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In this study, we used comprehensive multigene panels that included 35 known or suspected cancer susceptibility genes to examine BRCA1/2 mutation-negative Korean patients who had clinical features indicative of hereditary breast cancer
Pre-menopausal BRCA1/2 mutation carriers aged 30 to 47years chose screening, RRSO, or BS/DO. For those undergoing BS/DO, the delayed oophorectomy was recommended at age 40years for BRCA1 and age 45years for BRCA2 (zeige BRCA2 Proteine) patients.
Based on a cumulative risk of 0.55% to age 35 for BRCA1 mutation carriers and of 0.56% to age 45 for BRCA2 (zeige BRCA2 Proteine) mutation carriers, we recommend bilateral salpingo-oophorectomy before age 40, but by age 35, for women with a BRCA1 mutation and by age 45 for those with a BRCA2 (zeige BRCA2 Proteine) mutation to maximize prevention and to minimize adverse effects.
We demonstrate that homologous recombination deficiency (HRD)mutation signatures may offer clinically relevant information independently of BRCA1/2 mutation status and hope this work will guide the development of clinical trials
Overall, 65/648 (10%) study participants were BRCA1/2 mutation carriers.
BRCA1*R1699Q confers an intermediate risk for breast cancer and ovarian cancer.
patient-derived xenografts capture the molecular and phenotypic heterogeneity of triple-negative breast cancer . Here we show that PARP inhibition can have activity beyond germline BRCA1/2 altered tumors, causing regression in a variety of molecular subtypes. These models represent an opportunity for the discovery of rational combinations with targeted therapies and predictive biomarkers
Putative BRCA1/2 reversion mutations can be detected by cfDNA sequencing analysis in patients with ovarian and breast cancer. Our findings warrant further investigation of cfDNA sequencing to identify putative BRCA1/2 reversion mutations and to aid the selection of patients for PARP inhibition therapy
The frequency of the BRCA1 5382insC mutation in ovarian cancer patients from Ukraine
Tumor suppressor functions of MCPH1/BRIT1 (zeige MCPH1 Proteine) and BRCA1; links with the inactivation of the functional form of hTERT and the activation of dominant negative splice variants of hTERT.
Investigation on BRCA1 SNPs and its effects on mastitis in Chinese commercial cattle.
The gene-specific SNP marker analysis showed a significant association of BRCA1 C28300A with milk somatic cell scores.
In general, OC use, childbearing and breastfeeding do not differ between BRCA1/2 carriers and non-carriers with ovarian cancer. However, the effects of tubal ligation may differ between BRCA1 carriers and non-carriers.
Bovine BRCA1 was phosphorylated and nuclear speckling was enhanced in response to DNA-damaging agents.These results provide evidence that phosphorylation and nuclear relocalization are highly conserved features of the BRCA1 response to genotoxic stress.
Consensus-based recombinant adeno-associated virus-BRCA1 knock out virus vectors failed to induce BRCA1 knockout in Gottingen fibroblasts.
Recent work in a TP53(-/-)BRCA1-mutant murine breast cancer model indicates that double blockade with two immune checkpoint inhibitors increases the number of tumor-infiltrating lymphocytes and overall survival after DNA damaging chemotherapy, whereas single blockade does not
Data indicate the importance of breast cancer 1 protein (BRCA1)/breast cancer 2 protein (BRCA2 (zeige BRCA2 Proteine)) function in cranial neural crest cells (CNCCs) during craniofacial skeletal formation.
ATM (zeige ATM Proteine) has a role in homology-directed repair (HDR (zeige GATA3 Proteine)) independent of the BRCA1-53BP1 (zeige TP53BP1 Proteine) antagonism; its HDR (zeige GATA3 Proteine) function can become critical in certain contexts
BRCA1, but not BRCA2, suppresses the formation of tandem duplications at a site-specific chromosomal replication fork barrier imposed by the binding of Tus proteins to an array of Ter sites. BRCA1 has no equivalent role at chromosomal double-stranded DNA breaks, indicating that tandem duplications form specifically at stalled forks.
Loss of p16INK4 protein (p16) transforms breast cancer 1 (Brca1)-deficient mammary epithelial cell (MEC (zeige CCL28 Proteine)) and induces mammary tumors.
Brca1 is necessary for hematopoietic stem cells maintenance and normal hematopoiesis and that distinct mutations lead to different degrees of hematopoietic dysfunction.
TGFbeta (zeige TGFB1 Proteine) stabilized the abundance of BRCA1 by reducing the abundance of microRNA-182 (miR (zeige MLXIP Proteine)-182). Ectopic expression of BRCA1 or antagonism of miR (zeige MLXIP Proteine)-182 in cultured TGFbeta (zeige TGFB1 Proteine)-deficient mammary epithelial cells restored luminal lineage commitment.
BRCA1 inactivation can increase expression of miR (zeige MLXIP Proteine)-155, contributing to cardiac hypertrophy. And Rev produces their beneficial effects partially by down-regulating miR (zeige MLXIP Proteine)-155 expression, which might be a novel strategy for treatment of cardiac hypertrophy.
both murine Brca1185stop tumors and human BRCA1185delAG breast cancer cells express a new gene domain-less (RING-less) BRCA1 protein that mediated resistance to homologous recombination deficient-targeted therapies
Genomic instability can be rescued by deletion of Trp53bp1 (zeige TP53BP1 Proteine), encoding the DNA damage response factor 53BP1 (zeige TP53BP1 Proteine); mice expressing RING-less BRCA1 do not show an increased susceptibility to tumors in the absence of 53BP1 (zeige TP53BP1 Proteine); Genomic instability in cells expressing RING-less BRCA1 correlates with loss of BARD1 (zeige BARD1 Proteine) and a defect in restart of replication forks after hydroxyurea treatment
MRN (Mre11 (zeige MRE11A Proteine), Rad50 (zeige RAD50 Proteine), and Nbs1 (zeige NLRP2 Proteine)) complex, CtIP (zeige RBBP8 Proteine), and BRCA1 are required for both the removal of Top2 (zeige TOP2 Proteine)-DNA adducts and the subsequent resection of Top2 (zeige TOP2 Proteine)-adducted DSB ends.
BRCA1-dependent helicase unloading is a critical, early event in DNA interstrand crosslink repair.
This gene encodes a nuclear phosphoprotein that plays a role in maintaining genomic stability, and it also acts as a tumor suppressor. The encoded protein combines with other tumor suppressors, DNA damage sensors, and signal transducers to form a large multi-subunit protein complex known as the BRCA1-associated genome surveillance complex (BASC). This gene product associates with RNA polymerase II, and through the C-terminal domain, also interacts with histone deacetylase complexes. This protein thus plays a role in transcription, DNA repair of double-stranded breaks, and recombination. Mutations in this gene are responsible for approximately 40% of inherited breast cancers and more than 80% of inherited breast and ovarian cancers. Alternative splicing plays a role in modulating the subcellular localization and physiological function of this gene. Many alternatively spliced transcript variants, some of which are disease-associated mutations, have been described for this gene, but the full-length natures of only some of these variants has been described. A related pseudogene, which is also located on chromosome 17, has been identified.
BRCA1/BRCA2-containing complex, subunit 1
, RING finger protein 53
, breast and ovarian cancer susceptibility protein 1
, breast and ovarian cancer sususceptibility protein 1
, breast cancer type 1 susceptibility protein
, protein phosphatase 1, regulatory subunit 53
, BRCA1 homologue
, breast cancer type 1 susceptibility protein homolog
, breast cancer 1, early onset
, BRCA1 homolog
, breast and ovarian cancer susceptibility protein
, breast cancer associated 1