FANCE siRNA_Lentivectors
- Known as:
- FANCE siRNA_Lentivectors
- Catalog number:
- i007682b
- Product Quantity:
- 500ng
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FANCE siRNA_Lentivectors
Related genes to: FANCE siRNA_Lentivectors
- Gene:
- FANCE NIH gene
- Name:
- FA complementation group E
- Previous symbol:
- FACE
- Synonyms:
- FAE
- Chromosome:
- 6p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 1996-04-09
- Date modifiied:
- 2019-04-23
Related products to: FANCE siRNA_Lentivectors
Related articles to: FANCE siRNA_Lentivectors
- Germline mutations in homologous recombination-related genes significantly increase the lifetime risk of breast, ovarian, and other cancers; thus, the concept of BRCAness has been extensively studied. In this study, we aimed to investigate the association between germline mutations and breast cancer in clinical and experimental settings. Germline pathogenic or likely pathogenic variants in were identified through multigene panel testing in the PLEASANT studies. Fourteen cases of breast cancer with germline pathogenic or likely pathogenic variants in were identified. Compared to 1,446 wild-type cases of breast cancer, they appeared to be more aggressive. The proportion of patients with triple-negative breast cancer (TNBC) was higher and larger tumors (>2 cm) were more common. RAD51D-deficient tumors showed better pathological complete responses, defined as ypT0 ypN0, to neoadjuvant chemotherapy. Based on clinical findings, we analyzed the impact of RAD51D-deficiency on drug sensitivity to identify targetable vulnerabilities in RAD51D-deficient tumors. These TNBC cells were significantly more sensitive to cisplatin than wild-type TNBC cells, consistent with our clinical data. In conclusion, RAD51D-deficient tumors were shown to have a phenotype similar to that of BRCA1-deficient tumors, and further investigation of responses to DNA-damaging agents, particularly platinum-based chemotherapy, is warranted. - Source: PubMed
Publication date: 2026/05/21
Jo SeongyeonShim Wan CheolPark ShinyoungKweon TaeyongRyu Won-JiHwang YumiKim Min WooAhn Jee HyunLee Yoon JungLee Sun HwaWon DongjuNam Eun JiHan Jung WooKim Tae IlPark Ji SooPark Hyung Seok - Homologous Recombination Repair (HRR) genes alterations are a resistance mechanism to therapies by taxanes or Androgen Receptor Signalling inhibitors in Metastatic Castration Resistant Prostate Cancer (mCRPC). BRCA-mutated mCRPC patients are eligible to poly adenosine diphosphateribose polymerase inhibitors (PARPi). Therefore, assessing the population-specific prevalence of HRR-related genes alterations is of public healthcare importance. - Source: PubMed
Publication date: 2026/06/16
Allaume PierreRaby MaximeNourieh MayaLespagnol AlexandraTallet AnnePéricart SarahTantot JulietLindner VéroniqueDecaussin MyriamCallens CélineDescotes FrançoiseAllory YvesRioux-Leclercq NathalieKammerer-Jacquet Solène-FlorenceFromont Gaëlle - Breast cancer etiology involves a complex interplay of various risk factors, with genetic alterations playing a significant role in susceptibility to the disease. While mutations in genes such as BRCA1 and BRCA2 are well established in elevating breast cancer risk, their potential role in predicting metastatic progression remains unclear. A recent study by Mei et al. suggested that a common germline variant in the PCSK9 gene (rs562556) may increase metastasis risk and lower survival rates in breast cancer patients. To investigate this association, we evaluated the relationship between the PCSK9 rs562556 variant genotypes and survival outcomes in two cohorts: patients with BRCA1 mutations and those with familial breast cancer lacking mutations in known susceptibility genes. Our study included 1052 BRCA1 mutation carriers, 467 familial breast cancer patients of unknown genetic etiology, and 1404 controls. Genotyping was performed using TaqMan genotyping and whole-exome sequencing. Survival analyses were conducted using Kaplan-Meier survival curves and Cox proportional hazards models. We found no significant association between PCSK9 rs562556 variant and breast cancer mortality or time to death following distant recurrence in either cohort. This finding does not support PCSK9 prognostic impact in breast cancer that may be modified by additional genetic or environmental factors. - Source: PubMed
Publication date: 2026/06/15
Cybulski CezaryKluźniak WojciechWokołorczyk DominikaZamani NedaStempa KlaudiaGliniewicz KatarzynaHuzarski TomaszFalco MichalSun PingGronwald JacekLubiński JanNarod StevenAkbari Mohammad R - In this study, we synthesized novel 2-aryl-6-carboxamide-substituted benzoxazole derivatives and evaluated their anticancer potential against breast cancer cell lines, with a focus on mTOR inhibitory activity. The compounds were synthesized via a three-step method and characterized by NMR analysis. studiesincluding molecular docking, molecular dynamics simulations, and ADMET predictionswere conducted to predict interactions with the target protein and support the observed biological activity. IC0 values were determined in MCF-7 and MDA-MB-231 cells, with MCF-7 cells exhibiting greater sensitivity to the compound. The most active compounds, COH-17 and COH-19, demonstrated cytotoxicity as indicated by LDH release assays. Apoptotic effects were investigated at both molecular and cellular levels: Western blot analysis assessed key apoptotic proteins (Bcl-2, Bax, caspase-3, and p53), while RT-qPCR quantified the expression of BRCA1, BRCA2, PTEN, TP53, BCL-2, BAX, Caspase-3, PI3K, AKT, and BRAD1 genes. Morphological changes associated with apoptosis were confirmed by DAPI staining and fluorescence microscopy, and early and late apoptosis were quantified using Annexin V-FITC/PI flow cytometry. Cell cycle analysis revealed phase-specific arrest, further supporting the antiproliferative activity of the compound. Overall, COH-17 and COH-19 demonstrated potent anticancer effects through mTOR inhibition, induction of apoptosis, and cell cycle arrest, highlighting their potential as targeted therapeutic agents for breast cancer. - Source: PubMed
Publication date: 2026/05/22
Hepokur CeylanAykaç OkanMisir SemaAkin ŞeydaKuzu BurakKosar NaveenKurnaz RecepAlgül Öztekin - Personalised medicine approaches are redefining the therapeutic landscape for men with metastatic castration-resistant prostate cancer (mCRPC). While poly(ADP-ribose) polymerase (PARP) inhibitors have demonstrated clinical benefit in patients with BRCA1/2 mutant tumours, the therapeutic efficacy of these inhibitors in Ataxia-telangiectasia mutated (ATM)-mutated prostate cancer patients remains modest, highlighting the need for alternative treatment strategies. This study aimed to elucidate the impact of ATM loss on radiobiological and immune responses to different radiation modalities in prostate cancer models. - Source: PubMed
Publication date: 2026/05/30
Dunne Victoria LWright Timothy CToner AislinnWilson Melissa LaBonteSavage Kienan IO'Sullivan Joe MPrise Kevin M