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
- The utility of whole-genome sequencing (WGS) for detecting childhood leukemia predisposition remains unclear. We perform a nationwide, prospective, population-based study of 181 children with acute leukemia to assess diagnostic yield and clinical utility of a uniformly applied three-pronged strategy, including systematic phenotyping, germline WGS-based 189-gene panel and tumor sequencing of positive cases. Trio-WGS is performed in 11 high-suspicion families. Nine patients have pathogenic germline alterations: six (3.3%) with leukemia predisposition syndromes (TP53, CEBPA, DNMT3A, trisomy 21) and three (1.6%) with solid tumor predisposition syndromes (MSH6, PALB2, SDHA). Trio-WGS identifies one likely-pathogenic de novo DNMT3A variant. Six of nine diagnoses are previously unrecognized. Findings lead to tailored surveillance in 8/9 patients and treatment modifications in 4/9. Here, we show that this strategy gives a modest diagnostic yield. Nevertheless, the actionability of the findings supports its feasibility and validity in practice. Whether to restrict analysis to leukemia-relevant genes or broaden the panel should reflect local resources and counseling capacity. - Source: PubMed
Publication date: 2026/09/28
Taylan FulyaStaffas AnnaSjögren SaraLagerstedt-Robinson KristinaKuchinskaya EkaterinaPoluha AnnaIvarsson SofieHellberg MariaKlar JoakimAbel FridaAbrahamsson JonasPronk Cornelis JanBelander Strålin KarinHarila ArjaVogt HartmutNorén-Nyström UlrikaGrillner PernillaPalmqvist LarsArvidsson LindaPandzic TatjanaBondeson Marie-LouiseMu NinniEkholm KatjaAnderlid Britt-MarieGolovleva IrinaMaya-González CarolinaGideonsson PärTham EmmaBarbany GiselaLähteenmäki PäiviSandgren JohannaRosenquist RichardWirta ValtteriLjungman GustafGisselsson DavidPalle JosefineTesi BiancaNordgren Ann - Colorectal carcinoma (CRC) metastatic to the breast is exceedingly rare, with 46 cases compiled in a 2019 literature review and additional isolated reports since. The diagnostic challenge is substantially amplified in patients with a prior breast cancer history, in whom new breast lesions are reflexively attributed to recurrence rather than extramammary metastasis. A 71-year-old woman with a significant family history of malignancy presented with invasive lobular carcinoma of the left breast, treated with lumpectomy and hormonal therapy. Four months later, she was diagnosed with stage I endometrioid adenocarcinoma of the uterus; immunohistochemistry of the hysterectomy specimen revealed isolated PMS2 loss with preserved MLH1, MSH2, and MSH6 expression, and comprehensive germline testing of 35 hereditary cancer predisposition genes was negative, establishing a Lynch-like phenotype in that tumor. Approximately four years after her breast cancer diagnosis, she developed a maculopapular rash with skin thickening of the left breast, without a discrete mass; the clinical and mammographic presentation was concerning for inflammatory breast carcinoma. Punch biopsy demonstrated poorly differentiated adenocarcinoma with signet ring cell features, immunohistochemically positive for SATB2, CDX2, CK20, and CEA and negative for CK7, ER, PR, HER2, and GATA3, confirming colorectal origin and excluding breast cancer recurrence. Mismatch repair immunohistochemistry on the same specimen demonstrated retained expression of all four proteins, discordant with the endometrial primary and concordant with microsatellite instability-stable status and a tumor mutational burden of 3.7 mutations/Mb. Next-generation sequencing identified a TP53 splice region loss-of-function variant with RAS and BRAF wild-type status. Positron emission tomography revealed stage IV disease with hepatic metastasis, and colonoscopy identified synchronous cecal and recto-sigmoid masses. She was treated with four lines of systemic therapy and palliative radiation to the breast, and died approximately 20 months after the metastatic diagnosis. This case illustrates two points. First, any new breast lesion in a patient with prior malignancy requires histopathologic confirmation with comprehensive immunohistochemical analysis, as neither recurrence nor a primary breast process can be assumed. Second, mismatch repair status is a property of the individual tumor rather than of the patient; in patients with multiple primaries, each tumor requires independent testing, and molecular findings from one cannot be extrapolated to another. - Source: PubMed
Publication date: 2026/08/28
