hsa-let-7a-1	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7a-1	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7a-2	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7a-2	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7a-3	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7a-3	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7b	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7b	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7c	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7c	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7d	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7d	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7e	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7e	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7f-1	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7f-1	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7f-2	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7f-2	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7g	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7g	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7i	Colonic Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-let-7i	Lung Neoplasms	17965831	"Furthermore, a reduction in the expression of let-7 was associated with lung cancers and in particular with reduced survival./ Mayr et al. demonstrated that a chromosomal translocation at 12q5 disrupts let-7 expression and consequently curtails inhibition of the oncogene High Mobility Group A2 (Hmga2). Let-7 has also been implicated in the development of colon cancers and the progression of colorectal cancers."
hsa-mir-1-2	Heart Defects, Congenital	17397913	deletion
hsa-mir-125b-1	Leukemia, B-Cell	16885332	In a precursor B-cell acute lymphoblastic leukemia, an insertion of miR-125b-1 into a rearranged immunoglobulin heavy chain locus was described.
hsa-mir-125b-1	Leukemia, B-Cell	17028302	It is of note that insertion of miR-125b-1 into a rearranged immunoglobulin heavy chain gene locus was recently reported in a patient with precursor B-cell acute lymphoblastic leukemia, though the expression miR-125b-1 was not investigated.
hsa-mir-125b-1	Lung Neoplasms	14973191	deletion
hsa-mir-125b-1	Ovarian Neoplasms	14973191	deletion
hsa-mir-125b-1	Precursor B-Cell Lymphoblastic Leukemia-Lymphoma	16151463	an insertion of pre-miRNA into the immunoglobulin heavy-chain locus
hsa-mir-125b-1	Uterine Cervical Neoplasms	14973191	deletion
hsa-mir-142	Leukemia, B-Cell	16885332	It was shown later that miR-142 is located at the chromosome 17 breakpoint and that c-Myc was rearranged under the control of the promoter of miR-142 with consequent overexpression.
hsa-mir-146b	Thyroid Neoplasms	17468766	somatic mutations altering binding sites for miR-221, miR-222 and miR-146 have been observed in the 3?? UTR of the KIT oncogene in papillary thyroid carcinoma.
hsa-mir-15a	Breast Neoplasms	17012848	Later on, deletion of mir-16-1 and mir-15a deletion were also identified in epithelial tumors, such as pituitary adenomas, ovarian and breast cancer.
hsa-mir-15a	Leukemia	16166262	the deletion or downregulation of mir-15a results in increased expression of BCL2.
hsa-mir-15a	Leukemia	12434020	deletion or downregulation
hsa-mir-15a	Leukemia, B-Cell	16885332	Deleted and down-regulated in the majority of B-CLLs
hsa-mir-15a	Leukemia, Lymphocytic, Chronic, B-Cell	17965831	miR-15a and miR-16 are often deleted from chromosome 13q14.2 in patients with B cell CLL, suggesting that these miRNAs may be involved in tumour suppression. Additionally, introduction of exogenous miR-16 into a malignant B-1 cell line resulted in increased apoptosis.
hsa-mir-15a	Leukemia, Lymphocytic, Chronic, B-Cell	17940623	The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells.
hsa-mir-15a	Leukemia, Lymphocytic, Chronic, B-Cell	17012848	It was found that mir-16-1 and mir-15a at 13q14 are deleted in more than 50% patients, with concurrent reduced expression in ~65% patients. Further studies demonstrated that these two miRNAs suppress BCL2 expression and may serve as tumor suppressor genes in this disease.
hsa-mir-15a	Leukemia, Lymphocytic, Chronic, B-Cell	17234972	After years of futile attemptsto identify the gene(s) in the deleted 13q14 region that participatein the pathogenesis of chronic lymphocytic leukemia, Calin etal discovered that miR-15 and miR-16 are located within thissequence and that both are downregulated in  68% of cases.
hsa-mir-15a	Leukemia, Lymphocytic, Chronic, B-Cell	12434020	deletion or downregulation
hsa-mir-15a	Lymphoma	16166262	the deletion or downregulation of mir-15a results in increased expression of BCL2.
hsa-mir-15a	Lymphoma, Mantle-Cell	17940623	The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells.
hsa-mir-15a	Multiple Myeloma	17940623	The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells.
hsa-mir-15a	Pituitary Neoplasms	16885332	a type of benign tumors displaying deletions at 13q14.3 and reduced expression of miR-16-1 and miR-15a
hsa-mir-15a	Prostatic Neoplasms	17940623	The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells.
hsa-mir-15b	Leukemia, Lymphocytic, Chronic, B-Cell	17234972	After years of futile attemptsto identify the gene(s) in the deleted 13q14 region that participatein the pathogenesis of chronic lymphocytic leukemia, Calin etal discovered that miR-15 and miR-16 are located within thissequence and that both are downregulated in  68% of cases.
hsa-mir-16-1	Leukemia	16166262	the deletion or downregulation of mir-15a results in increased expression of BCL2.
hsa-mir-16-1	Leukemia	12434020	deletion or downregulation
hsa-mir-16-1	Leukemia, B-Cell	16885332	Deleted and down-regulated in the majority of B-CLLs
hsa-mir-16-1	Leukemia, Lymphocytic, Chronic, B-Cell	16251535	mutation
hsa-mir-16-1	Leukemia, Lymphocytic, Chronic, B-Cell	17012848	It was found that mir-16-1 and mir-15a at 13q14 are deleted in more than 50% patients, with concurrent reduced expression in ~65% patients. Further studies demonstrated that these two miRNAs suppress BCL2 expression and may serve as tumor suppressor genes in this disease.
hsa-mir-16-1	Leukemia, Lymphocytic, Chronic, B-Cell	17940623	The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells.
hsa-mir-16-1	Leukemia, Lymphocytic, Chronic, B-Cell	17234972	After years of futile attemptsto identify the gene(s) in the deleted 13q14 region that participatein the pathogenesis of chronic lymphocytic leukemia, Calin etal discovered that miR-15 and miR-16 are located within thissequence and that both are downregulated in  68% of cases.
hsa-mir-16-1	Leukemia, Lymphocytic, Chronic, B-Cell	17965831	miR-15a and miR-16 are often deleted from chromosome 13q14.2 in patients with B cell CLL, suggesting that these miRNAs may be involved in tumour suppression. Additionally, introduction of exogenous miR-16 into a malignant B-1 cell line resulted in increased apoptosis.
hsa-mir-16-1	Leukemia, Lymphocytic, Chronic, B-Cell	17028302	Detailed analyses of deletion and expression status revealed these two miRNAs to be located within a 30 kb minimally deleted region in chronic lymphocytic leukemia (CLL) patients, both of which were deleted or downregulated in most CLL cases, suggesting that miR-15a and miR-16-1 may function as tumor suppressor genes.
hsa-mir-16-1	Leukemia, Lymphocytic, Chronic, B-Cell	12434020	deletion or downregulation
hsa-mir-16-1	Lymphoma	16166262	the deletion or downregulation of mir-15a results in increased expression of BCL2.
hsa-mir-16-1	Lymphoma, Mantle-Cell	17940623	The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells.
hsa-mir-16-1	Multiple Myeloma	17940623	The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells.
hsa-mir-16-1	Ovarian Neoplasms	17012848	Later on, deletion of mir-16-1 and mir-15a deletion were also identified in epithelial tumors, such as pituitary adenomas, ovarian and breast cancer.
hsa-mir-16-1	Pituitary Neoplasms	16885332	a type of benign tumors displaying deletions at 13q14.3 and reduced expression of miR-16-1 and miR-15a
hsa-mir-16-1	Pituitary Neoplasms	17012848	Later on, deletion of mir-16-1 and mir-15a deletion were also identified in epithelial tumors, such as pituitary adenomas, ovarian and breast cancer.
hsa-mir-16-1	Prostatic Neoplasms	17940623	The common loss of miR-15a and miR-16-1 in CLL, as well as the loss of 13q14 in mantle cell lymphoma (50 percent of cases), multiple myeloma (16 to 40 percent) and prostate cancer (60 percent), strongly suggests that these two miRNAs act as tumor suppressor genes. While their full target complement is unknown, they appear to mediate their effects largely by down-regulating the anti-apoptotic protein BCL2. This protein is often found expressed at high levels in CLL and is thought to be important for the survival of the malignant cells.
hsa-mir-16-2	Leukemia, Lymphocytic, Chronic, B-Cell	17965831	miR-15a and miR-16 are often deleted from chromosome 13q14.2 in patients with B cell CLL, suggesting that these miRNAs may be involved in tumour suppression. Additionally, introduction of exogenous miR-16 into a malignant B-1 cell line resulted in increased apoptosis.
hsa-mir-17	Breast Neoplasms	16940181	The genomic location of Mir-17-5p also undergoesloss of heterozygosity in different types of cancer, including breast cancer.
hsa-mir-17	Carcinoma, Hepatocellular	15944709	loss of heterozygosity of this cluster
hsa-mir-17	Colonic Neoplasms	17965831	The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation.
hsa-mir-17	Hematologic Neoplasms	17011485	The miR-17-92 cluster is amplified in hematopoietic malignancies.
hsa-mir-17	Lymphoma	16940181	Mir-17-5p, also known as Mir-91,is located on chromosome 13q31; this gene is amplified in childhoodlymphoma.
hsa-mir-181b-2	Urinary Bladder Neoplasms	17470785	mir-181b-2 and mir-199b are 3.3 Mb from the peak of the colon Scc2 locus on Chr 2; homologous human miRNAs are located inside a cancer-associated genomic region, which is a region commonly deleted in bladder cancer.
hsa-mir-18a	Carcinoma, Hepatocellular	15944709	loss of heterozygosity of this cluster
hsa-mir-198	Schizophrenia	17849003	SNP (rs1700) disease susceptibility
hsa-mir-199a-1	Carcinoma, Hepatocellular	17188425	This region encodes miRNA-199a-1 (19p13.2), whose expression levels are lower in HCC compared to nontumor liver [59] and is deleted in several other tumor types.
