Anti - Mouse, MSH2 Clone FE11
- Known as:
- Anti - Mouse, MSH2 Clone FE11
- Catalog number:
- 60-0046
- Product Quantity:
- 6 mL
- Category:
- -
- Supplier:
- Genemed
- Gene target:
- Anti - Mouse MSH2 Clone FE11
Related genes to: Anti - Mouse, MSH2 Clone FE11
- 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: Anti - Mouse, MSH2 Clone FE11
Related articles to: Anti - Mouse, MSH2 Clone FE11
- MutS Homolog 3 (MSH3), part of the MutSβ DNA mismatch repair complex with MSH2, can reversibly translocate from the nucleus to cytosol via IL-6 signaling, abrogating nuclear MutSβ function and is associated with metastasis and poor patient survival. A polymorphism consisting of deletion of 27-bp proximate to the nuclear localization signal (NLS) (Δ27bpMSH3) allows MSH3 cytosolic retention with IL-6 or oxidative stress. Here, we examined for IL-6-induced post-translational modifications associated with MSH3 cytosolic translocation. - Source: PubMed
Publication date: 2026/03/25
Tseng-Rogenski Stephanie SKoi MinoruCarethers John M - Lynch syndrome predisposes to multiple cancer types, including urological malignancies. However, no evidence-based recommendations for surveillance of urological malignancies currently exist. In this systematic review, we aim to describe the current evidence regarding surveillance for these cancers. A systematic literature search was conducted using MEDLINE, searching for urological malignancies, Lynch syndrome, and surveillance including the results of the surveillance methods. Sensitivity and specificity were calculated, when possible, preferably for pooled data from each surveillance method. The risk of bias was assessed using the Newcastle–Ottawa Scale. After full text-screening, nine studies published in 2008–2025 met the inclusion criteria, including two on prostate cancer and seven on urothelial cancer. Prostate cancer-antigen (PSA) surveillance led to 38 prostate cancer diagnoses in 865 individuals with Lynch syndrome, with 71% being clinically significant prostate cancers. In 1564 individuals, 11 urothelial carcinomas were diagnosed by different surveillance methods and 15 diagnoses were missed. Sensitivity of urinalysis, urine cytology, urine MSI, and CT and cystoscopy was 11%, 30%, 100%, and 100% respectively. Specificity was 90%, 97%, 99%, and 100% respectively for these methods. Further data is needed but for prostate cancer surveillance PSA shows promise, while for carriers at least, urine microsatellite instability analysis shows promise as a urothelial cancer surveillance test. - Source: PubMed
Publication date: 2026/04/24
Doornweerd B H JRasmussen M W - Gallbladder adenocarcinoma has limited global prevalence but occurs more frequently in certain regions. The disease is often diagnosed at advanced stages, restricting therapeutic options and contributing to poor outcomes. The molecular mechanisms underlying its development remain largely undefined, complicating the discovery of targeted therapies. Microsatellite instability (MSI), resulting from defective DNA mismatch repair, plays a well-established role in several malignancies; however, its significance in gallbladder adenocarcinoma remains unclear. Characterizing MSI status may help identify patients eligible for novel therapeutic approaches. This study investigates the loss of DNA mismatch repair protein expression in gallbladder adenocarcinoma. - Source: PubMed
Publication date: 2026/03/09
Ghosh RanajoyMondal AninditaHalder AniketRay SukantaChatterjee Uttara - Approximately 5-10% of the cases with colorectal cancers have a hereditary cancer syndrome. MUTYH is a DNA base excision repair gene, and its mutation can induce the development of polyposis and colorectal cancer. Additionally, MUTYH repair gene may interact with the DNA mismatch repair system. The aim of this study was to investigate the clinicopathological features of colorectal cancer cases carrying germline MUTYH mutations. - Source: PubMed
Publication date: 2026/04/20
Guzelis IsmailGasimli RoyaSubaşıoğlu AslıSari Aysegul - Microsatellite instability (MSI) is a clinically actionable molecular phenotype in cancer, but MSI-associated findings remain fragmented across tumor types, study designs, and biomarker categories, limiting systematic cross-cancer comparison and evidence-guided biomarker prioritization. To address this problem, we developed the Microsatellite Instability Cancer Knowledgebase (MSICKB), a manually curated and literature-traceable resource for MSI-associated molecular and clinical features. We collected and curated 1,382 MSI-related features from 492 publications covering 31 cancer types and organized the evidence into 4 major dimensions: genetic and molecular alterations, clinicopathological features, prognostic factors, and therapeutic response. Based on curated gene-cancer associations, we constructed a simple bipartite network to examine the cross-cancer organization of MSI-associated genes. In the primary network, 99 genes were linked to 13 cancer types through 147 unique gene-cancer edges. Gene degree was strongly right-skewed, with most genes linked to a single cancer type and a small subset showing broader cross-cancer connectivity. Using an operational cutoff of degree ≥ 3, we identified 9 hub genes: BRAF, CD274, KRAS, MLH1, MSH2, PTEN, RNF43, TGFBR2, and TP53. These hubs were enriched in canonical MSI-related pathways, including mismatch repair, cancer signaling, and immune regulation. To provide external molecular support, we further evaluated the hub genes in 3 The Cancer Genome Atlas cohorts with established MSI relevance. In pooled analyses of 336 MSI-high and 1,214 non-MSI-high tumors, all 9 hub genes showed significant differences in mutation prevalence and expression. Overall, MSICKB provides a structured framework for MSI-related evidence synthesis, cross-cancer comparison, and biomarker prioritization and is freely available at http://www.sysbio.org.cn/MSICKB/. - Source: PubMed
Publication date: 2026/04/20
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