MSH2 - Mouse monoclonal [25D12] to MSH2; MutS protein homolog 2 Monoclonal
- Known as:
- MSH2 - Mouse mab [25D12] MSH2; MutS protein homolog 2 Monoclonal
- Catalog number:
- 20-272-192367
- Product Quantity:
- 0.5 ml
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- MSH2 - Mouse monoclonal [25D12] MSH2; MutS protein homolog 2 Monoclonal
Related genes to: MSH2 - Mouse monoclonal [25D12] to MSH2; MutS protein homolog 2 Monoclonal
- Gene:
- MSH2 NIH gene
- Name:
- mutS homolog 2
- Previous symbol:
- COCA1
- Synonyms:
- HNPCC, HNPCC1
- Chromosome:
- 2p21-p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1993-07-28
- Date modifiied:
- 2019-04-23
Related products to: MSH2 - Mouse monoclonal [25D12] to MSH2; MutS protein homolog 2 Monoclonal
Related articles to: MSH2 - Mouse monoclonal [25D12] to MSH2; MutS protein homolog 2 Monoclonal
- Subtotal colectomy is usually the therapy of choice in Lynch syndrome patients diagnosed with colon cancer. In patients who develop cancer after the age of 50-60 years, segmental colectomy is considered a good alternative. Although the endoscopic treatment of early colorectal cancer in non-Lynch patients has increased in the last decades, almost all patients with a Lynch syndrome-associated colorectal malignancy undergo surgery, even if the tumour is diagnosed in a (very) early stage. One of the endoscopic treatment options for early colorectal cancer is an endoscopic full thickness resection (eFTR). This treatment modality allows optimal pathological examination of the resection specimen, as a transmural resection is performed with optimal T-staging of the tumour. We report a case of a 62 year old man, diagnosed with MSH2-Lynch syndrome, who underwent successful eFTR treatment of an early (pT1) colon cancer located in the ascending colon, with no signs of recurrence 12 months after treatment. We discuss the pros and cons of endoscopic resection of early colorectal carcinoma in Lynch syndrome patients. - Source: PubMed
Publication date: 2019/05/20
Langers Alexandra M JBoonstra Jurjen JHardwick James C Hvan der Kraan JoleinFarina Sarasqueta ArantzaVasen Hans F A - To examine the mechanism of pathogenity of Thr767Ile variant on MSH6 protein. - Source: PubMed
Publication date: 2019/04/22
Stembalska AgnieszkaKlapecki JakubPławski AndrzejKarpinski Paweł - It is increasingly important for clinicians involved in the management of prostate cancer to understand the relevance of heritable (germline) mutations that, for select patients, affect prostate cancer risk and cancer biology, and acquired (somatic) mutations that occur in prostate cancer cells. In the advanced disease setting, mutations in homologous recombination repair genes (eg, BRCA1, BRCA2, ATM, CHEK2, PALB2) suggest candidacy for platinum chemotherapy and PARP inhibitor trials. Similarly, microsatellite instability and mismatch repair deficiency, which may arise in the setting of MLH1, MSH2, MSH6, and PMS2 mutations, suggest potential vulnerability to PD-1 inhibitors. Germline genetic testing has potential importance in the treatment and assessment of familial risk, and tumor-directed somatic sequencing may guide treatment decision-making. This review provides clinicians with knowledge of basic genetic terminology, awareness of the importance of family history of cancer (not limited to prostate cancer), contrasts between the different but potentially related objectives of germline versus somatic testing of tumor tissue, and indications for genetic counseling. Specific clinical scenarios, objectives of testing, and nature of the assays are reviewed. Germline and somatic mutations of known and potential relevance to prostate cancer are discussed in the context of treatment options, and algorithms to assist clinicians in approaching this area are proposed. - Source: PubMed
Cheng Heather HSokolova Alexandra OSchaeffer Edward MSmall Eric JHigano Celestia S - Sir: Lynch Syndrome (LS), an inherited predisposition to a variety of cancers, is caused in the vast majority of cases by a pathogenic mutation within the mismatch repair (MMR) genes (MLH1, MSH2, MSH6 and PMS2). Women with LS have a lifetime risk of approximately 50-60% of developing colorectal carcinoma (CRC) and endometrial carcinoma (EC), with EC often being the first or sentinel malignancy. EC occurring in LS has an excellent outcome, and screening for LS in all newly diagnosed EC patients therefore offers an opportunity to detect undiagnosed LS, with a view to enroll the patient and afflicted family members to appropriate surveillance programs. Universal screening of newly diagnosed EC cases is therefore recommended (1, 2), but has not been widely adopted. In the United Kingdom, universal screening for LS in CRC has been recommended by the National Institute of Health and Care Excellence since February 2017 and similar guidance on EC is awaited. This article is protected by copyright. All rights reserved. - Source: PubMed
Publication date: 2019/05/11
Niu Bonnie THammond Rory F LLeen Sarah L SGilks C BlakeSingh Naveena - DNA mismatch repair (MMR) deficiency is a major pathway of genomic instability in cancer. It leads to the accumulation of numerous mutations predominantly at microsatellite sequences, a phenotype known as microsatellite instability (MSI). MSI tumors have a distinct clinical behavior and commonly respond well to immune checkpoint blockade, irrespective of their origin. Data about the prevalence of MSI among gallbladder cancer (GBC) have been conflicting. We here analyzed a well-characterized cohort of 69 Western-world GBCs. - Source: PubMed
Publication date: 2019/05/08
Goeppert BenjaminRoessler StephanieRenner MarcusLoeffler MoritzSinger StephanRausch MelinaAlbrecht ThomasMehrabi ArianebVogel Monika NadjaPathil AnitaCzink ElenaKöhler BrunoSpringfeld ChristophRupp ChristianWeiss Karl HeinzSchirmacher Petervon Knebel Doeberitz MagnusKloor Matthias