hsa-mir-199b	Urinary Bladder Neoplasms	17470785	mir-181b-2 and mir-199b are 3.3 Mb from the peak of the colon Scc2 locus on Chr 2; homologous human miRNAs are located inside a cancer-associated genomic region, which is a region commonly deleted in bladder cancer.
hsa-mir-19a	Hematologic Neoplasms	17011485	The miR-17-92 cluster is amplified in hematopoietic malignancies.
hsa-mir-19a	Lung Neoplasms	17965831	The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation.
hsa-mir-19b-1	Carcinoma, Hepatocellular	15944709	loss of heterozygosity of this cluster
hsa-mir-19b-1	Hematologic Neoplasms	17011485	The miR-17-92 cluster is amplified in hematopoietic malignancies.
hsa-mir-19b-1	Lung Neoplasms	17965831	The miRNA cluster miR-17-92 is located at 13q31.3 and has been associated with several types of cancer, including colorectal cancer and lung cancer, and is thought to be a potential oncogene [86, 87] that enhances cell proliferation.
hsa-mir-206	Schizophrenia	17849003	SNP (rs17578796) disease susceptibility
hsa-mir-20a	Hematologic Neoplasms	17011485	The miR-17-92 cluster is amplified in hematopoietic malignancies.
hsa-mir-215	Uterine Cervical Neoplasms	17470785	The list of miRNAs at or near sites commonly altered in human cancers includes mir-215 and mir-194-1, which are <0.17 kb from D1Mit208, a marker that defines the peak of the colon Scc3 locus on Chr 1. Homologous human miRNAs are located inside the FRA1H at Chr 1q42.1; this fragile site is an HPV16 integration site involved in cervical cancer.
hsa-mir-221	Thyroid Neoplasms	17468766	somatic mutations altering binding sites for miR-221, miR-222 and miR-146 have been observed in the 3?? UTR of the KIT oncogene in papillary thyroid carcinoma.
hsa-mir-222	Thyroid Neoplasms	17468766	somatic mutations altering binding sites for miR-221, miR-222 and miR-146 have been observed in the 3?? UTR of the KIT oncogene in papillary thyroid carcinoma.
hsa-mir-24-1	Tourette Syndrome	17462786	A mutation in the 3'UTR of the SLITRK1 gene which is associated with Tourette's syndrome was found to enhance repression of the SLITRK mRNA by miR-189, presumably preventing SLITRK1's promotion of dendritic growth.
hsa-mir-29a	Neoplasms	17965831	Many miRNAs are located at chromosomal break points or fragile sites associated with cancer. Indeed miR-29a and miR-29b are associated with the fragile site FRA7H. In addition, miR-29b along with miR-181b may target the oncogene TCL1 in CLL patients [163], while miR-29b reduced Mcl-1 protein and rendered cholangiocarcinoma cells more susceptible to apoptosis.
hsa-mir-29b-1	Neoplasms	17965831	Many miRNAs are located at chromosomal break points or fragile sites associated with cancer. Indeed miR-29a and miR-29b are associated with the fragile site FRA7H. In addition, miR-29b along with miR-181b may target the oncogene TCL1 in CLL patients [163], while miR-29b reduced Mcl-1 protein and rendered cholangiocarcinoma cells more susceptible to apoptosis.
hsa-mir-92a-1	Hematologic Neoplasms	17011485	The miR-17-92 cluster is amplified in hematopoietic malignancies.
hsa-mir-29a	Alzheimer Disease	18434550	loss
hsa-mir-29b-1	Alzheimer Disease	18434550	loss
hsa-mir-296	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-1-1	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-133a-2	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-153-2	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-339	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-103a-2	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-106b	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-25	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-93	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-219-1	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-135b	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-194-1	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-215	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-338	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-199a-2	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-214	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-151a	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-30b	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-30d	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-200a	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-200b	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-429	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-9-1	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-488	Ovarian Neoplasms	16754881	copy number gain
hsa-mir-296	Breast Neoplasms	16754881	copy number gain
hsa-mir-1-1	Breast Neoplasms	16754881	copy number gain
hsa-mir-133a-2	Breast Neoplasms	16754881	copy number gain
hsa-mir-153-2	Breast Neoplasms	16754881	copy number gain
hsa-mir-339	Breast Neoplasms	16754881	copy number gain
hsa-mir-103a-2	Breast Neoplasms	16754881	copy number gain
hsa-mir-106b	Breast Neoplasms	16754881	copy number gain
hsa-mir-25	Breast Neoplasms	16754881	copy number gain
hsa-mir-93	Breast Neoplasms	16754881	copy number gain
hsa-mir-219-1	Breast Neoplasms	16754881	copy number gain
hsa-mir-135b	Breast Neoplasms	16754881	copy number gain
hsa-mir-194-1	Breast Neoplasms	16754881	copy number gain
hsa-mir-215	Breast Neoplasms	16754881	copy number gain
hsa-mir-338	Breast Neoplasms	16754881	copy number gain
hsa-mir-199a-2	Breast Neoplasms	16754881	copy number gain
hsa-mir-214	Breast Neoplasms	16754881	copy number gain
hsa-mir-151a	Breast Neoplasms	16754881	copy number gain
hsa-mir-30b	Breast Neoplasms	16754881	copy number gain
hsa-mir-30d	Breast Neoplasms	16754881	copy number gain
hsa-mir-200a	Breast Neoplasms	16754881	copy number gain
hsa-mir-200b	Breast Neoplasms	16754881	copy number gain
hsa-mir-429	Breast Neoplasms	16754881	copy number gain
hsa-mir-9-1	Breast Neoplasms	16754881	copy number gain
hsa-mir-488	Breast Neoplasms	16754881	copy number gain
hsa-mir-296	Melanoma	16754881	copy number gain
hsa-mir-1-1	Melanoma	16754881	copy number gain
hsa-mir-133a-2	Melanoma	16754881	copy number gain
hsa-mir-153-2	Melanoma	16754881	copy number gain
hsa-mir-339	Melanoma	16754881	copy number gain
hsa-mir-103a-2	Melanoma	16754881	copy number gain
hsa-mir-106b	Melanoma	16754881	copy number gain
hsa-mir-25	Melanoma	16754881	copy number gain
hsa-mir-93	Melanoma	16754881	copy number gain
hsa-mir-219-1	Melanoma	16754881	copy number gain
hsa-mir-135b	Melanoma	16754881	copy number gain
hsa-mir-194-1	Melanoma	16754881	copy number gain
hsa-mir-215	Melanoma	16754881	copy number gain
hsa-mir-338	Melanoma	16754881	copy number gain
hsa-mir-199a-2	Melanoma	16754881	copy number gain
hsa-mir-214	Melanoma	16754881	copy number gain
hsa-mir-151a	Melanoma	16754881	copy number gain
hsa-mir-30b	Melanoma	16754881	copy number gain
hsa-mir-30d	Melanoma	16754881	copy number gain
hsa-mir-200a	Melanoma	16754881	copy number gain
hsa-mir-200b	Melanoma	16754881	copy number gain
hsa-mir-429	Melanoma	16754881	copy number gain
hsa-mir-9-1	Melanoma	16754881	copy number gain
hsa-mir-488	Melanoma	16754881	copy number gain
hsa-mir-302a	Melanoma	16754881	copy number loss
hsa-mir-302b	Melanoma	16754881	copy number loss
hsa-mir-302c	Melanoma	16754881	copy number loss
hsa-mir-302d	Melanoma	16754881	copy number loss
hsa-mir-367	Melanoma	16754881	copy number loss
hsa-mir-218-1	Melanoma	16754881	copy number loss
hsa-mir-383	Melanoma	16754881	copy number loss
hsa-mir-17	Melanoma	16754881	copy number loss
hsa-mir-18a	Melanoma	16754881	copy number loss
hsa-mir-19a	Melanoma	16754881	copy number loss
hsa-mir-19b-1	Melanoma	16754881	copy number loss
hsa-mir-20a	Melanoma	16754881	copy number loss
hsa-mir-320a	Melanoma	16754881	copy number loss
hsa-mir-302a	Breast Neoplasms	16754881	copy number loss
hsa-mir-302b	Breast Neoplasms	16754881	copy number loss
hsa-mir-302c	Breast Neoplasms	16754881	copy number loss
hsa-mir-302d	Breast Neoplasms	16754881	copy number loss
hsa-mir-367	Breast Neoplasms	16754881	copy number loss
hsa-mir-218-1	Breast Neoplasms	16754881	copy number loss
hsa-mir-383	Breast Neoplasms	16754881	copy number loss
hsa-mir-17	Breast Neoplasms	16754881	copy number loss
hsa-mir-18a	Breast Neoplasms	16754881	copy number loss
hsa-mir-19a	Breast Neoplasms	16754881	copy number loss
hsa-mir-19b-1	Breast Neoplasms	16754881	copy number loss
hsa-mir-20a	Breast Neoplasms	16754881	copy number loss
hsa-mir-320a	Breast Neoplasms	16754881	copy number loss
hsa-mir-302a	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-302b	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-302c	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-302d	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-367	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-218-1	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-383	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-17	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-18a	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-19a	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-19b-1	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-20a	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-320a	Ovarian Neoplasms	16754881	copy number loss
hsa-mir-146a	Breast Neoplasms	18634034	miR-146: rs2910164 were associated with increased risk of breast cancer in Chinese women
hsa-mir-146a	Breast Neoplasms	18660546	miR-146a: A functional polymorphism (rs2910164) in the miR-146a gene and age of familial breast/ovarian cancer diagnosis
hsa-mir-146b	Breast Neoplasms	18634034	miR-146: rs2910164 were associated with increased risk of breast cancer in Chinese women
hsa-mir-149	Breast Neoplasms	18634034	miR-149: rs2292832 were associated with increased risk of breast cancer in Chinese women
hsa-mir-17	Breast Neoplasms	19048628	miR-17: mutations
hsa-mir-196a-2	Breast Neoplasms	18634034	miR-196a-2: rs11614913 were associated with increased risk of breast cancer in Chinese women
hsa-mir-499a	Breast Neoplasms	18634034	miR-499: rs3746444 were associated with increased risk of breast cancer in Chinese women
hsa-mir-101-1	Neoplasms	19008416	miR-101: Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer
hsa-mir-101-2	Neoplasms	19008416	miR-101: Genomic loss of microRNA-101 leads to overexpression of histone methyltransferase EZH2 in cancer
hsa-mir-34a	Neoplasms	18834855	miR-34a: reduced or lost
hsa-mir-659	Dementia	18723524	miR-659: Common variation in the miR-659 binding-site of GRN is a major risk factor for TDP43-positive frontotemporal dementia
hsa-mir-146a	Carcinoma, Hepatocellular	18711148	miR-146a: A functional polymorphism (rs2910164) in the miR-146a gene is associated with the risk for hepatocellular carcinoma
hsa-let-7a-1	Lung Neoplasms	18922928	let-7a: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7a-2	Lung Neoplasms	18922928	let-7a: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7a-3	Lung Neoplasms	18922928	let-7a: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7b	Lung Neoplasms	18922928	let-7b: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7c	Lung Neoplasms	18922928	let-7c: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7d	Lung Neoplasms	18922928	let-7d: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7e	Lung Neoplasms	18922928	let-7e: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7f-1	Lung Neoplasms	18922928	let-7f: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7f-2	Lung Neoplasms	18922928	let-7f: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7g	Lung Neoplasms	18922928	let-7g: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-let-7i	Lung Neoplasms	18922928	let-7i: A SNP in a let-7 microRNA complementary site in the KRAS 3' untranslated region increases non-small cell lung cancer risk
hsa-mir-96	Hearing Loss	19363479	miR-96: Mutations in the seed region
hsa-mir-146a	Ovarian Neoplasms	18660546	miR-146a: A functional polymorphism (rs2910164) in the miR-146a gene and age of familial breast/ovarian cancer diagnosis
hsa-mir-146a	Thyroid Neoplasms	19164563	miR-146a: SNP rs2910164 contribute to thyroid cancer
hsa-mir-128-2	Precursor Cell Lymphoblastic Leukemia-Lymphoma	20237425	A novel mutation in the miR-128b gene reduces miRNA processing and leads to glucocorticoid resistance of MLL-AF4 acute lymphocytic leukemia cells.
