MSH6 BLOCKING PEPTIDE
- Known as:
- MSH6 BLOCKING PEPTIDE
- Catalog number:
- ABS9581
- Product Quantity:
- 50 µg
- Category:
- Peptides
- Supplier:
- AbD
- Gene target:
- MSH6 BLOCKING PEPTIDE
Ask about this productRelated genes to: MSH6 BLOCKING PEPTIDE
- 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 BLOCKING PEPTIDE
Related articles to: MSH6 BLOCKING PEPTIDE
- Ovarian aging, marked by the gradual decline in both the number and quality of oocytes, significantly impacts women's reproductive lifespan and overall health. However, the biological mechanisms driving ovarian aging remain poorly understood and current treatment strategies are limited. - Source: PubMed
Publication date: 2026/05/28
Lian XuanSong ShuangLou ChenZhu MingLi YanLi WenjianJiang XintongWang GuiquanYang HaiyanWang LinHe LiyingMa YunlongDong XiChen YijieChang Hsun-MingZhu WenchengWang JiaYu YangWu YangZhao YueMu Liangshan - To investigate oncological and reproductive outcomes in patients with mismatch repair-deficient (MMRd) endometrial endometrioid carcinoma (EEC) or atypical endometrial hyperplasia (AEH) undergoing fertility-preserving treatment to inform clinical management of this molecular subtype. - Source: PubMed
Publication date: 2026/05/27
Zhang TianyuYang JieCao DongyanYu MeiWu HuanwenXiang YangZhang XinyueZong XuanZhang RundongJin XinyangZhang KezhenZheng JingYang Jiaxin - The aim of this study is to assess the mismatch repair (MMR) status and immunohistochemical changes in cases of recurrent endometrial cancer following primary surgery and to evaluate the impact of these changes on prognosis. Thirty-one patients diagnosed with endometrial cancer who underwent surgery and had pathologically confirmed recurrences were evaluated. Changes in MMR protein expression, estrogen receptor (ER)/progesterone receptor (PR), and p53 expression in primary surgery and recurrent tumor tissues were assessed using immunohistochemical methods. Prognostic factors influencing these parameters and survival data were investigated. : In the assessment of recurrent materials, there were four cases where the MLH-1&PMS-2 staining status changed from intact to loss and four cases that changed from loss to intact. No changes were observed in regard to MSH-2 &MSH-6 staining. The ratios of pMMR and dMMR following the primary surgery were 55% (n = 17) and 45% (n = 14), respectively. Four cases transitioned from pMMR to dMMR, and four cases transitioned from dMMR to pMMR. After recurrence, changes in the ER, PR, and P53 status were observed in seven, three, and three patients, respectively. : Changes in the MMR status, receptors, and P53 were observed. It is necessary to re-evaluate prognostic parameters via biopsies in recurring cases and to adjust rescue treatments accordingly. - Source: PubMed
Publication date: 2026/04/27
Guzeloz ZelihaKutlu OzceErdogan OzgurDemir GonulGulle Bugra TaygunSancı MuzafferErdogan MihribanTalu Canan Kelten - Endometrial carcinoma (EC) is now classified primarily by molecular subtype--ultramutated, mismatch repair-deficient (dMMR), -mutant/copy-number-high (CNH), and "no specific molecular profile" (NSMP)-a framework that has reshaped prognostic counseling and adjuvant therapy decisions. Yet several practically important questions remain insufficiently addressed in real-world cohorts: whether all four mismatch repair genes confer an equivalent favorable prognosis, whether all alterations carry the same survival benefit or only specific pathogenic variants, and whether molecular subtypes retain prognostic value after adjustment for histology and tumor burden. We addressed these questions in 2901 patients pooled from the MSK-IMPACT 50K Clinical Sequencing Cohort ( = 2372; discovery) and the TCGA UCEC PanCancer Atlas ( = 529; validation)-the largest dual-cohort genomic analysis of EC reported to date. We performed individual MMR gene and combined dMMR survival stratification, multivariable Cox regression adjusted for age, histology, and sample type, and a pathogenicity-aware sensitivity analysis for POLE variants, with tumor mutational burden (TMB) compared across subgroups. Across both cohorts, all four MMR gene-mutant subgroups (, , , ) conferred equivalently favorable overall survival (OS) (six-group log-rank = 7.66 × 10 in discovery; = 6.78 × 10 in validation), confirming dMMR as a class-level prognostic designation independent of which MMR gene is altered. Multivariable Cox regression demonstrated that -ultramutated status retained an independent favorable effect (HR = 0.62, = 0.038 in MSK; HR = 0.35, = 0.028 in TCGA) after adjustment for age, histology, and sample type, while the favorable dMMR effect was largely accounted for by histologic context. Critically, a pathogenicity-aware sensitivity analysis revealed that the exceptional survival of the subgroup is confined to canonical exonuclease-domain hotspot mutations (event rate 0.9% in MSK), whereas variants of uncertain significance behave indistinguishably from NSMP-like tumors. Consistent with this finding, TMB was markedly elevated in canonical pathogenic cases (median 138.7 mut/Mb in MSK; 247.4 in TCGA) but not in -VUS-only cases (median 29.0 and 15.0, respectively; < 0.001 between groups in both cohorts), confirming that the ultramutator phenotype is confined to canonical pathogenic variants. We additionally characterize Uterine Clear Cell Carcinoma as a distinct histologic entity ( = 73; 3.0%) and report the + co-mutant group ( = 90; 3.8%). These findings refine the molecular classification of EC in clinically meaningful ways: they support class-level immunotherapy eligibility based on dMMR status regardless of the specific MMR gene altered, demonstrate that -ultramutated classification requires variant-level pathogenicity assessment, and identify -mutant/CNH patients as the population with the most urgent unmet therapeutic need. - Source: PubMed
Publication date: 2026/05/21
Sertesen Çamöz ElifKarabuğa BerkanKaraçin CengizTerzi Yunus KasımYılmaz Çelik Zerrin - To characterize tumor-site distribution, age at diagnosis, sex distribution, and tumor multiplicity in a Brazilian institutional Lynch syndrome (LS) cohort stratified by mismatch repair (MMR) gene and genetic testing status, and to assess the impact of including nontested (NT) relatives. - Source: PubMed
Publication date: 2026/05/20
Bassaneze ThiagoOliveira Ferreira FábioSandoval Renata LazariPisani Janina PontesVanessa Quirino CarlaRodrigues de Nicola Pablo DomingosAchatz Maria IsabelDominguez-Valentin MevRossi Benedito Mauro