Walters Morgan LFigueroa Quast Andres - Lynch syndrome (LS) is the most common cause of hereditary colorectal and endometrial cancer. LS is caused by germline pathogenic variants (PV) in the mismatch repair genes (MLH1, MSH2, MSH6, PMS2) and EPCAM. Little is known about LS in Iraqi/Chaldean and broader Middle Eastern and North African populations. We describe our institution's experience with a unique MSH2 PV in a cohort of Iraqi/Chaldean patients. Records of patients with LS and Iraqi/Chaldean ancestry seen in a high-volume cancer genetics center between January 2008 and March 2024 were analyzed. A total of 483 LS patients were identified, of whom 60 (12.4%) reported Iraqi/Chaldean ancestry. Of those, 53 individuals (88.3%) from 22 unique families harbored the same PV in MSH2, c.932delA (p.N311Tfs*20) and were analyzed in this study. This variant was detected only in our Iraqi/Chaldean population. Of individuals with this variant, 28 (52.8%) had at least one LS-related cancer diagnosis (17 colorectal, 12 endometrial, 7 renal/urothelial, 6 ovarian, one sebaceous carcinoma), of whom 16 (57.1%) had multiple malignancies. The average age of colorectal cancer onset was 49.6 years. Additionally, 14 families (63.6%) underwent cascade testing, identifying 31 of the MSH2 carriers in this cohort and 25 true negatives. This is the first report of a recurrent MSH2 c.932delA PV in Iraqi/Chaldean patients with LS. These findings suggest a putative LS founder variant in the Iraqi/Chaldean population, and further studies are needed to characterize LS in this population. - Source: PubMed
Publication date: 2026/09/27
Bradley MikaelaRangarajan TaraZakalik Dana - Endometrial carcinoma is the most common malignancy of the female genital tract, and endometrial intraepithelial neoplasia (EIN, also termed atypical endometrial hyperplasia) is its recognized precursor lesion. Mismatch repair (MMR) deficiency, identified through loss of MLH1, PMS2, MSH2, and MSH6 expression on immunohistochemistry (IHC), is an important molecular event in endometrial carcinogenesis with diagnostic, prognostic, and hereditary (Lynch syndrome) implications. Comparatively few studies have examined the frequency of MMR loss in EIN. This study evaluated the proportion and patterns of MMR protein loss in EIN and endometrial carcinoma, with descriptive assessment of MMR protein loss according to histopathological grade of endometrial carcinoma. - Source: PubMed
Publication date: 2026/08/25
Maheshwari UjwalaAnand RamanaShah Vrutika - Tarin exhibits immunomodulatory and antiproliferative properties against several tumor cell lines. Nano-encapsulation in liposomes enhances its therapeutic potential by improving protein stability, bioavailability, and sustained release. Previous studies demonstrated that nano-encapsulated tarin induces cell cycle arrest, migration inhibition, apoptosis, and autophagy in triple-negative breast cancer cells; however, the molecular mechanisms underlying these effects remain poorly understood. To investigate the proteomic response elicited by nano-encapsulated tarin, MDA-MB-231 cells were treated for 24 and 48 h. Intracellular proteins were extracted, digested with trypsin, and analyzed by label-free LC-2D-MS/MS using HDMSE acquisition. Differentially expressed proteins were identified and quantified using the Progenesis QI platform, and then functional classification and pathway enrichment analyses were performed. A total of 2818 proteins were identified, of which 2150 displayed time-dependent modulation following treatment. After 24 h, cells exhibited an adaptive stress response profile characterized by increased DNA repair proteins (, ), migration/remodeling factors (, , ), and immune/cell cycle regulators (, ), while antioxidant proteins (, ) and BRCA1 were reduced, indicating oxidative stress and DNA damage. After 48 h, the proteomic profile shifted toward cell death, with increased , , , and CASP8 expression, disruption of DNA repair and cell cycle regulators (, , , ), and decreased migration-related proteins (, , , ). Nano-encapsulated tarin promotes a time-dependent transition from early adaptive stress responses to apoptosis, autophagy, cell cycle disruption, and loss of migratory capacity. These findings provide novel insights into the molecular mechanisms underlying tarin antitumoral activity and support its potential as a promising therapeutic strategy against triple-negative breast cancer. - Source: PubMed
Publication date: 2026/09/07
Cardoso Raiane VPereira Patricia RFreitas Cyntia SSouza Yuri PKalume Dário EVerissimo da Costa Giovani CarloConte-Junior Carlos APaschoalin Vania Margaret Flosi