hsa-mir-196a-1	Glioma	20229273	A polymorphism of microRNA196a genome region was associated with decreased risk of glioma in Chinese population
hsa-mir-196a-2	Glioma	20229273	A polymorphism of microRNA196a genome region was associated with decreased risk of glioma in Chinese population
hsa-mir-191	Ovarian Neoplasms	20167074	Novel genetic variants in miR-191 gene and familial ovarian cancer
hsa-mir-125b-1	Leukemia, Biphenotypic, Acute	20485370	miR-125b-1:A new recurrent translocation t(11;14)(q24;q32) involving IGH@ and miR-125b-1 in B-cell progenitor acute lymphoblastic leukemia
hsa-mir-126	Precursor Cell Lymphoblastic Leukemia-Lymphoma	20621067	miR-126:Alteration of processing induced by a single nucleotide polymorphism in pri-miR-126
hsa-mir-143	Neoplasms	20439436	miR-143:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-145	Neoplasms	20439436	miR-145:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-15a	Multiple Myeloma	20031211	miR-15a:Micro-RNA-15a and micro-RNA-16 expression and chromosome 13 deletions in multiple myeloma
hsa-mir-16-1	Multiple Myeloma	20031211	miR-16:Micro-RNA-15a and micro-RNA-16 expression and chromosome 13 deletions in multiple myeloma
hsa-mir-16-2	Multiple Myeloma	20031211	miR-16:Micro-RNA-15a and micro-RNA-16 expression and chromosome 13 deletions in multiple myeloma
hsa-mir-122	Hypertension	19067360	a polymorphism of the 3'UTR of the SLC7A1 gene affects the binding with miR-122
hsa-mir-196a-2	Stomach Neoplasms	19834808	miR-196a-2:Association of microRNA-196a-2 gene polymorphism with gastric cancer risk
hsa-mir-30e	Schizophrenia	20347265	miR-30e:mir-30e ss178077483 plays a role in schizophrenia susceptibility
hsa-mir-34a	Leukemia, Lymphocytic, Chronic, B-Cell	20393129	miR-34a:We found that miR-15a, miR-21, miR-34a, miR-155, and miR-181b were differentially expressed between CLLs with chromosome 17p deletion and CLLs with normal 17p and normal karyotype, and that miR-181b was down-regulated in therapy-refractory cases
hsa-mir-451a	Erythropoiesis	20424607	miR-451:a loss of miR-451, a small RNA important for erythropoiesis
hsa-mir-17	Neoplasms	20439436	mir-17:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-18a	Neoplasms	20439436	mir-18a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-19a	Neoplasms	20439436	mir-19a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-19b-1	Neoplasms	20439436	mir-19b:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-19b-2	Neoplasms	20439436	mir-19b:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-204	Neoplasms	20439436	miR-204:hsa-miR-30 and hsa-miR-204, were found to be physically altered at the DNA copy number level as well
hsa-mir-20a	Neoplasms	20439436	mir-20a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-92a-1	Neoplasms	20439436	mir-92a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-92a-2	Neoplasms	20439436	mir-92a:We correctly identified hsa-miR-17/92 family as amplified and the hsa-miR-143/145 cluster as deleted
hsa-mir-196a-2	Cardiomyopathy, Dilated	20488170	mir-196a2:Common genetic polymorphisms in pre-microRNAs were associated with increased risk of dilated cardiomyopathy
hsa-mir-499a	Cardiomyopathy, Dilated	20488170	mir-499:Common genetic polymorphisms in pre-microRNAs were associated with increased risk of dilated cardiomyopathy
hsa-mir-27a	Stomach Neoplasms	20666778	mir-27a:mir-27a genetic variant contributes to gastric cancer susceptibility
hsa-mir-491	Colorectal Neoplasms	21128281	deleted
hsa-mir-646	Colorectal Neoplasms	21128281	deleted
hsa-mir-17	Breast Neoplasms	21140207	SNP (rs3739008) located at 3'UTR of NPAS2 and the C to T changing of the SNP may disrupt the binding of microRNA- (miR-)17-5p and miR-519e to the 3'UTR of NPAS2
hsa-mir-519e	Breast Neoplasms	21140207	SNP (rs3739008) located at 3'UTR of NPAS2 and the C to T changing of the SNP may disrupt the binding of microRNA- (miR-)17-5p and miR-519e to the 3'UTR of NPAS2
hsa-mir-15a	Leukemia, Lymphocytic, Chronic, B-Cell	21156224	often absent
hsa-mir-16-1	Leukemia, Lymphocytic, Chronic, B-Cell	21156224	often absent
hsa-mir-569	Lupus Erythematosus, Systemic	21162035	Association of a functional polymorphism in the 3' untranslated region of SPI1 with systemic lupus erythematosus.
hsa-mir-196a-2	Colorectal Neoplasms	21241442	A variant ( rs11614913 ) in microRNA-196a2 is not associated with susceptibility to and progression of colorectal cancer in Chinese.
hsa-mir-196a-1	Crohn Disease	21278745	The common exonic synonymous SNP (c.313C>T) in IRGM alters a binding site for miR-196 and causes deregulation of IRGM-dependent xenophagy in Crohn's disease.
hsa-mir-196a-2	Crohn Disease	21278745	The common exonic synonymous SNP (c.313C>T) in IRGM alters a binding site for miR-196 and causes deregulation of IRGM-dependent xenophagy in Crohn's disease.
hsa-mir-196b	Crohn Disease	21278745	The common exonic synonymous SNP (c.313C>T) in IRGM alters a binding site for miR-196 and causes deregulation of IRGM-dependent xenophagy in Crohn's disease.
hsa-mir-200b	Neoplasms	21292642	Depletion of miR-200 in arsenite-transformed cells involved induction of the EMT-inducing transcription factors ZEB1 (zinc-finger E-box-binding homeobox factor 1) and ZEB2 and increased methylation of miR-200 promoters.
hsa-mir-124-1	Breast Neoplasms	21318219	Genetic variants (SNP rs1042538 A/T) at the miR-124 binding site on the cytoskeleton-organizing IQGAP1 gene confer differential predisposition to breast cancer.
hsa-mir-124-2	Breast Neoplasms	21318219	Genetic variants (SNP rs1042538 A/T) at the miR-124 binding site on the cytoskeleton-organizing IQGAP1 gene confer differential predisposition to breast cancer.
hsa-mir-124-3	Breast Neoplasms	21318219	Genetic variants (SNP rs1042538 A/T) at the miR-124 binding site on the cytoskeleton-organizing IQGAP1 gene confer differential predisposition to breast cancer.
hsa-mir-499a	Esophageal Neoplasms	21319225	SNP (rs3746444 A/G): Significantly increased CSCC risks were found to be associated with G allele of rs3746444
hsa-mir-146a	Esophageal Neoplasms	21319225	SNP (rs2910164 G/C): Significantly increased CSCC risks were found to be associated with G allele of rs2910164
hsa-mir-499a	Carcinoma, Squamous Cell	21319225	SNP (rs3746444 A/G): Significantly increased CSCC risks were found to be associated with G allele of rs3746444
hsa-mir-146a	Carcinoma, Squamous Cell	21319225	SNP (rs2910164 G/C): Significantly increased CSCC risks were found to be associated with G allele of rs2910164
hsa-mir-569	Lupus Erythematosus, Systemic	21360505	rs1057233 alters a target sequence for microRNA hsa-miR-569 (miR-569).
hsa-mir-18a	Urinary Bladder Neoplasms	21388952	Specific deletion of p53 in urothelial cells is associated with specific overexpression of miR-18a and miR-19a and down-regulation of miR-107.
