FANCE Peptide
- Known as:
- FANCE Peptide
- Catalog number:
- 42-799P
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- FANCE Peptide
Related genes to: FANCE Peptide
- 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 Peptide
Related articles to: FANCE Peptide
- Constitutional epimutations arise early in development and are present across normal tissues, including peripheral blood. Constitutional promoter methylation has emerged as a risk factor for -associated cancers, such as ovarian cancer (OC), and may serve as a biomarker for OC risk. This study retrospectively evaluated the clinical relevance of constitutional promoter methylation in 473 patients with OC enrolled in the observational AGO-TR1 study (ClinicalTrials.gov identifier: NCT02222883). - Source: PubMed
Publication date: 2026/06/12
Kayali MohamadHahnen EricBurges AlexanderReuss AlexanderCaro-Valenzuela Juliade Gregorio NikolausHeitz FlorianSchmidt SandraMarmé FrederikHilpert FelixWimberger PaulineKommoss StefanPrieske KatharinaEngel ChristophBuderath PaulDietrich DimoSchmutzler RitaSehouli JalidRhiem KerstinHarter PhilippHauke Jan - Poly(ADP-ribose) polymerase (PARP) inhibitors have emerged as an important therapeutic option for patients with homologous recombination repair (HRR)-deficient cancers, especially those with BRCA1/2 mutations. Since the initial US Food Administration approval of olaparib in 2014, PARP inhibitors have shown efficacy across ovarian, breast, and prostate cancers, although differences in trial design and biomarker strategies have resulted in tumor-specific indications. Homologous recombination deficiency (HRD) arises from germline or somatic mutations in HRR genes or from epigenetic inactivation, and it can be assessed through genomic "scars" such as loss of heterozygosity and mutational signatures. Although BRCA1/2 alterations confer the strongest sensitivity to PARP inhibitors, non-BRCA HRR gene mutations demonstrate heterogeneous responses, highlighting the need for more precise HRD assessment, including the role of biallelic vs monoallelic inactivation. Despite initial success, both primary and acquired resistance-through reversion mutations, replication fork stabilization, and therapy-induced clonal hematopoiesis-limit the durability of the response to PARP inhibition. Ongoing studies are evaluating rational combinations targeting complementary DNA damage response pathways (ATR/CHK1/WEE1, PI3K/AKT) and integrating immunotherapy or hormonal agents to extend benefit. Moving forward, harmonizing HRD testing across tumor types, accounting for germline, somatic, and liquid biopsy-derived alterations, and refining patient selection will be essential to maximize therapeutic efficacy and safely expand PARP inhibitor use beyond canonical BRCA-mutated cancers. - Source: PubMed
Linville Laura MCanzoniero Jenna VMarshall Catherine HArmstrong Deborah KMarkowski Mark CCarducci Michael A - - Source: PubMed
Publication date: 2026/06/11
Álvarez-Salafranca MarcialPuértolas TeresaDiago AdriánGómez-Mateo María Carmen - Prostate cancer (PCa) is the most common malignancy among men in the United Arab Emirates (UAE) and is often diagnosed at advanced stages with aggressive features. Germline mutations in DNA-repair genes, especially and , increase PCa risk, with conferring up to 8.6-fold and a 3.7-fold risk. The objective is to determine the prevalence, zygosity, and clinical significance of mutations in high-grade PCa among UAE and Arab patients and describe their potential role in disease aggressiveness. - Source: PubMed
Publication date: 2026/05/26
Al Shareef Zainab MAl-Shahrabi Rula MBhamidimarri Poorna ManasaYener BurcuBouzid AmalHamad Alaa MohamedMurad ShirinElbarkouky AhmedSaheb Sharif-Askari FatemehBendardaf RiyadHamoudi Rifat AHachim Mahmood Y - Inherited (germline) pathogenic and likely pathogenic variants (gPVs) in key genes associated with increased risk of prostate cancer (PCa) now warrant more attentive PCa screening per National Comprehensive Cancer Network (NCCN) guidelines-e.g., BRCA2, HOXB13, ATM, BRCA1, MSH2, MSH6, CHEK2 and TP53. However, the optimal early detection strategy for gPV carriers, including use of age-adjusted PSA thresholds and prostate imaging may be refined. and as a means to investigate novel biomarkers. - Source: PubMed
Publication date: 2026/06/09
Cheng Heather HMaxwell Kara NSalari KeyanCooperberg Matthew RFollmer KristinJeter Joanne MJun GraceLee Daniel JPatel Hiten DSchaeffer Edward MSokolova Alexandra OWolff Erika MLin Daniel W