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
Ask about this productRelated 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
- Papillary thyroid carcinoma (PTC) is the most common type of thyroid malignancy and is generally associated with a favorable prognosis. However, a subset of these tumors exhibits more aggressive behavior, underscoring the need for refined molecular and immunohistochemical characterization to improve diagnostic precision and prognostic stratification. Given the shared embryologic origin of the thyroid gland and gastrointestinal tract from the endoderm, intestinal differentiation markers (CDX2 and SATB2) and alterations in DNA mismatch repair (MMR) pathways, including MLH1 promoter methylation, may represent biologically relevant features in thyroid tumors. This study performed MLH1 promoter methylation analysis by pyrosequencing and protein expression of MLH1, PMS2, MSH2, MSH6, SATB2 and CDX2 by immunohistochemistry in 63 PTCs. Clinicopathological and molecular data were also collected for comparative analyses and correlation with progression-free survival (PFS). All PTCs retained expression of MMR proteins (MLH1, PMS2, MSH2, and MSH6), including the three tumors with MLH1 promoter hypermethylation. CDX2 positivity was detected in only two (3.2%) PTCs (classic and follicular subtypes), and SATB2 expression was absent in all cases. No significant association was identified between MLH1 promoter methylation, MMR protein expression, CDX2 or SATB2 expression, and PFS. In contrast, venous invasion was confirmed as a significant predictor of worse PFS (HR = 3.34; 95% CI 1.27-8.76; p = 0.014) in univariate analysis. MLH1 promoter methylation, MMR deficiency, and CDX2 are rare events in PTC and do not appear to influence PFS. Although infrequent, the expression of CDX2 is not exclusive to any PTC subtype. - Source: PubMed
Publication date: 2026/05/07
Silva Fábio França Vieira EPrada-Ramallal GuillermoDi Domenico MarinaPadín-Iruegas María ElenaRojo-Álvarez Laura IsabelBravo-López Susana BelénDella Monica PaolaColapietra FedericaBallini AndreaCameselle-Teijeiro José Manuel - Malignant teratomas are rare germ cell tumors characterized by undifferentiated embryonic components, exhibiting invasive and metastatic potential. While teratomas commonly arise in the gonads, such as the ovaries and testes, as well as midline locations like the sacrococcygeal region and mediastinum, the occurrence of a malignant teratoma in the femur (right femur) is exceedingly rare, with limited research available. We report the case of a 19-year-old female presented with a subcutaneous mass in the right posterior thigh for 2 months, which was later confirmed as immature teratoma (CK5/6, CK8/18, CK7, CK20, villin , S-100, Syn, GFAP, NF, Neu-N, CgA, CD99, Dasmin, SMA) with higher expression of Ki-67. Two key like pathogenic germline variants were revealed through whole exome sequencing: BLM c.2634C>A (p. Tyr878 *) and MSH6 c.3986C>A (p. Ser1329 *). This report provides information on the clinical course of rare malignant teratoma in the right posterior thigh, including treatment strategy and prognosis. - Source: PubMed
Publication date: 2026/04/21
Shi YanhuiLeng PengfeiTan XiaohuaLiu LinlinZhao Miaoqing - Comprehensive genomic profiling test (CGPT) using next-generation sequencing (NGS) plays a vital role in cancer diagnosis, treatment option, and prognostic evaluation. In Japan, three tissue-based CGPTs, FoundationOne® CDx, GenMineTOP, and NCC OncoGuide™, are reimbursed under public health insurance. However, their comparative performance in central nervous system (CNS) tumors remains unclear. - Source: PubMed
Publication date: 2026/05/06
Kawauchi DaisukeOhno MakotoTakahashi MasamichiKoyama TakafumiSunami KunikoHirata MakotoYanagisawa ShunsukeOmura TakakiAoki TakumaFujii GentaSaito KojiYamamoto TetsuyaSuzuki HiromichiNarita Yoshitaka - Prostate cancer (PCa) is a heterogeneous and prevalent neoplasm, traditionally stratified by PSA and Gleason Score. However, these biomarkers have prognostic limitations, driving the search for new molecular markers. Alterations in DNA mismatch repair (MMR) system proteins are associated with genomic instability, therapeutic resistance, and poorer clinical outcomes. Their relevance in PCa remains poorly understood, highlighting MMR status as a potential prognostic biomarker. This systematic review, following PRISMA 2020 guidelines, evaluated the relationship between MMR protein (MSH2, MSH6, MLH1, PMS2) expression and clinical-pathological outcomes in PCa. Ten studies assessing MMR protein expression in prostate adenocarcinoma samples were included. Risk of bias was assessed using the Newcastle-Ottawa Scale. Studies revealed heterogeneous MMR protein expression. Loss of MSH2 consistently correlated with poorer clinical outcomes, including biochemical recurrence, higher Gleason Scores, and perineural invasion. MSH6 was more prevalent in high-grade tumors, without clear prognostic association. Cytoplasmic MLH1 expression was linked to aggressive histological patterns; PMS2 results were conflicting. Two studies assessed Microsatellite Instability (MSI), correlating with MSH2 and PMS2. Overall, MMR protein alterations, particularly MSH2 loss, may indicate worse PCa prognosis. However, methodological heterogeneity and lack of standardization hinder definitive conclusions. Further studies, integrating MSI analyses are crucial to confirm their prognostic. - Source: PubMed
Publication date: 2026/05/01
Silva Karina SerafimPasotti Maria Clara Del PintorSouza Luiz Gustavo Neiva ReisLeite Katia Ramos MoreiraReis Sabrina T - This case highlights a novel genotype-phenotype correlation in the field of endocrinology. Specific endocrine and imaging assessment, in addition to next-generation sequencing (NGS), was performed on the Illumina MiSeq platform, using a TruSight One Sequencing Panel kit for genomic analysis of coding regions of 4813 genes. A 54-year-old female was confirmed with a papillary thyroid carcinoma after total thyroidectomy and underwent radioiodine ablative therapy. Three years later, a left femoral enchondroma of almost 3 cm was identified at computed tomography (CT) scan and magnetic resonance imaging (MRI). She experienced hypertension (in addition to obesity, dyslipidaemia and impaired glucose tolerance) and was later confirmed with ACTH-independent cortisol excess [lack of cortisol suppression at 1 mg dexamethasone testing of 13.9 (normal < 1.8 µg/dL)], noting bilateral adrenal tumors, of 4.7 cm (right), respectively, and of 1.6 cm (left) at CT. Right laparoscopic adrenalectomy was performed with post-operative adrenal insufficiency, requiring glucocorticoid replacement and stopping the anti-hypertensive medication. Pathology report confirmed an adrenocortical adenoma (a Ki67 proliferation index of 2%). Noting the unusual association of the mentioned conditions, NGS was performed in the peripheral blood and identified a heterozygote missense variant of the gene (c.5759G>A, p.Arg1920Gln), a heterozygote missense variant of the gene (c.2092C>G, p.Gln698Glu), and an incidental additional finding: a heterozygote stop gain pathogenic variant of the gene (c.2707C>T, p.Arg903*). The first two are currently classified as variants of uncertain significance. Whether the co-presence of a triple mutation may change the clinical picture and the life-long outcomes across reciprocal influence is still an open matter. Further research will point out the clinical implications of this genotype-phenotype association, which, to our best knowledge, has not been previously reported. - Source: PubMed
Publication date: 2026/04/16
Carsote MaraSchipor Sorina VioletaDumitrascu AndaGheorghe Ana-MariaSima Oana-ClaudiaManda DanaCostachescu MihaiMuresan AndreiPreda Emi MarinelaTerzea Dana