hsa-mir-19a	Urinary Bladder Neoplasms	21388952	Specific deletion of p53 in urothelial cells is associated with specific overexpression of miR-18a and miR-19a and down-regulation of miR-107.
hsa-mir-107	Urinary Bladder Neoplasms	21388952	Specific deletion of p53 in urothelial cells is associated with specific overexpression of miR-18a and miR-19a and down-regulation of miR-107.
hsa-mir-328	Myopia	21421876	SNPs rs644242 and rs662702 had marginal significance (p=0.063) and further analyses showed that these SNPs were associated with extreme myopia. The OR for extreme myopia was 2.1 (empirical p=0.007) for the CC genotype at SNP rs662702 at 3' UTR. The functional assay for SNP rs662702 demonstrated that the C allele had a significantly lower expression level than the T allele (P=0.0001). SNP rs662702 was predicted to be located in the microRNA-328 binding site, which may explain the differential allelic effect on gene expression.
hsa-let-7a-1	Ovarian Neoplasms	21482675	rs12194974 (G>A), a SNP in a putative transcription factor binding site in the LIN28B promoter region (summary OR=0.90, 95% CI: 0.82-0.98; P=0.015). LIN28B LIN28B over-expression in epithelial ovarian cancer (EOC) contributes to tumorigenesis by repressing tumor suppressor let-7 expression.
hsa-let-7a-2	Ovarian Neoplasms	21482675	rs12194974 (G>A), a SNP in a putative transcription factor binding site in the LIN28B promoter region (summary OR=0.90, 95% CI: 0.82-0.98; P=0.015). LIN28B LIN28B over-expression in epithelial ovarian cancer (EOC) contributes to tumorigenesis by repressing tumor suppressor let-7 expression.
hsa-let-7a-3	Ovarian Neoplasms	21482675	rs12194974 (G>A), a SNP in a putative transcription factor binding site in the LIN28B promoter region (summary OR=0.90, 95% CI: 0.82-0.98; P=0.015). LIN28B LIN28B over-expression in epithelial ovarian cancer (EOC) contributes to tumorigenesis by repressing tumor suppressor let-7 expression.
hsa-mir-196a-2	Breast Neoplasms	21483822	rs11614913 polymorphism:Overall, individuals with the TC/CC genotypes were associated with higher cancer risk than those with the TT genotype (OR?=?1.18, 95% CI?=?1.03-1.34, P<0.001 for heterogeneity test). In the stratified analyses, we observed that the CC genotype might modulate breast cancer risk (OR?=?1.11, 95%CI?=?1.01-1.23, P(heterogeneity)?=?0.210) and lung cancer risk (OR?=?1.25, 95%CI?=?1.06-1.46, P(heterogeneity)?=?0.958), comparing with the TC/TT genotype. Moreover, a significantly increased risk was found among Asian populations in a dominant model (TC/CC versus TT, OR?=?1.24, 95% CI?=?1.07-1.43, P(heterogeneity)?=?0.006).
hsa-mir-196a-2	Lung Neoplasms	21483822	rs11614913 polymorphism:Overall, individuals with the TC/CC genotypes were associated with higher cancer risk than those with the TT genotype (OR?=?1.18, 95% CI?=?1.03-1.34, P<0.001 for heterogeneity test). In the stratified analyses, we observed that the CC genotype might modulate breast cancer risk (OR?=?1.11, 95%CI?=?1.01-1.23, P(heterogeneity)?=?0.210) and lung cancer risk (OR?=?1.25, 95%CI?=?1.06-1.46, P(heterogeneity)?=?0.958), comparing with the TC/TT genotype. Moreover, a significantly increased risk was found among Asian populations in a dominant model (TC/CC versus TT, OR?=?1.24, 95% CI?=?1.07-1.43, P(heterogeneity)?=?0.006).
hsa-mir-218-1	Urinary Bladder Neoplasms	21519788	miR-218 on the genomic loss region of chromosome 4p15.31 functions as a tumor suppressor in bladder cancer.
hsa-mir-218-2	Urinary Bladder Neoplasms	21519788	miR-218 on the genomic loss region of chromosome 4p15.31 functions as a tumor suppressor in bladder cancer.
hsa-mir-499a	Tuberculosis, Pulmonary	21524676	There was no association between rs3746444 (in hsa-mir-499) and PTB risk (p = 0.118) in the Han population, but subjects carrying the C allele exhibited decreased PTB risk (odds ratio [OR] = 0.403 [95% confidence interval (95% CI) 0.278-0.583]). There was an association between rs3746444 and PTB in the Tibetan population, and individuals carrying the C allele exhibited increased PTB risk (OR = 1.870 [95% CI 1.218-2.871]).
hsa-mir-146a	Tuberculosis, Pulmonary	21524676	A polymorphism (rs2910164 G>C, in miR-146a) indicated an association with PTB risk in both Tibetan (p = 0.031) and Han (p = 0.000) populations. However, the role of the G allele of rs2910164, like the C allele in rs3746444, differed in the Tibetan (OR = 1.509, p < 0.05) and Han (OR = 0.575, p < 0.05) groups.
hsa-mir-146a	Uterine Cervical Neoplasms	21529907	Polymorphism (rs2910164) of the pre-miR-146a is associated with risk of cervical cancer in a Chinese population. The subjects carrying GG homozygote had a 1.496-foldincreased risk than those carrying CG/CC genotypes. The carriers of GG genotype had obviously more reduced miR-146a expression level compared with the carriers of CC genotype.
hsa-mir-125b-1	Prostatic Neoplasms	21556765	rs1434536 in the 3'UTR of BMPR1B gene affects the binding ability of miR-125b to BMPR1B mRNA and contributes to the genetic hspredisposition to localized prostate cancer and patients aged >70years.
hsa-mir-125b-2	Prostatic Neoplasms	21556765	rs1434536 in the 3'UTR of BMPR1B gene affects the binding ability of miR-125b to BMPR1B mRNA and contributes to the genetic hspredisposition to localized prostate cancer and patients aged >70years.
hsa-mir-637	Hypertension	21558123	A common genetic variant (rs938671) in the 3'-UTR of Vacuolar H+-ATPase ATP6V0A1 creates a micro-RNA (hsa-miR-637) motif to alter Chromogranin A (CHGA) processing and hypertension risk.
hsa-mir-519a-1	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-519a-2	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-519b	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-519c	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-519d	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-519e	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-520a	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-520b	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-520e	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-520d	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-520f	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-520g	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-520h	Gout	21558165	There was a clear link between the rs1333049 genotypic and allelic frequencies between gout cases and controls. There was a significantly increased risk of gout in carriers of the CC genotype.This SNP is homologous to miR-519 and miR-520.
hsa-mir-196a-2	Pulmonary Disease, Chronic Obstructive	21565178	The TT genotype and T allele of miR-196a2 rs11614913 were significantly associated with a decreased risk for COPD (Chronic obstructive pulmonary disease), compared with the CC genotype and C allele. Similarly, the GG genotype and G allele of miR-499 rs3746444 were associated with a decreased risk for COPD, compared with the AA genotype and A allele.
hsa-mir-499a	Pulmonary Disease, Chronic Obstructive	21565178	The TT genotype and T allele of miR-196a2 rs11614913 were significantly associated with a decreased risk for COPD (Chronic obstructive pulmonary disease), compared with the CC genotype and C allele. Similarly, the GG genotype and G allele of miR-499 rs3746444 were associated with a decreased risk for COPD, compared with the AA genotype and A allele.
hsa-mir-196a-2	Colorectal Neoplasms	21565628	A Functional Variant in MicroRNA-196a2 (rs11614913 SNP) Is Associated with Susceptibility of Colorectal Cancer in a Chinese Population.
hsa-mir-1302-1	Infertility, Male	21601192	Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro.
hsa-mir-1302-2	Infertility, Male	21601192	Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro.
hsa-mir-1302-3	Infertility, Male	21601192	Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro.
hsa-mir-1302-4	Infertility, Male	21601192	Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro.
hsa-mir-1302-5	Infertility, Male	21601192	Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro.
hsa-mir-1302-6	Infertility, Male	21601192	Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro.
hsa-mir-1302-7	Infertility, Male	21601192	Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro.
hsa-mir-1302-8	Infertility, Male	21601192	Two SNPs from two genes (rs6631 of CGA and rs2303846 of CPEB1)(binding sites of miR-1302) were found to be associated with idiopathic male infertility. Functionally, the substitution of A by T in rs6631 results in decreased binding affinity of miR-1302 and overexpression of CGA in vitro.
hsa-mir-196a-2	Hepatitis C	21604580	SNP rs11614913 on miR196a-2 gene is associated with  the antiviral therapy efficacy of hepatitis C patients.The TT genotype or T alleles be associated with the SVR while the CC genotype or C allele could be related to the NVR or recurrence.
hsa-mir-196a-2	Carcinoma, Non-Small-Cell Lung	21617338	MicroRNA196a2 rs11614913 Genotypes are associated with the Risk of Non-Small Cell Lung Cancer in Korean Population.
hsa-mir-492	Psoriasis	21655935	The rs8259 T allele was associated with significantly decreased psoriasis susceptibility (OR?=?0.758, 95% CI 0.638-0.901, p?=?0.002) compared to A allele. the rs8259 polymorphism was located in a seed region for miR-492 binding.
hsa-mir-1827	Carcinoma, Small Cell	21676885	Genetic Variation in an miRNA-1827 Binding Site in MYCL1 Alters Susceptibility to Small-Cell Lung Cancer. The rs3134615T allele was associated with a significantly increased risk of SCLC, with the OR for carrying the GT or TT genotype being 2.08 (95% confidence interval, 1.39-3.21; P = 0.0004) compared with the GG genotype.
hsa-mir-146a	Lupus Erythematosus, Systemic	21738483	A functional variant in microRNA-146a promoter modulates its expression and confers disease risk for systemic lupus erythematosus.
