scholarly journals MLH1 Gene

2020 ◽  
Author(s):  
Keyword(s):  
Mlh1 Gene

Loss of the wild type MLH1 gene is a feature of hereditary nonpolyposis colorectal cancer

1994 ◽  
Vol 8 (4) ◽  
pp. 405-410 ◽  
Author(s):  
Akseli Hemminki ◽  
Päivi Peltomäki ◽  
Jukka-Pekka Mecklin ◽  
Heikki Järvinen ◽  
Reijo Salovaara ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Hereditary Nonpolyposis Colorectal Cancer ◽  
Wild Type ◽  
Mlh1 Gene ◽  
Hereditary Nonpolyposis

scholarly journals Modulation of histone methylation and MLH1 gene silencing by hexavalent chromium

2009 ◽  
Vol 237 (3) ◽  
pp. 258-266 ◽  
Author(s):  
Hong Sun ◽  
Xue Zhou ◽  
Haobin Chen ◽  
Qin Li ◽  
Max Costa
Keyword(s):  
Gene Silencing ◽  
Hexavalent Chromium ◽  
Histone Methylation ◽  
Mlh1 Gene

COMMON VARIANTS ON MLH1 GENE AND THEIR ASSOCIATIONS WITH PROSTATE CANCER IN EUROPEAN AMERICANS

2008 ◽  
Vol 179 (4S) ◽  
pp. 227-227
Author(s):  
Huifeng Xi ◽  
Prodipto Pal ◽  
Saurav Guha ◽  
Guangyun Sun ◽  
Joshua J Meeks ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Common Variants ◽  
Mlh1 Gene ◽  
European Americans

scholarly journals Clinical Implications of Microsatellite Instability and MLH1 Gene Inactivation in Sporadic Insulinomas

2009 ◽  
Vol 94 (9) ◽  
pp. 3448-3457 ◽  
Author(s):  
Mei Mei ◽  
Dajun Deng ◽  
Tong-Hua Liu ◽  
Xin-Ting Sang ◽  
Xin Lu ◽  
...  
Keyword(s):  
Clinical Outcome ◽  
Microsatellite Instability ◽  
Promoter Methylation ◽  
Clinicopathological Characteristics ◽  
High Rate ◽  
Mlh1 Gene ◽  
Multivariate Statistic ◽  
Incurable Disease ◽  
Multivariate Statistic Analysis ◽  
Mlh1 Protein

Context: The molecular pathogenesis of sporadic insulinomas is unknown. There is a lack of biomarker to distinguish benign and malignant form of insulinoma. Objective: Our objective was to confirm the occurrence of microsatellite instability (MSI) in insulinomas, to identify alterations of mismatch repair (MMR) genes in the tumors, and to evaluate the possibility to distinguish benign and malignant insulinoma or to predict the clinical outcome of patients with these alterations. Design and Patients: We detected MSI and inactivation of MLH1 gene in 55 sporadic insulinomas by PCR, immunohistochemical staining, allelic typing, analysis of promoter methylation, and exon mutations. Their correlations with clinicopathological characteristics were analyzed with univariate and multivariate statistic analysis. Results: A high rate of MSI (MSI-H) was found in 33% of sporadic insulinomas. Reduced expression of mutL homolog 1 (MLH1) protein was observed in 36% of insulinomas and correlated with MSI-H (P = 0.008). Promoter methylation and loss of heterozygosity of MLH1 gene was found in 31 and 49% of insulinomas, respectively. Reduced expression of MLH1 and MSI-H were significantly associated with both tumor malignancy (P = 0.033 and P = 4.8 × 10−6, respectively) and incurable disease (P = 0.006 and P = 0.001, respectively). Conclusion: High frequency of MSI occurred in sporadic insulinomas. The silencing of MLH1 gene may partially contribute to the MSI-H in the tumors. Assessing MSI-H and expressions of MLH1 could be used to distinguish benign and malignant insulinomas and to predict the outcome of patients. Detecting of a high rate of microsatellite instability can be used to distinguish malignancy from benign, and predict clinical outcome of the sporadic insulinomas.

scholarly journals Saccharomyces cerevisiae pms2 mutations are alleles of MLH1, and pms2-2 corresponds to a hereditary nonpolyposis colorectal carcinoma-causing missense mutation.

1996 ◽  
Vol 16 (6) ◽  
pp. 3008-3011 ◽  
Author(s):  
A Jeyaprakash ◽  
R Das Gupta ◽  
R Kolodner
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Amino Acid ◽  
Colorectal Carcinoma ◽  
Missense Mutation ◽  
Model System ◽  
Missense Mutations ◽  
Mlh1 Gene ◽  
Dna Mismatch ◽  
Hereditary Nonpolyposis ◽  
Hereditary Nonpolyposis Colorectal Carcinoma

A number of mutant Saccharomyces cerevisiae strains having phenotypes consistent with defects in DNA mismatch repair have been described, but not all have been extensively characterized. In this study we demonstrate that the pms2-1 and pms2-2 alleles arise from missense mutations in the MLH1 gene which inactivate MLH1. One of these alleles, pms2-2, causes the same amino acid substitution in a highly conserved region of the known MutL homologs as that caused by a proposed missense mutation observed in a Swedish hereditary nonpolyposis colorectal carcinoma kindred. This observation supports the functional significance of missense mutations found in hereditary nonpolyposis colorectal carcinoma kindreds and indicates that in some cases S. cerevisiae can serve as a useful model system for the analysis of such mutations.

scholarly journals Common mutations identified in the MLH1 gene in familial Lynch syndrome

2017 ◽  
Vol 1 (Special Issue-Supplement) ◽  
pp. 254-254
Author(s):  
Jisha Elias ◽  
Coral Karunakaran ◽  
Snigdha Majumder ◽  
Malini Manoharan ◽  
Rakshit Shah ◽  
...  
Keyword(s):  
Lynch Syndrome ◽  
Mlh1 Gene
Sign in / Sign up

Export Citation Format

Share Document