MSH6 antibody Monoclonal Antibodies Primary antibodies
- Known as:
- MSH6 (anti-) Monoclonal Antibodies Primary antibodies
- Catalog number:
- orb119630
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- MSH6 antibody Monoclonal Antibodies Primary antibodies
Related genes to: MSH6 antibody Monoclonal Antibodies Primary antibodies
- 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 Monoclonal Antibodies Primary antibodies
Related articles to: MSH6 antibody Monoclonal Antibodies Primary antibodies
- DNA mismatch repair (MMR) deficiency is a clinically important biomarker in human oncology, yet its relevance in feline neoplasia remains poorly understood due to limited characterisation and the absence of validated reagents. In this study, we established a practical immunohistochemistry (IHC) approach for evaluating feline MMR proteins by confirming the cross-reactivity of anti-human MLH1, MSH2 and MSH6 antibodies using CRISPR/Cas9-engineered feline tumour cell lines lacking each target gene. Using these validated antibodies, we conducted a pilot screening to assess MMR protein expression in 83 feline tumours and observed variable reductions or losses of MLH1, MSH2 and MSH6 across several tumour types. Notably, MLH1 expression was lost in all melanoma cases (6/6, 100%) and in most osteosarcomas (14/15, 93%), indicating that MMR perturbations may be particularly relevant in these malignancies. These findings provide the first analytically validated framework for assessing MMR proteins in feline oncology and suggest that MMR dysregulation may be more widespread than previously recognised. Although the clinical sample size is limited, this initial pilot screening maps the preliminary landscape of feline MMR protein expression. Further large-scale validation studies incorporating microsatellite instability testing, methylation analysis and genomic profiling are warranted to clarify the biological significance of these alterations. - Source: PubMed
Publication date: 2026/08/16
Nishibori ShomaSakurai MasashiKagawa YumikoNishigaki KazuoNakagawa TakayukiInanaga SakuyaIgase MasayaMizuno Takuya - Pathogenic mutations in the mismatch repair (MMR) genes cause Lynch syndrome. Adenoma resection can prevent colorectal cancer (CRC), but the occurrence of precancerous lesions is understudied in Lynch syndrome. - Source: PubMed
Publication date: 2026/07/08
Atarere JosephBilalaga Maria MalakVasireddy RamyaMensah BonifaceGaddipati Greeshma NSingh SimardeepAkhiwu Ted OWoo StephanieDash ChiranjeevKanth Priyanka - To analyze the type and frequency druggable mutations in patients with progressive metastatic castration-resistant prostate cancer (mCRPC). - Source: PubMed
Publication date: 2026/08/13
Steenbock OliviaRieger ConstantinHeidenreich JulianPaffenholz PiaPfister DavidBrandenstein Melanie vonHeidenreich Axel - Tumors exhibiting mismatch repair deficiency without detectable germline mutations via standard multigene panel testing are often classified as Lynch-like syndrome. In the present report, we describe the case of a 47-year-old man presenting with synchronous axillary sebaceous carcinoma and colonic medullary carcinoma. Although initial germline multigene panel testing failed to identify pathogenic variants, a high degree of pathological suspicion for Muir-Torre syndrome remained. Immunohistochemistry revealed a concordant loss of MSH2 and MSH6 expression in both the extraocular sebaceous carcinoma and the colonic medullary carcinoma. This identical protein-loss pattern detected across anatomically distinct tumors served as decisive pathological evidence of an underlying germline defect rather than independent biallelic somatic mutations. Consequently, whole-genome sequencing was performed to resolve the discrepancy between the pathological findings and multigene panel testing results, successfully identifying a germline intronic MSH2 variant (NM_000251.3:c.2459-12A>G). Subsequent RNA analysis confirmed aberrant splicing with an 11-bp insertion. In conclusion, the present case illustrates that concordant mismatch repair protein loss across multiple tumors provides compelling morphological evidence to guide pathologists in reconsidering negative panel results and pursuing comprehensive genomic investigation to identify pathogenic intronic variants. - Source: PubMed
Noda KeisukeKurohama HirokazuMatsuda KatsuyaKinoshita AkiraMishima HiroyukiMatsumoto MegumiMatsuda RikoUeki NozomiKishikawa MasaoMiura KiyonoriNonaka TakashiYoshiura Koh-IchiroMatsumoto KeitaroNakashima Masahiro - Mismatch repair deficiency (MMRd) is a critical biomarker in endometrial cancer (EC) for prognostication, Lynch syndrome screening, and immunotherapy eligibility. This study aimed to determine the prevalence of MMRd and its correlation with clinicopathological characteristics in EC. This prospective observational cohort included 93 patients with EC undergoing primary surgical treatment, managed as per the European Society of Gynaecological Oncology (ESGO) guidelines. , , , and expression was assessed through immunohistochemistry (IHC) on formalin-fixed, paraffin-embedded hysterectomy specimens. Associations between mismatch repair (MMR) status and histology, grade, lymphovascular space invasion (LVSI), myometrial invasion, FIGO 2023 stage, nodal status, recurrence, and survival were analyzed. The median age was 66 years. Most tumors were endometrioid (86%), 29% were grade 3, 45.2% showed deep myometrial invasion, and 23.7% had substantial LVSI. MMRd was identified in 41.9% of cases, with MLH1 and PMS2 loss being most frequent, and was significantly associated with endometrioid histology ( = 0.027) and deep myometrial invasion ( = 0.011). No significant correlations were found with grade, LVSI, FIGO stage, nodal involvement, recurrence, or overall survival. Routine MMR assessment may refine risk stratification and guide individualized treatment decisions. - Source: PubMed
Publication date: 2026/07/31
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