hsa-mir-146a	Glioblastoma	21744077	A functional polymorphism in the pre-miR-146a gene is associated with risk and prognosis in adult glioma. An increased glioma risk was observed among rs2910164 minor allele (C) carriers (per allele OR (95%CI)?=?1.22 (1.01-1.46, p (trend)?=?0.039)). The association was stronger among older subjects carrying at least one copy of the C allele (OR (95% CI)?=?1.38 (1.04-1.83, P?=?0.026). Mortality was increased among minor allele carriers (HR(95% CI)=1.33 (1.03-1.72, P?=?0.029)), with the association largely restricted to females (HR (95% CI)=2.02 (1.28-3.17, P=0.002)).
hsa-mir-155	Hepatitis C	21750860	Coordinated increase of miRNA-155 and miRNA-196b expression correlates with the detection of the antigenomic strand of hepatitis C virus in peripheral blood mononuclear cells.
hsa-mir-196b	Hepatitis C	21750860	Coordinated increase of miRNA-155 and miRNA-196b expression correlates with the detection of the antigenomic strand of hepatitis C virus in peripheral blood mononuclear cells.
hsa-mir-155	Hypertrophy	21771600	the C allele of rs5186 was associated with a significant increase in SWT (p=0.003) and LVM (p=0.001). This functional polymorphism increases expression of AGTR1 by altering the binding site for miR-155
hsa-mir-155	Hypertrophy	21771600	A polymorphic miR-155 binding site ( rs5186) in AGTR1 is associated with cardiac hypertrophy in Friedreich ataxia.
hsa-mir-125a	Abortion, Habitual	21788734	Two common SNPs (rs41275794, rs12976445) in pri-miR-125a alter the mature miRNA expression and associate with Abortion, Habitual in a Han-Chinese population.
hsa-mir-186	Medulloblastoma	21793975	deletion
hsa-mir-135a-1	Medulloblastoma	21793975	deletion
hsa-mir-548d-1	Medulloblastoma	21793975	deletion
hsa-mir-548d-2	Medulloblastoma	21793975	deletion
hsa-mir-512-2	Medulloblastoma	21793975	deletion. Antisense-based knockdown of miR-512-5p (mature sequence of miR-512-2) resulted in significant upregulation of MYCC expression in HeLa and A549 cells, while forced overexpression of miR-512-2 in medulloblastoma/PNET cell lines DAOY, UW-228-2, PFSK resulted in downregulation of MYCC protein.
hsa-mir-135a-2	Medulloblastoma	21793975	deletion or amplification
hsa-mir-135b	Medulloblastoma	21793975	deletion or amplification
hsa-mir-33b	Medulloblastoma	21793975	deletion, amplification or a mutation at the precursor miRNA
hsa-mir-132	Supranuclear Palsy, Progressive	21807765	MicroRNA-132 loss is associated with tau exon 10 inclusion in Supranuclear Palsy, Progressive.
hsa-mir-367	Breast Neoplasms	21810988	Functional SNP (rs1044129, is present in binding region) in the microRNA-367 binding site in the 3'UTR of the calcium channel ryanodine receptor gene 3 (RYR3) affects breast cancer risk and calcification.
hsa-mir-196a-2	Colorectal Neoplasms	21815818	A Functional Polymorphism (rs11614913 (T>C)) in miRNA-196a2 Is Associated with Colorectal Cancer Risk in a Chinese Population.
hsa-mir-542	Colorectal Neoplasms	21822307	A common single-nucleotide polymorphism (T8473CA) in cyclooxygenase-2 disrupts microRNA (miR-542-3p)-mediated regulation.
hsa-mir-637	Hypertension	21846868	ATP6V0A1 Polymorphism and MicroRNA-637 may have A Pathogenetic Role for MicroRNAs in Essential Hypertension.
hsa-mir-101-1	Lung Neoplasms	21849855	miR-101 DNA Copy Loss is a Prominent Subtype Specific Event in Lung Cancer.
hsa-mir-101-2	Lung Neoplasms	21849855	miR-101 DNA Copy Loss is a Prominent Subtype Specific Event in Lung Cancer.
hsa-mir-17	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-18a	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-19a	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-20a	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-19b-1	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-92a-1	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-17	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-18a	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-19a	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-20a	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-19b-1	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-92a-1	Musculoskeletal Abnormalities	21892160	Germline deletion of the miR-17-92 cluster causes skeletal and growth defects in humans.
hsa-mir-137	Schizophrenia	21926974	GWAS analysis revealed that rs1625579 within an intron of a putative primary transcript for MIR137 (microRNA 137), a known regulator of neuronal development was associated with schizophrenia.
hsa-mir-101-1	Pancreatic Neoplasms	21932133	Loss of MicroRNA-101 Promotes Overexpression of Histone Methyltransferase EZH2.
hsa-mir-101-2	Pancreatic Neoplasms	21932133	Loss of MicroRNA-101 Promotes Overexpression of Histone Methyltransferase EZH2.
hsa-mir-184	Carcinoma, Squamous Cell	21934093	The authors found that, compared with the rs8126 TT (a SNP of miR-184 Binding Site in TNFAIP2) genotype, the variant C allele were associated with increased SCCHN risk in an allele-dose response manner (adjusted odds ratio=1.48 and 95% confidence interval=1.06-2.05 for CC, respectively; P(trend)=0.009).
hsa-mir-149	Stomach Neoplasms	21976437	Marginally significant associations were found both for hsa-miR-149 rs2292832 with gastric cancer risk (TC?+?CC vs. TT, OR?=?0.68, 95% CI: 0.44-1.04) and for hsa-miR-605 rs2043556 with colorectal cancer risk (AG?+?GG vs. AA, OR?=?0.70, 95% CI: 0.48-1.02) in males.
hsa-mir-605	Stomach Neoplasms	21976437	Marginally significant associations were found both for hsa-miR-149 rs2292832 with gastric cancer risk (TC?+?CC vs. TT, OR?=?0.68, 95% CI: 0.44-1.04) and for hsa-miR-605 rs2043556 with colorectal cancer risk (AG?+?GG vs. AA, OR?=?0.70, 95% CI: 0.48-1.02) in males.
hsa-mir-17	Burkitt Lymphoma	21981616	The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse.
hsa-mir-18a	Burkitt Lymphoma	21981616	The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse.
hsa-mir-19a	Burkitt Lymphoma	21981616	The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse.
hsa-mir-20a	Burkitt Lymphoma	21981616	The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse.
hsa-mir-19b-1	Burkitt Lymphoma	21981616	The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse.
hsa-mir-92a-1	Burkitt Lymphoma	21981616	The minimum common amplified region on 13q was at 13q31 and included the MIR17HG (MIR17-92) locus. Samples with this gain had higher levels of MIR17 RNA and showed a tendency for early relapse.
hsa-mir-137	Alzheimer Disease	21994399	We identified that the loss of miR-137, -181c, -9, and 29a/b-1 increases SPT and in turn Abeta levels, and provides a mechanism for the elevated risk of AD associated with age, high-saturated-fat diet, and gender. Finally, these results suggest SPT and the respective miRNAs may be potential therapeutic targets for sporadic AD.
hsa-mir-181c	Alzheimer Disease	21994399	We identified that the loss of miR-137, -181c, -9, and 29a/b-1 increases SPT and in turn Abeta levels, and provides a mechanism for the elevated risk of AD associated with age, high-saturated-fat diet, and gender. Finally, these results suggest SPT and the respective miRNAs may be potential therapeutic targets for sporadic AD.
hsa-mir-9-1	Alzheimer Disease	21994399	We identified that the loss of miR-137, -181c, -9, and 29a/b-1 increases SPT and in turn Abeta levels, and provides a mechanism for the elevated risk of AD associated with age, high-saturated-fat diet, and gender. Finally, these results suggest SPT and the respective miRNAs may be potential therapeutic targets for sporadic AD.
hsa-mir-9-2	Alzheimer Disease	21994399	We identified that the loss of miR-137, -181c, -9, and 29a/b-1 increases SPT and in turn Abeta levels, and provides a mechanism for the elevated risk of AD associated with age, high-saturated-fat diet, and gender. Finally, these results suggest SPT and the respective miRNAs may be potential therapeutic targets for sporadic AD.
hsa-mir-9-3	Alzheimer Disease	21994399	We identified that the loss of miR-137, -181c, -9, and 29a/b-1 increases SPT and in turn Abeta levels, and provides a mechanism for the elevated risk of AD associated with age, high-saturated-fat diet, and gender. Finally, these results suggest SPT and the respective miRNAs may be potential therapeutic targets for sporadic AD.
hsa-mir-29a	Alzheimer Disease	21994399	We identified that the loss of miR-137, -181c, -9, and 29a/b-1 increases SPT and in turn Abeta levels, and provides a mechanism for the elevated risk of AD associated with age, high-saturated-fat diet, and gender. Finally, these results suggest SPT and the respective miRNAs may be potential therapeutic targets for sporadic AD.
hsa-mir-29b-1	Alzheimer Disease	21994399	We identified that the loss of miR-137, -181c, -9, and 29a/b-1 increases SPT and in turn Abeta levels, and provides a mechanism for the elevated risk of AD associated with age, high-saturated-fat diet, and gender. Finally, these results suggest SPT and the respective miRNAs may be potential therapeutic targets for sporadic AD.
hsa-mir-218-1	Carcinoma, Hepatocellular	22011248	The AG genotype of pri-miR-218 rs11134527 A/G was associated with family history (p=0.018, odds ratio [OR]=2.96, 95% confidence interval [CI]: 1.16-7.56) and elevated serum α-fetoprotein (serum alpha-fetoprotein [AFP]) levels (�0?ng/mL; p=0.009, OR=1.92, 95% CI: 1.17-3.14) in HCC patients. These findings suggested that the AG genotype of pri-miR-218 rs11134527 might relate to genetic predisposition and be involved in regulating the expression of AFP in Chinese HCC patients.
