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In the very high-risk Bladder Cancer patients , several genes had a higher frequency of mutations than reported in the The Cancer Genome Atlas database, including BRCA2 . Mutation associations with receipt of neoadjuvant chemotherapy, nodal involvement, metastatic disease development, and survival were analyzed.
we show that this combined approach allows the rapid and reliable detection of both germline and somatic aberrations affecting BRCA1 and BRCA2 in DNA derived from FFPE OCs, enabling improved hereditary cancer risk assessment and clinical treatment of ovarian cancer patients.
BRCA1/2 mutation carriers who have been treated with PS have a substantially reduced breast cancer incidence and mortality.
Of note is the recent U.S. Food and Drug Administration breakthrough therapy designation of olaparib for the treatment of BRCA1/2- or ATM (Montrer ATM Kits ELISA)-mutated metastatic castration-resistant prostate cancer. The implications of this new knowledge for clinical practice now and in the future are discussed.
In this review, we will discuss the emerging importance of somatic and epigenetic alterations of BRCA- and BRCA-related genes(BRCA1 and BRCA2 ) in the management of ovarian cancer.
three patients had biallelic inactivation of BRCA2, a tumor suppressor gene critical for homologous DNA repair. two had germline BRCA2 mutations. The third patient had somatic BRCA2 homozygous copy loss. Biallelic BRCA2 inactivation in Metastatic Castration-resistant Prostate Cancer warrants further exploration as a predictive biomarker for sensitivity to platinum c
The current model places BRCA2 as a central regulator of genome stability by repairing DNA double strand breaks and limiting replication stress. [review]
Increasing evidence on the molecular role of the BRCA2 protein in the homologous recombination of DNA damages suggest that BRCA2-related PDAC are sensitive to agents causing DNA cross-linking damage, such as platinum salts, and treatments targeting rescue DNA repair pathways, such as poly(ADP-ribose) polymerase (Montrer PARP1 Kits ELISA) inhibitors that are currently under investigation.[ review]
In a population without strong germline founder mutations, the likelihood of a BRCA1/2 mutation found in a breast carcinoma being somatic was approximately 1/3 and germline 2/3. This may have implications for treatment and genetic counseling
Durable responses to olaparib were observed in patients with relapsed germline BRCA1/2 mutation ovarian cancer who had received >/=3 lines of prior chemotherapy
persistent meiotic DNA double-strand breaks might correspond to crossovers, which are mobilized to the nuclear envelope for their repair; Brca2-Pds5 complexes may be key mediators of this process.
A mutation in Cyp6d2, a cytochrome P450 gene, when combined with a brca2 mutation, resulted in synergistic hypersensitivity to camptothecin.
DNA repair by homologous recombination is dramatically decreased in CG30169 (brca2 homolog) mutants.
the data suggest for the first time that brca2/fancd1 is essential for vertebrate kidney ontogeny.
Carcinogenesis in zebrafish with combined mutations in tp53 (Montrer TP53 Kits ELISA) and brca2 typically requires biallelic mutation or loss of at least one of these genes.
The novel role of Brca2 in organizing the vertebrate egg nucleus may provide new insights into the origin of ovarian cancer
critical roles for brca2 in ovarian development and tumorigenesis in reproductive tissues
we generated a Brca2 knock-in mouse model lacking exons 4-7 and demonstrated that these exons are dispensable for viability as well as tumor-free survival. This study provides the first in vivo evidence of the functional significance of a minor transcript of BRCA2 that can play a major role in the survival of humans who are homozygous for a clearly pathogenic mutation.
we describe a genetic approach to examine the functional significance of the interaction between BRCA2 and PALB2 (Montrer PALB2 Kits ELISA) by generating a knock-in mouse model of Brca2 carrying a single amino acid change (Gly25Arg, Brca2G25R) that disrupts this interaction. In addition, we have combined Brca2G25R homozygosity as well as hemizygosity with Palb2 (Montrer PALB2 Kits ELISA) and Trp53 (Montrer TP53 Kits ELISA) heterozygosity .
Merit40 (Montrer BABAM1 Kits ELISA) mutation exacerbated ICL-induced chromosome instability in the context of concomitant Brca2 deficiency but not in conjunction with Fancd2 (Montrer FANCD2 Kits ELISA) mutation.
Heterozygous and homozygous Brca2 mutation may lead to dysfunction in T cell populations.
BRCA2 exon 27 domain maintains chromosomal integrity at both stalled and collapsed replication forks consistent with involvement in both replication fork maintenance and double strand break repair.
we use a genetically engineered mouse model of BRCA2-associated hereditary breast cancer to study drug resistance to several types of chemotherapy and PARP (Montrer PARP1 Kits ELISA) inhibition.
BRCA2-mediated sequestration of nuclear RAD51 (Montrer RAD51 Kits ELISA) serves to prevent inappropriate DNA interactions.
BRCA2 directly represses the expression of IFN-related genes
the models reveal novel aspects of cancer evolution in carriers of germline BRCA2 mutations, provide new insights into the tumour suppressive role of BRCA2
genetic stability, and hematopoietic differentiation potential of gene-corrected Brca2(Delta) (27/) (Delta) (27) iPSCs, achievements and limitations in the application of current reprogramming approaches in hematopoietic stem cell therapy are also discussed.
Inherited mutations in BRCA1 and this gene, BRCA2, confer increased lifetime risk of developing breast or ovarian cancer. Both BRCA1 and BRCA2 are involved in maintenance of genome stability, specifically the homologous recombination pathway for double-strand DNA repair. The BRCA2 protein contains several copies of a 70 aa motif called the BRC motif, and these motifs mediate binding to the RAD51 recombinase which functions in DNA repair. BRCA2 is considered a tumor suppressor gene, as tumors with BRCA2 mutations generally exhibit loss of heterozygosity (LOH) of the wild-type allele.
BRCA1/BRCA2-containing complex, subunit 2
, breast and ovarian cancer susceptibility gene, early onset
, breast cancer 2 tumor suppressor
, breast cancer type 2 susceptibility protein
, fanconi anemia group D1 protein
, truncated breast and ovarian cancer susceptibility protein 2
, breast cancer 2, early onset homolog
, breast cancer 2, mutation 1, University of Wisconsin-Madison
, breast cancer susceptibility protein 2
, breast cancer type 2 susceptibility protein homolog
, fanconi anemia group D1 protein homolog
, breast and ovarian cancer susceptibility protein 2
, breast cancer 2, early onset
, breast cancer type 2 susceptibility protein-like