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discover a translocation disrupting MLH1 and three mutations in MSH6 and PMS2 that increase endometrial, colorectal, brain and ovarian cancer risk
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Whole exome sequencing in triple negative breast cancer cases revealed MSH6 rs2020912 (MAF: 56.25% vs. 1.04%, OR 122.13, 95% CI 12.29-2985.48) are risk factors for triple negative breast cancer.
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CSE1L expression was correlated with MSH6 expression in tumor samples and was associated with poor prognosis in patients with osteosarcoma. Taken together, our results demonstrate that the CSE1L-MSH6 axis has an important role in osteosarcoma progression.
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our data suggests thatMSH6 Glu39Gly polymorphism is associated with the risk of developing sporadic colorectal cancer in polish population. Linkage to the female gender, onset above 60 years old and further increase of risk when combined with wild-type allele of PMS2 IVS1-1121C >
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Results from a study on gene expression variability markers in early-stage human embryos shows that is a putative expression variability marker for the 3-day, 8-cell embryo stage.
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hMSH6 Glu39Gly polymorphism is associated with the risk of developing colorectal cancer in the Polish population.
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Expression of MSH6 and MSH2 was positively associated with tumor volume doubling time. Gene expression was positively associated with ATR expression. Reduction of MSH6 and MSH2 expression at the messenger RNA and protein levels could be involved in direct Pituitary Adenoma proliferation by promoting cell-cycle progression or decreasing the rate of apoptosis through interference with the function of the ATR-Chk1 pathway.
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Our results suggest that increased expression of MSH6, or other MMR, may be a new mechanism contributing to the acquired resistance during TMZ therapy; and may serve as an indicator to the resistance in GBM.
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study to estimate frequency of point mutations and chromosomal rearrangements in 3 mismatch repair (MMR) genes MLH1, MSH2, and MSH6 among unselected patients with ovarian cancer; estimate that approximately 0.6% of unselected ovarian cancer patients have mutations in the MMR genes
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MSH6 frameshift variants incompletely segregate with the Lynch syndrome phenotype in two families.
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Patients with mutations 6 showed higher rate of achieving major molecular response than those<6 (P=0.0381). Mutations in epigenetic regulator, ASXL1, TET2, TET3, KDM1A and MSH6 were found in 25% of patients. TET2 or TET3, AKT1 and RUNX1 were mutated in one patient each. ASXL1 was mutated within exon 12 in three cases
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The MSH6 gene polymorphisms are likely to play an important role in the progression of AIDS in the northern Chinese population.
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MSH6 mutations contribute to colorectal cancer susceptibility in Algerian families with suspected Lynch syndrome.
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Neoadjuvant therapy in microsatellite-stable colorectal carcinoma induces concomitant loss of MSH6 and Ki-67 expression.
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High MSH6 expression is associated with the development of genetic instability and is linked to tumor aggressiveness and early PSA recurrence in prostate cancer.
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In path_MSH6 10-year survival was 84%, relative incidence of subsequent cancer compared with incidence of first cancer was slightly but insignificantly higher than cancer incidence in patients with Lynch syndrome without previous cancer.
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human Pol alpha interacts with MSH2-MSH6 complex
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In colorectal neoplasms, negative expression of the MMR proteins MLH1, MSH2 or MSH6 was seen in 15% (47 of 313) of the patients. Defect MLH1 was most common and detected in 12% of the cases. Defect MLH1 and MSH2 were identified in each patient's normal adjacent mucosa.
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unlike MutSbeta, MutSalpha may also act to protect against repeat contractions in the Fmr1 gene
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A total of 201 unique disease-predisposing mismatch repair gene mutations were identified in 369 Lynch syndrome families. These mutations affected MLH1 in 40%, MSH2 in 36%, MSH6 in 18% and PMS2 in 6% of the families
