MSH6 (168-417) antibody Host Rabbit
- Known as:
- MSH6 (168-417) (anti-) Host Rabbit
- Catalog number:
- 'GTX111660
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- ACR
- Gene target:
- MSH6 (168-417) antibody Host Rabbit
Related genes to: MSH6 (168-417) 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 (168-417) antibody Host Rabbit
Related articles to: MSH6 (168-417) antibody Host Rabbit
- The objective of the study was to evaluate the prevalence of pathogenic variants in 18 cancer predisposition genes in a national cohort of women with breast cancer diagnosed at age 40 or younger. - Source: PubMed
Publication date: 2026/06/23
Metcalfe KellyNarod Steven APoll AlettaHoey ChristianneWarner EllenBaxter Nancy NIsherwood SusanMacDougall EllenZemani NedaYang FloraSuwito Jason SamuelQuan May-LynnAkbari Mohammad R - Colorectal cancer (CRC) is one of the most prevalent malignancies worldwide, with up to 50% of patients developing metastatic disease, predominantly involving the liver. Hepatectomy remains the gold standard for resectable hepatic metastases; however, recurrence rates remain high and reliable prognostic biomarkers are lacking. Phosphorylated ribosomal protein S6 (pS6), a surrogate marker of PI3K/AKT/mTORC1 pathway activation, has been implicated in tumor aggressiveness across multiple cancer types, but its prognostic role after hepatectomy for metastatic colorectal cancer (mCRC) has not been established. - Source: PubMed
Publication date: 2026/06/22
Henriques Cavalcanti Torres de Melo Rafaellade Barros Silva Paulo GoberlianioNeto Heladio Feitosa E CastroNunes Rayane Cardoso de Souzade Moura Torres de Melo José RicardoBezerra Maria Julia BarbosaDornelas Conceição AparecidaHirth Carlos Gustavo - Hepatocellular carcinoma (HCC) remains a lethal malignancy with limited therapeutic options. While Poly (ADP-ribose) polymerase inhibitors (PARPi) exploit synthetic lethality in tumors with DNA repair defects, their clinical utility in HCC is hindered by the low prevalence of canonical repair gene mutations and the enhancing DNA repair capacity. Through proteomic analysis of two independent cohorts (=260), we identified the THO complex component THOC2 as a master regulator of DNA damage response (DDR) via mRNA nuclear export control. Clinically, THOC2 overexpression predicted poor survival (HR=2.68-6.84, <0.001) and correlated with enhanced DDR gene expression. Mechanistically, THOC2 chaperones mRNA nuclear export of DDR effectors (MDC1, PRKDC, MSH6) and proliferation drivers (TOP2A), thereby establishing a dual pro-repair/pro-growth program. Targeting this vulnerability, THOC2 knockdown induced synthetic lethality with PARPi, reducing Olaparib IC50 by up to 61% and suppressing tumor growth by 76% (<0.001). Our study illuminates mRNA transport as a druggable DDR modulator and establishes THOC2 as both a prognostic biomarker and a therapeutic target to overcome PARPi resistance in HCC. This work pioneers a strategy to expand synthetic lethality beyond genetic defects by targeting post-transcriptional regulation. - Source: PubMed
Publication date: 2026/06/10
Li XinliYang SongpengZhang MengxinGuo ZhaoyuWang YanMeng YanruLiu YuanpingZhang HuXu KaikunZhang XiuyuanZhai YuanjunJin JingzhuoHe FuchuTian ChunyanSun Aihua - Lynch syndrome (LS), also known as hereditary nonpolyposis colorectal cancer, is caused by mutations in the mismatch repair genes and confers genetic predisposition to colorectal and other cancers. Germ cell tumors, the majority of which are seminomas, usually arise sporadically and predominantly occur in younger patients; their association with Lynch syndrome rarely occurs. Insight into such associations will provide knowledge about genetic predispositions and their management implications. A 56-year-old man was brought in with lower back pain and a testicle mass, and constant pain. Enlarged lymph nodes in the retroperitoneal and paravertebral regions suggested testicular cancer by CT scans. The right radical orchiectomy was performed for him and the tests proved that it was a classic seminoma. He had received four cycles of VIP chemotherapy because the cancer had extended to the lungs. The retroperitoneal lymph node dissection (RPLND) was performed after treatment because some lymph nodes were still enlarged, but no cancer was found in those nodes. Further examinations confirmed that the patient had anemia, and colorectal adenocarcinoma was the result of further investigations. The immunohistochemical analysis revealed that there was a loss of MSH6 protein expression while MLH1, MSH2, and PMS2 were preserved. These findings raise suspicion for Lynch syndrome. This case is interesting because seminoma and colorectal cancer were both identified in a patient with features suggestive of a hereditary cancer syndrome. - Source: PubMed
Publication date: 2026/06/18
Kamandi MostafaBoozari MaryamSoltani EhsanSoltani Salman - The expression of mismatch repair (MMR) proteins does not follow a simple "intact" or "loss" pattern. Rather, "nonclassic loss" patterns can be presented. - Source: PubMed
Yu JinchuanXiao XuexueHe WeiyingYang YananYue Junqiu