hsa-mir-218-2	Carcinoma, Hepatocellular	22011248	The AG genotype of pri-miR-218 rs11134527 A/G was associated with family history (p=0.018, odds ratio [OR]=2.96, 95% confidence interval [CI]: 1.16-7.56) and elevated serum α-fetoprotein (serum alpha-fetoprotein [AFP]) levels (�0?ng/mL; p=0.009, OR=1.92, 95% CI: 1.17-3.14) in HCC patients. These findings suggested that the AG genotype of pri-miR-218 rs11134527 might relate to genetic predisposition and be involved in regulating the expression of AFP in Chinese HCC patients.
hsa-mir-499a	Arthritis, Rheumatoid	22019503	There was a significant difference in the levels of CRP and ESR among different genotypes in rs3746444 (hsa-mir-499) (p = 0.031 and p = 0.047, respectively) in Chinese Han people. The heterozygote CT had significantly higher levels of CRP and ESR compared with homozygotes CC and TT.
hsa-mir-423	Colorectal Neoplasms	22028396	Two SNPs were identified to be significantly associated with recurrence-free survival and overall survival of the patients. The most significant SNP was rs6505162 in pre-miR-423. Compared to the homozygous wild-type genotype, the variant-containing genotypes of this SNP were significantly associated with both the overall survival (HR=2.12, 95% CI1.34--3.34, P=0.001) and the recurrence-free survival (HR=1.59, 95% CI1.08--2.36, P=0.019). Another SNP, rs4919510 in pre-miR-608, was also associated with altered recurrence-free survival (HR=0.61, 95% CI 0.41-0.92, P=0.017). These effects were evident only in patients receiving chemotherapy but not in those without chemotherapy. In addition, the combined analysis of the two SNPs conferred a 2.84-fold (95% CI 1.50-5.37, P=0.001) increased risk of recurrence and/or death. Similarly, this effect was only prominent in those receiving chemotherapy (P<0.001) but not in those without chemotherapy (P=0.999).
hsa-mir-608	Colorectal Neoplasms	22028396	Two SNPs were identified to be significantly associated with recurrence-free survival and overall survival of the patients. The most significant SNP was rs6505162 in pre-miR-423. Compared to the homozygous wild-type genotype, the variant-containing genotypes of this SNP were significantly associated with both the overall survival (HR=2.12, 95% CI1.34--3.34, P=0.001) and the recurrence-free survival (HR=1.59, 95% CI1.08--2.36, P=0.019). Another SNP, rs4919510 in pre-miR-608, was also associated with altered recurrence-free survival (HR=0.61, 95% CI 0.41-0.92, P=0.017). These effects were evident only in patients receiving chemotherapy but not in those without chemotherapy. In addition, the combined analysis of the two SNPs conferred a 2.84-fold (95% CI 1.50-5.37, P=0.001) increased risk of recurrence and/or death. Similarly, this effect was only prominent in those receiving chemotherapy (P<0.001) but not in those without chemotherapy (P=0.999).
hsa-mir-199b	Thyroid Neoplasms	22049245	miR-199b-5p and miR-144 which were essentially lost in the carcinomas.
hsa-mir-144	Thyroid Neoplasms	22049245	miR-199b-5p and miR-144 which were essentially lost in the carcinomas.
hsa-mir-30c-1	Stomach Neoplasms	22108846	The genotype frequencies of pre-miR-30c A/G (Polymorphism rs928508 in pre-miR-30c) in gastric cancer patients were obviously different from those in the controls (P = 0.022). AA genotype carriers were associated with an increased risk of gastric cancer compared with GG genotype (adjusted odds ratio (OR) = 1.83, 95% confidence interval (CI): 1.07-3.15, P = 0.029). Moreover, the gastric cancer risk especially elevated in older individuals (aged >60 years), males, nonsmokers, and Helicobacter pylori (H. pylori)-infected individuals (adjusted OR = 2.66, 95% CI: 1.38-5.13, P = 0.004; adjusted OR = 1.90, 95% CI: 1.10-3.27, P = 0.022; adjusted OR = 1.94, 95% CI: 1.12-3.35, P = 0.018; adjusted OR = 1.83, 95% CI: 1.08-3.10, P = 0.024, respectively). Further stratified analysis indicated that AA genotype facilitated developing of gastric cancer with lymph node metastasis (adjusted OR = 2.23, 95% CI: 1.07-4.64, P = 0.032). Expression analysis detected that rs928508 AA showed a significantly increased level of mature miR-30c compared with GG or AG/GG genotype (P = 0.011 or P = 0.013). Patients with AA genotype were associated with unfavorable outcome in overall survival compared with AG/GG genotype (Log rank 5.848, P = 0.016). This study demonstrates that pre-miR-30c A/G polymorphism may be associated with an increased risk of gastric cancer in a Chinese population through altering mature miR-30c expression.
hsa-mir-30c-2	Stomach Neoplasms	22108846	The genotype frequencies of pre-miR-30c A/G (Polymorphism rs928508 in pre-miR-30c) in gastric cancer patients were obviously different from those in the controls (P = 0.022). AA genotype carriers were associated with an increased risk of gastric cancer compared with GG genotype (adjusted odds ratio (OR) = 1.83, 95% confidence interval (CI): 1.07-3.15, P = 0.029). Moreover, the gastric cancer risk especially elevated in older individuals (aged >60 years), males, nonsmokers, and Helicobacter pylori (H. pylori)-infected individuals (adjusted OR = 2.66, 95% CI: 1.38-5.13, P = 0.004; adjusted OR = 1.90, 95% CI: 1.10-3.27, P = 0.022; adjusted OR = 1.94, 95% CI: 1.12-3.35, P = 0.018; adjusted OR = 1.83, 95% CI: 1.08-3.10, P = 0.024, respectively). Further stratified analysis indicated that AA genotype facilitated developing of gastric cancer with lymph node metastasis (adjusted OR = 2.23, 95% CI: 1.07-4.64, P = 0.032). Expression analysis detected that rs928508 AA showed a significantly increased level of mature miR-30c compared with GG or AG/GG genotype (P = 0.011 or P = 0.013). Patients with AA genotype were associated with unfavorable outcome in overall survival compared with AG/GG genotype (Log rank 5.848, P = 0.016). This study demonstrates that pre-miR-30c A/G polymorphism may be associated with an increased risk of gastric cancer in a Chinese population through altering mature miR-30c expression.
hsa-mir-629	Lung Neoplasms	22114071	The rs2735383CC (NBS1 gene) genotype had a significantly increased risk of lung cancer under a recessive genetic model in the total 1559 cases versus 1679 controls (OR = 1.40, 95% C.I. = 1.18-1.66, P = 0.0001) when compared with GG or GC genotypes; the rs2735383CC genotype carriers had lower mRNA and protein expression levels in tumor tissues than those of other genotypes as qPCR and western blot shown. Luciferase assay revealed that the rs2735383C allele had a lower transcription activity than G allele; and the hsa-miR-629 but not hsa-miR-499-5P had effect on modulation of NBS1 gene in vitro. We further observed that the X-ray radiation induced more chromatid breaks in lymphocyte cells from the carriers of rs2735383CC homozygote than those from the subjects with other genotypes (P = 0.0008). Our data suggested that the rs2735383G>C variation contributes to an increased risk of lung cancer by diminishing gene's expression through binding of microRNA-629 to the polymorphic site in the 3'-UTR of NBS1 gene.
hsa-mir-196a-2	Coronary Artery Disease	22159951	The variant genotypes CC/CT of hsa-mir-196a2 rs11614913 T �C were not associated with a significantly increased risk of CAD (adjusted OR = 1.02, 95% CI = 0.76-1.38), compared with wide genotype TT, but CC and CC/CT genotypes were associated with 34 and 35% increased risks of serious prognosis of CAD (adjusted HR = 1.34, 95% CI = 1.02-1.75 for CC; adjusted HR = 1.35, 95% CI = 1.03-1.75 for CC/CT). In the variant of hsa-mir-499 rs3746444A �G, GG was associated with the 223% increased risk of CAD (adjusted OR = 3.23, 95% CI = 1.56-6.67). Cox regression analysis showed that age, smoking status, numbers of pathological changes in coronary arteries, rs11614913 T �C, and diabetes mellitus were associated with serious prognosis of CAD.
hsa-mir-499a	Coronary Artery Disease	22159951	The variant genotypes CC/CT of hsa-mir-196a2 rs11614913 T �C were not associated with a significantly increased risk of CAD (adjusted OR = 1.02, 95% CI = 0.76-1.38), compared with wide genotype TT, but CC and CC/CT genotypes were associated with 34 and 35% increased risks of serious prognosis of CAD (adjusted HR = 1.34, 95% CI = 1.02-1.75 for CC; adjusted HR = 1.35, 95% CI = 1.03-1.75 for CC/CT). In the variant of hsa-mir-499 rs3746444A �G, GG was associated with the 223% increased risk of CAD (adjusted OR = 3.23, 95% CI = 1.56-6.67). Cox regression analysis showed that age, smoking status, numbers of pathological changes in coronary arteries, rs11614913 T �C, and diabetes mellitus were associated with serious prognosis of CAD.
hsa-mir-196a-2	Colorectal Neoplasms	22161766	The authors found a significantly increased colorectal cancer risk with the miR-196a2CC (rs11614913) genotype compared with the TT/CT genotype (AOR?=?1.50; 95% CI?=?1.11-2.04; P?=?0.01; FDR-P?=?0.04) in Korean population.
hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.	hsa-mir-570	Stomach Neoplasms	22190470	A guanine-to-cytosine mutation at the 3'-UTR of CD274 mRNA led to CD274 over-expression by disrupting the miR-570 binding. A frequent somatic mutation in CD274 3'-UTR leads to protein over-expression in gastric cancer by disrupting miR-570 binding.
hsa-mir-146a	Lupus Erythematosus, Systemic	22218224	The SNP (rs2431697) was associated with the microRNA-146a, where the risk allele correlates with lower expression of the miRNA.
