MSH6 antibody Host Rabbit
- Known as:
- MSH6 (anti-) Host Rabbit
- Catalog number:
- 'GTX111661
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- MSH6 antibody Host Rabbit
Related genes to: MSH6 antibody Host Rabbit
- Gene:
- MSH6 NIH gene
- Name:
- mutS homolog 6
- Previous symbol:
- GTBP
- Synonyms:
- -
- Chromosome:
- 2p16.3
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-29
- Date modifiied:
- 2019-04-23
Related products to: MSH6 antibody Host Rabbit
Related articles to: MSH6 antibody Host Rabbit
- To evaluate the prognostic significance of mismatch repair (MMR) markers in head and neck squamous cell carcinoma (HNSCC) patients. We performed a systematic review of prognostic factors following PRISMA 2020 using the PI(E)COS framework. Observational studies evaluating MMR protein expression (MSH2, MLH1, MSH6, PMS2) in HNSCC were identified through searches in five databases and gray literature. Eligible studies were qualitatively synthesized. Risk of bias was assessed using the QUIPS tool. Seven observational studies involving 846 HNSCC patients met the eligibility criteria. Most patients were males (78.3%), the age ranged from 59 to 63.6 years, and the oral cavity was the most common tumor site. MMR protein expression associated with clinicopathological features was heterogeneous, with prognostic effects varying according to tumor subsite, HPV/p16 status, and analytical approach. Across the available studies, low or loss of MSH2 expression was consistently associated with poorer overall survival, with reported hazard ratios ranging from 2.75 to 4.38, all indicating a clinically meaningful increased risk of death. In contrast, the prognostic value of MLH1, MSH6, and PMS2 varied by tumor subsite, HPV/p16 status, and patient age, lacking sufficient consistency for quantitative pooling. Due to the limited number of methodologically comparable studies, a quantitative meta-analysis was not appropriate. In conclusion, the pooled results showed that reduced or absent MSH2 expression is linked to poorer outcomes in HNSCC, suggesting that MSH2 may be the most promising prognostic biomarker, pending further validation. - Source: PubMed
Publication date: 2026/08/11
de Carvalho Gomes José RenatoCosta Raisa Ferreirade Lima-Souza Reydson AlcidesAntolini-Tavares ArthurTincani Alfio JoséChone Carlos TakahiroAltemani AlbinaMariano Fernanda Viviane - CpG dinucleotides are mutational hotspots due to spontaneous deamination of 5-methylcytosine (5mC), resulting in T:G mismatches that can lead to CpG>TpG transitions. These mutations are a hallmark of aging and cancer and play a central role in the evolution of vertebrate genomes. We have previously uncovered MBD4 as the primary base excision repair (BER) glycosylase responsible for 5mC deamination repair. Here, we employ an APOBEC1 deaminase fused to a catalytically dead Cas9 to induce targeted 5mC deamination independently of DNA replication and track its repair in human cells. This approach reveals that MBD4 elicits a coordinated repair response with a non-canonical branch of mismatch repair (MMR) involving complexes MutLβ (MLH1-PMS1) and MutSα (MSH2-MSH6). We uncover the physical interaction between MBD4 and MutLβ and demonstrate that MBD4-mediated repair requires MLH1. We show that PMS1 deficiency phenocopies the CpG>TpG hypermutation signature characteristic of MBD4 loss, establishing 5mC deamination repair as a key function of human PMS1. In alignment with our experimental data, we show that the CpG>TpG mutational burden in MMR-deficient tumors is partly explained by replication-independent processes. Altogether, we uncover a novel function of non-canonical MMR that underscores its interplay with BER in safeguarding genomic integrity against damage to methylated DNA. - Source: PubMed
Le Ven AnaïsVanhuele SandraGanier OlivierHouy AlexandreKahn AmandaRodrigues ManuelStern Marc-HenriGuerois RaphaelSilveira André Bortolini - In humans, about 5-10% of all cancers are caused by germline pathogenic variants (PVs) in cancer-predisposing genes, and their identification enables precision oncology approaches, such as surveillance for early detection, preventive medicine, and targeted therapy. Although cancer is a leading cause of death in cats, PVs have not been investigated for precision oncology. We developed a feline-specific multiplex targeted sequencing method to analyze 813 cats for putative PVs in 27 candidate feline cancer-predisposing genes. A total of 784 variants were identified, 13 of which were classified as putative PVs based on predicted truncating impact of amino acid sequence, clinical interpretation of corresponding variants in human, and in silico prediction on amino acid functions. Among 18 cats with one of the 13 putative PVs, seven (38.9%) had various types of confirmed or suspected tumor. Although PV carriers do not always develop cancer even in humans, putative PV carriers without tumors tended to be younger (1.83-16.58, years old, 9.16 years old on average) than the median age of tumor-bearing putative PV carriers (11.83 years old), suggesting that the proportion of affected cats may increase over time. Moreover, five cats with putative PVs in homologous recombination repair genes (BRCA2, RAD51C, or ATM) and two cats with those in mismatch repair genes (MSH2 and MSH6) may be candidates for targeted therapy with PARP inhibitors and immunotherapy with immune checkpoint inhibitors, respectively. These findings provide the first characterization of putative PVs in feline candidate cancer-predisposing genes, representing an important step toward genomics-informed oncology and risk stratification in cats. - Source: PubMed
Publication date: 2026/08/08
Ikeda NamikoMizukami KeijiroYamada RyokoToyoda HirotoAoi TomomiEndo MikikoIwasaki YusukeKato DaikiNakagawa TakayukiNishimura RyoheiTomiyasu HirotakaMomozawa Yukihide - Multiple germline variants are associated with prostate cancer (PCa) susceptibility and aggressive features; however, their value for predicting prostate cancer-specific mortality (PCSM) at the time of diagnosis remains uncertain, particularly among men with clinically localized disease. - Source: PubMed
Publication date: 2026/08/04
Lu LucyXu JulianShi ZhuqingEngelmann ValentinaTran HuyWei JunAshworth AnnabelleCornell BrandonPieczonka ChristopherIsaacs William BZheng S LillyHelfand Brian TLuo JunXu JianfengLu Jim - All individuals with colorectal cancer (CRC) should undergo genetic cancer risk assessment given its implications for personalized treatment, surveillance, risk-reduction strategies, and cascade testing. Universal screening using immunohistochemistry (IHC) for mismatch repair (MMR) proteins in tumor tissue, when combined with clinical criteria, is essential for identifying individuals at higher risk for carrying germline pathogenic variants (PVs) in resource limited countries. - Source: PubMed
Publication date: 2026/08/04
Rodríguez-Olivares José LuisAguilar-Y-Méndez DioneKimball Tamara NRivero-García PamelaRios-Valencia JavierSantuario-Facio SandraRojas-Martinez AugustoOrtiz-López RocíoBarraza-Arellano Angélica LeticiaAranda-Gutierrez AlejandroArteaga-Vazquez JazmínDe-La-Mora-Molina HéctorHerzog JosefJeter Joanne MWeitzel Jeffrey NChávarri-Guerra Yanin