The biochemical basis of microsatellite instability and abnormal immunohistochemistry and clinical behavior in Lynch syndrome: from bench to bedside - Test2 - elhamkhani - TriplyDB

The biochemical basis of microsatellite instability and abnormal immunohistochemistry and clinical behavior in Lynch syndrome: from bench to bedside

The biochemical basis of microsatellite instability and abnormal immunohistochemistry and clinical behavior in Lynch syndrome: from bench to bedside

http://www.wikidata.org/entity/Q33762979

about

Review of the Lynch syndrome: history, molecular genetics, screening, differential diagnosis, and medicolegal ramifications Molecular origins of cancer: Molecular basis of colorectal cancer Microsatellite instability in colorectal cancer The clinical phenotype of Lynch syndrome due to germ-line PMS2 mutations Lynch syndrome and Lynch syndrome mimics: The growing complex landscape of hereditary colon cancer EMAST is a Form of Microsatellite Instability That is Initiated by Inflammation and Modulates Colorectal Cancer Progression Causal link between microsatellite instability and hMRE11 dysfunction in human cancers Risk of metachronous colorectal cancer following colectomy in Lynch syndrome: a systematic review and meta-analysis.Pyloric gland adenoma in Lynch syndrome Genetic testing for hereditary colorectal cancer.Performance of clinical guidelines compared with molecular tumour screening methods in identifying possible Lynch syndrome among colorectal cancer patients: a Norwegian population-based study A case report of Muir-Torre syndrome in a woman with breast cancer and MSI-Low skin squamous cell carcinoma.Genomic and epigenetic instability in colorectal cancer pathogenesis.Mismatch repair protein expression and colorectal cancer in Hispanics from Puerto Rico MSH6 and PMS2 mutation positive Australian Lynch syndrome families: novel mutations, cancer risk and age of diagnosis of colorectal cancer.Frameshift mutagenesis and microsatellite instability induced by human alkyladenine DNA glycosylase.Clinical relevance of microsatellite instability in colorectal cancer.Low frequency of Lynch syndrome among young patients with non-familial colorectal cancer.Microsatellite alterations at selected tetranucleotide repeats are associated with morphologies of colorectal neoplasias Evidence for an hMSH3 defect in familial hamartomatous polyps.Tumor hypoxia and genetic alterations in sporadic cancers.Hereditary ovarian carcinoma: heterogeneity, molecular genetics, pathology, and management.DNA mismatch repair-related protein loss as a prognostic factor in endometrial cancers.Characteristics of hereditary nonpolyposis colorectal cancer patients with double primary cancers in endometrium and colorectum.Mismatch repair genes expression defects & association with clinicopathological characteristics in colorectal carcinoma.Tumor microsatellite instability and clinicopathologic features in Iranian colorectal cancer patients at risk for Lynch syndrome.Anticipation in lynch syndrome: where we are where we go Clinical and Molecular Characterization of Brazilian Patients Suspected to Have Lynch Syndrome.Phenotype diversity in type 1 Gaucher disease: discovering the genetic basis of Gaucher disease/hematologic malignancy phenotype by individual genome analysis.CpG Island Methylation, Microsatellite Instability, and BRAF Mutations and Their Clinical Application in the Treatment of Colon Cancer.Immunohistochemistry and microsatellite instability analysis in molecular subtyping of colorectal carcinoma based on mismatch repair competency.Trinucleotide repeat expansions catalyzed by human cell-free extracts Isolated Loss of PMS2 Immunohistochemical Expression is Frequently Caused by Heterogenous MLH1 Promoter Hypermethylation in Lynch Syndrome Screening for Endometrial Cancer Patients.Molecular pathways involved in colorectal cancer: implications for disease behavior and prevention Secondary mutation in a coding mononucleotide tract in MSH6 causes loss of immunoexpression of MSH6 in colorectal carcinomas with MLH1/PMS2 deficiency.Epitope-positive truncating MLH1 mutation and loss of PMS2: implications for IHC-directed genetic testing for Lynch syndrome.A two-antibody mismatch repair protein immunohistochemistry screening approach for colorectal carcinomas, skin sebaceous tumors, and gynecologic tract carcinomas.Dietary, endocrine, and metabolic factors in the development of colorectal cancer.Lynch syndrome diagnostics: decision-making process for germ-line testing.Research on plants for the understanding of diseases of nuclear and mitochondrial origin.

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The biochemical basis of microsatellite instability and abnormal immunohistochemistry and clinical behavior in Lynch syndrome: from bench to bedside

http://www.wikidata.org/entity/Q33762979

description

2007 nî lūn-bûn

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2007 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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The biochemical basis of micro ...... yndrome: from bench to bedside

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The biochemical basis of micro ...... yndrome: from bench to bedside

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Familial Cancer

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The biochemical basis of micro ...... yndrome: from bench to bedside

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C Richard Boland

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Dong K Chang

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John M Carethers

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Minoru Koi

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P2860

hMSH2 forms specific mispair-binding complexes with hMSH3 and hMSH6

Tumor microsatellite-instability status as a predictor of benefit from fluorouracil-based adjuvant chemotherapy for colon cancer

hMSH2-hMSH6 forms a hydrolysis-independent sliding clamp on mismatched DNA

Germ-line msh6 mutations in colorectal cancer families

Immunohistochemical analysis reveals high frequency of PMS2 defects in colorectal cancer

Germline mutation of MSH6 as the cause of hereditary nonpolyposis colorectal cancer

A National Cancer Institute Workshop on Microsatellite Instability for cancer detection and familial predisposition: development of international criteria for the determination of microsatellite instability in colorectal cancer

Methylation of the hMLH1 promoter correlates with lack of expression of hMLH1 in sporadic colon tumors and mismatch repair-defective human tumor cell lines

Steady-state regulation of the human DNA mismatch repair system.

Polymorphisms in a pseudogene highly homologous to PMS2.

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