hsa-mir-196a-2	Abortion, Habitual	22222140	RSA(recurrent spontaneous abortion) patients exhibited significantly different frequencies of the miR-196a2CC (TT+TC vs. CC; adjusted odds ratio [AOR], 1.587; 95% confidence interval [CI], 1.042-2.417) and miR-499AG+GG genotypes (AOR, 1.671; 95% CI, 1.054-2.651) compared with the control group.
hsa-mir-499a	Abortion, Habitual	22222140	RSA(recurrent spontaneous abortion) patients exhibited significantly different frequencies of the miR-196a2CC (TT+TC vs. CC; adjusted odds ratio [AOR], 1.587; 95% confidence interval [CI], 1.042-2.417) and miR-499AG+GG genotypes (AOR, 1.671; 95% CI, 1.054-2.651) compared with the control group.
hsa-mir-17	Ovarian Neoplasms	22235027	The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113
hsa-mir-18a	Ovarian Neoplasms	22235027	The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113
hsa-mir-19a	Ovarian Neoplasms	22235027	The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113
hsa-mir-20a	Ovarian Neoplasms	22235027	The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113
hsa-mir-19b-1	Ovarian Neoplasms	22235027	The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113
hsa-mir-92a-1	Ovarian Neoplasms	22235027	The most notable cluster is the tumorigenic miR-17-92 cluster with five microRNAs, all of which are significantly associated with rs3814113
hsa-mir-124-1	Glioma	22253443	Loss of brain-enriched miR-124 enhances the stem-like traits and invasiveness of glioma cells.
hsa-mir-124-2	Glioma	22253443	Loss of brain-enriched miR-124 enhances the stem-like traits and invasiveness of glioma cells.
hsa-mir-124-3	Glioma	22253443	Loss of brain-enriched miR-124 enhances the stem-like traits and invasiveness of glioma cells.
hsa-let-7e	Crohn Disease	22262659	The rs10889677 variant in the 3'-untranslated region of the IL-23R gene displays enhanced levels of both mRNA and protein production of IL-23R. This can be attributed to a loss of binding capacity for the microRNAs (miRNAs) Let-7e and Let-7f by the variant allele.
hsa-let-7f-1	Crohn Disease	22262659	The rs10889677 variant in the 3'-untranslated region of the IL-23R gene displays enhanced levels of both mRNA and protein production of IL-23R. This can be attributed to a loss of binding capacity for the microRNAs (miRNAs) Let-7e and Let-7f by the variant allele.
hsa-let-7f-2	Crohn Disease	22262659	The rs10889677 variant in the 3'-untranslated region of the IL-23R gene displays enhanced levels of both mRNA and protein production of IL-23R. This can be attributed to a loss of binding capacity for the microRNAs (miRNAs) Let-7e and Let-7f by the variant allele.
hsa-mir-145	Ovarian Neoplasms	22285623	The loss of miR-145 can result in the activation of factors that promote oncogenesis and cellular pluripotency which in turn could lead to the development of ovarian cancer.
hsa-mir-133a-1	Breast Neoplasms	22292984	Loss of miR-133a expression associated with poor survival of breast cancer and restoration of miR-133a expression inhibited breast cancer cell growth and invasion.
hsa-mir-133a-2	Breast Neoplasms	22292984	Loss of miR-133a expression associated with poor survival of breast cancer and restoration of miR-133a expression inhibited breast cancer cell growth and invasion.
hsa-mir-499a	Carcinoma, Hepatocellular	22311030	hsa-mir-499 (rs3746444; adenine to guanine [C-T]) .Significant differences were found in frequency and distribution of the genotypes of miRNA-499 between the HCC and the control group. Compared with miRNA-499 T/T, the odds ratio (OR) of patients with miRNA-499 C/C for developing HCC was 3.630 (95% CI: 1.545-8.532), and OR for developing HBV-related HCC was 3.133 (95% CI: 1.248-7.861).
hsa-mir-1207	Glomerulonephritis	22319602	A miR-1207-5p binding site polymorphism (C1936T, rs13385) abolishes regulation of HBEGF and is associated with disease severity in CFHR5 nephropathy.
hsa-mir-143	Neoplasms	22330136	Loss of microRNA-143/145 disturbs cellular growth and apoptosis of human epithelial cancers by impairing the MDM2-p53 feedback loop.
hsa-mir-145	Neoplasms	22330136	Loss of microRNA-143/145 disturbs cellular growth and apoptosis of human epithelial cancers by impairing the MDM2-p53 feedback loop.
hsa-mir-27a	Stomach Neoplasms	22350505	The SNP rs895819 in the miR-27a gene with the minor allele C presented significantly reduced risk to gastric cancer in Chinese population.
hsa-mir-196a-2	Breast Neoplasms	22363415	The authors found that hs-miR-196a2 in premenopausal patients, and hs-miR-499, hs-miR-146a and hs-miR-196a2 in postmenopausal patients, may discriminate breast cancer patients from healthy individuals. In addition, we found a significant association between two microRNA polymorphisms (hs-miR-196a2 and hs-miR-499) and breast cancer risk.
hsa-mir-499a	Breast Neoplasms	22363415	The authors found that hs-miR-196a2 in premenopausal patients, and hs-miR-499, hs-miR-146a and hs-miR-196a2 in postmenopausal patients, may discriminate breast cancer patients from healthy individuals. In addition, we found a significant association between two microRNA polymorphisms (hs-miR-196a2 and hs-miR-499) and breast cancer risk.
hsa-mir-146a	Breast Neoplasms	22363415	The authors found that hs-miR-196a2 in premenopausal patients, and hs-miR-499, hs-miR-146a and hs-miR-196a2 in postmenopausal patients, may discriminate breast cancer patients from healthy individuals. In addition, we found a significant association between two microRNA polymorphisms (hs-miR-196a2 and hs-miR-499) and breast cancer risk.
hsa-mir-146a	Breast Neoplasms	22363684	Increased Risk of Breast Cancer Associated with CC Genotype of Has-miR-146a Rs2910164 Polymorphism in Europeans.
hsa-mir-499a	Heart Failure	22374132	A naturally occurring miR-499 mutation(u17c in the 3' end) outside the critical seed sequence modifies mRNA targeting and end-organ function.
hsa-mir-106b	Carcinoma, Hepatocellular	22393390	A Genetic Variant (rs999885) in the Promoter Region of miR-106b-25 Cluster and Risk of HBV Infection and Hepatocellular Carcinoma.Compared with the HBV natural clearance subjects carrying rs999885 AA genotype, those with AG/GG genotypes had a decreased risk of chronic HBV infection with an adjusted odds ratio (OR) of 0.79 [95% confidence intervals (CIs)?=?0.67-0.93]. However, the AG/GG genotypes were significantly associated with an increased HCC risk in HBV persistent carriers (adjusted OR?=?1.25, 95% CIs?=?1.06-1.47). Expression analysis revealed that the expression level of miR-106b-25 cluster was significantly higher in AG/GG carriers than those in AA carriers in non-tumor liver tissues.
hsa-mir-25	Carcinoma, Hepatocellular	22393390	A Genetic Variant (rs999885) in the Promoter Region of miR-106b-25 Cluster and Risk of HBV Infection and Hepatocellular Carcinoma.Compared with the HBV natural clearance subjects carrying rs999885 AA genotype, those with AG/GG genotypes had a decreased risk of chronic HBV infection with an adjusted odds ratio (OR) of 0.79 [95% confidence intervals (CIs)?=?0.67-0.93]. However, the AG/GG genotypes were significantly associated with an increased HCC risk in HBV persistent carriers (adjusted OR?=?1.25, 95% CIs?=?1.06-1.47). Expression analysis revealed that the expression level of miR-106b-25 cluster was significantly higher in AG/GG carriers than those in AA carriers in non-tumor liver tissues.
hsa-mir-106b	Hepatitis B	22393390	A Genetic Variant (rs999885) in the Promoter Region of miR-106b-25 Cluster and Risk of HBV Infection and Hepatocellular Carcinoma.Compared with the HBV natural clearance subjects carrying rs999885 AA genotype, those with AG/GG genotypes had a decreased risk of chronic HBV infection with an adjusted odds ratio (OR) of 0.79 [95% confidence intervals (CIs)?=?0.67-0.93]. However, the AG/GG genotypes were significantly associated with an increased HCC risk in HBV persistent carriers (adjusted OR?=?1.25, 95% CIs?=?1.06-1.47). Expression analysis revealed that the expression level of miR-106b-25 cluster was significantly higher in AG/GG carriers than those in AA carriers in non-tumor liver tissues.
hsa-mir-25	Hepatitis B	22393390	A Genetic Variant (rs999885) in the Promoter Region of miR-106b-25 Cluster and Risk of HBV Infection and Hepatocellular Carcinoma.Compared with the HBV natural clearance subjects carrying rs999885 AA genotype, those with AG/GG genotypes had a decreased risk of chronic HBV infection with an adjusted odds ratio (OR) of 0.79 [95% confidence intervals (CIs)?=?0.67-0.93]. However, the AG/GG genotypes were significantly associated with an increased HCC risk in HBV persistent carriers (adjusted OR?=?1.25, 95% CIs?=?1.06-1.47). Expression analysis revealed that the expression level of miR-106b-25 cluster was significantly higher in AG/GG carriers than those in AA carriers in non-tumor liver tissues.
hsa-mir-29b-1	Muscular Dystrophy, Duchenne	22434133	Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis.
hsa-mir-29b-2	Muscular Dystrophy, Duchenne	22434133	Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis.
hsa-mir-29a	Muscular Dystrophy, Duchenne	22434133	Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis.
hsa-mir-29c	Muscular Dystrophy, Duchenne	22434133	Loss of miR-29 in Myoblasts Contributes to Dystrophic Muscle Pathogenesis.
hsa-mir-146a	Stomach Neoplasms	22455393	A Functional Polymorphism (rs2910164) in Pre-miR-146a Is Associated with Susceptibility to Gastric Cancer in a Chinese Population.
hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.	hsa-mir-938	Stomach Neoplasms	22537748	Genetic polymorphisms of IL17A ((rs2275913 (-197 G > A), rs3748067 (*1249 C > T)) and pri-microRNA-938 (pri-miR-938, rs2505901 (T > C).), targeting IL17A 3'-UTR, influence susceptibility to gastric cancer.
hsa-mir-21	Breast Neoplasms	22547075	DNA damage induces NF-kB-dependent microRNA-21 upregulation and promotes breast cancer cell invasion.
hsa-mir-520a	Colorectal Neoplasms	22553375	A  3' untranslated region (UTR) mutation was also shown to be associated with increased sensitivity to saracatinib and have a reduced affinity for miR-520a and miR-525a.
hsa-mir-608	Breast Neoplasms	22586447	Polymorphism rs4919510:C>G in mature sequence of human microRNA-608 contributes to the risk of HER2-positive breast cancer but not other subtypes.
hsa-mir-92a-1	Carcinoma, Hepatocellular	22587342	Oxidative DNA damage correlates with cell immortalization and mir-92 expression in hepatocellular carcinoma.
hsa-mir-423	Breast Neoplasms	22593246	A genetic variant (rs6505162:A>C) located in miR-423 is associated with reduced breast cancer risk.
hsa-mir-146a	Moyamoya Disease	22659075	Association of the miR-146aC>G, miR-196a2C>T, and miR-499A>G polymorphisms with moyamoya disease in the Korean population.
hsa-mir-196a-2	Moyamoya Disease	22659075	Association of the miR-146aC>G, miR-196a2C>T, and miR-499A>G polymorphisms with moyamoya disease in the Korean population.
hsa-mir-219-1	Colorectal Neoplasms	22661538	The mir219-1:rs213210 showed consistent association with death in the training set, the replication set, and combined data set
hsa-mir-608	Colorectal Neoplasms	22661538	In patients with stage III disease, mir608: rs4919510 was associated with increased risk for both recurrence and death.
hsa-mir-146a	Nasopharyngeal Neoplasms	22711332	A single nucleotide polymorphism (rs2910164) in microRNA-146a is associated with the risk for nasopharyngeal carcinoma.
hsa-mir-499a	Carcinoma, Squamous Cell	22761899	This study determined that a significant association of miRNA499 with CC genotype, as compared to the subjects with TT genotype, had a higher risk of oral squamous cell carcinoma.
hsa-mir-499b	Carcinoma, Squamous Cell	22761899	This study determined that a significant association of miRNA499 with CC genotype, as compared to the subjects with TT genotype, had a higher risk of oral squamous cell carcinoma.
hsa-mir-7-1	Urinary Bladder Neoplasms	22768238	A microRNA-7 binding site polymorphism (1010A/G) in HOXB5 leads to differential gene expression in bladder cancer.
hsa-mir-7-2	Urinary Bladder Neoplasms	22768238	A microRNA-7 binding site polymorphism (1010A/G) in HOXB5 leads to differential gene expression in bladder cancer.
hsa-mir-7-3	Urinary Bladder Neoplasms	22768238	A microRNA-7 binding site polymorphism (1010A/G) in HOXB5 leads to differential gene expression in bladder cancer.
hsa-mir-146a	Asthma	22823586	MiR-146a polymorphism is associated with asthma but not with systemic lupus erythematosus and juvenile rheumatoid arthritis in Mexican patients.
hsa-mir-1231	Carcinoma, Hepatocellular	22824466	A miR-1231 binding site polymorphism (rs17875871) in the 3'UTR of IFNAR1 is associated with hepatocellular carcinoma susceptibility.
hsa-mir-125b-1	Leukemia, Myeloid, Acute	22843432	MicroRNA-125b-1 accelerates a C-terminal mutant of C/EBPα (C/EBPa-C(m))-induced myeloid leukemia.
hsa-mir-34b	Intracranial Aneurysm	22844323	The CC genotype of miR-34b/c rs4938723 was significantly associated with a decreased risk of IA compared with the TT genotype. Moreover, a significant gene interaction of the carriers with the combined genotypes of miR-34b/c rs4938723CC and TP53 Arg72Pro CG/CC/GG had a decreased risk of IA, compared with those carrying miR-34b/c rs4938723CT/TT+TP53 Arg72Pro GG/CG/CC combined genotypes.
hsa-mir-34c	Intracranial Aneurysm	22844323	The CC genotype of miR-34b/c rs4938723 was significantly associated with a decreased risk of IA compared with the TT genotype. Moreover, a significant gene interaction of the carriers with the combined genotypes of miR-34b/c rs4938723CC and TP53 Arg72Pro CG/CC/GG had a decreased risk of IA, compared with those carrying miR-34b/c rs4938723CT/TT+TP53 Arg72Pro GG/CG/CC combined genotypes.
hsa-mir-126	Pancreatic Neoplasms	22845403	Loss of miR-126 is crucial to pancreatic cancer progression.
hsa-mir-146a	Urinary Bladder Neoplasms	22846912	miR-146a rs2910164 C allele inhibited cell proliferation and significantly downregulates expression of IRAK1 and TRAF6 in bladder cancer cells.
hsa-mir-196a-1	Esophageal Neoplasms	22859270	MiR-196a binding-site SNP (rs6573) regulates RAP1A expression contributing to esophageal squamous cell carcinoma risk and metastasis.
hsa-mir-196a-2	Esophageal Neoplasms	22859270	MiR-196a binding-site SNP (rs6573) regulates RAP1A expression contributing to esophageal squamous cell carcinoma risk and metastasis.
hsa-mir-502	Ovarian Neoplasms	22867998	A polymorphism (rs16917496) at the miR-502 binding site in the 3' untranslated region of the SET8 gene is associated with the risk of epithelial ovarian cancer.
hsa-mir-181a-1	Precursor Cell Lymphoblastic Leukemia-Lymphoma	22916024	Deletion of mir-181a-1/b-1 expression inhibits the development of Notch1 oncogene-induced T cell acute lymphoblastic leukemia (T-ALL). mir-181a-1/b-1 controls the strength and threshold of Notch activity in tumorigenesis in part by dampening multiple negative feedback regulators downstream of NOTCH and pre-T cell receptor (TCR) signaling pathways.
hsa-mir-181b-1	Precursor Cell Lymphoblastic Leukemia-Lymphoma	22916024	Deletion of mir-181a-1/b-1 expression inhibits the development of Notch1 oncogene-induced T cell acute lymphoblastic leukemia (T-ALL). mir-181a-1/b-1 controls the strength and threshold of Notch activity in tumorigenesis in part by dampening multiple negative feedback regulators downstream of NOTCH and pre-T cell receptor (TCR) signaling pathways.
hsa-mir-155	Heart Failure	22939041	Angiotensin Receptor Type 1 Single Nucleotide Polymorphism 1166A/C is Associated With Malignant Arrhythmias and Altered Circulating miR-155 Levels in Patients With Chronic Heart Failure.
hsa-mir-31	Melanoma	22948084	Genetic and epigenetic loss of microRNA-31 leads to feed-forward expression of EZH2 in melanoma.
hsa-mir-337	Leukemia, Myeloid, Acute	23065518	A polymorphism in the 3'-untranslated region of the NPM1 gene causes illegitimate regulation by microRNA-337-5p and correlates with adverse outcome in acute myeloid leukemia
hsa-mir-200c	Stomach Neoplasms	23065816	G-A variant in miR-200c binding site of EFNA1 alters susceptibility to gastric cancer
hsa-mir-27a	Carcinoma, Renal Cell	23118855	A genetic variant in pre-miR-27a is associated with a reduced renal cell cancer risk in a Chinese population
hsa-mir-30c-1	Lung Neoplasms	23159078	Single nucleotide polymorphism in flanking region of miR-30c influences the maturing process of miR-30c in lung carcinoma
hsa-mir-30c-2	Lung Neoplasms	23159078	Single nucleotide polymorphism in flanking region of miR-30c influences the maturing process of miR-30c in lung carcinoma
hsa-mir-146a	Melanoma	23222547	The rs2910164 G>C polymorphism in microRNA-146a is associated with the incidence  of malignant melanoma
hsa-mir-196a-1	Breast Neoplasms	23228090	Evaluation of single nucleotide polymorphisms in microRNAs (hsa-miR-196a2 rs11614913 C/T) from Brazilian women with breast cancer
hsa-mir-196a-2	Breast Neoplasms	23228090	Evaluation of single nucleotide polymorphisms in microRNAs (hsa-miR-196a2 rs11614913 C/T) from Brazilian women with breast cancer
hsa-mir-204	Neoplasms	23285024	Genomic Loss of Tumor Suppressor miRNA-204 Promotes Cancer Cell Migration and Invasion by Activating AKT/mTOR/Rac1 Signaling and Actin Reorganization
hsa-mir-218-1	Uterine Cervical Neoplasms	23320911	The pri-miR-218 rs11134527 SNP was significantly associated with the risk of cervical carcinoma in Eastern Chinese women
hsa-mir-218-2	Uterine Cervical Neoplasms	23320911	The pri-miR-218 rs11134527 SNP was significantly associated with the risk of cervical carcinoma in Eastern Chinese women
hsa-mir-367	Colorectal Neoplasms	23393343	the functional variant (rs1044129) in the miR-367 binding site of RYR3 may be a potential marker for prognosis in patients following curative surgery for CRC
hsa-mir-151b	Nasopharyngeal Neoplasms	23416081	A miR-151 binding site polymorphism in the 3'-untranslated region of the cyclin E1 gene associated with nasopharyngeal carcinoma
hsa-mir-125a	Breast Neoplasms	23420759	rs12976445 variant in the pri-miR-125a correlates with a lower level of hsa-miR-125a and ERBB2 overexpression in breast cancer patients
hsa-mir-184	Stomach Neoplasms	23724109	The miR-184 Binding-Site rs8126 T>C Polymorphism in TNFAIP2 Is Associated with Risk of Gastric Cancer.