anti-BRCA2 (BRCA2) Antikörper

Human Breast Cancer 2, Early Onset (BRCA2) Interaktionspartner

1. Eligible patients for this study were healthy women with >/= 17% lifetime risk of breast cancer or with a mutation in BRCA1 or BRCA2. A total of 632 women were screened between 2002 and 2012 (each for 6 years). During the study, 30 women were diagnosed with breast cancer, with 10 of these diagnoses occurring between screening visits, and six of the 10 diagnosed women were gene carriers

2. Among BRCA1/2 mutation wild-type patients, homologous recombination (HR) deficient(HRD) patients were more likely to achieve a pathologic complete response (OR 16, 95% CI 1.65-160.41, p = 0.0041) compared with HR non-deficient patients. Further, HRD scores were highly concordant pre- and post-therapy

3. these results provide a significant insight into certain mutations and proteins involved in the interaction network of BRCA1 and BRCA2, which may have common roles in breast cancer and ovarian cancer.

4. The overall frequencies of the BRCA germline mutations (BRCA1 and BRCA2 )were 10.2% in breast and 30.7% in ovarian cancer patients. These data shed new light into the prevalence of BRCA mutations in the Arab women population.

5. This study provides a comprehensive view of known and novel BRCA1/2 mutations in breast cancer (BC)patients from the Republic of Macedonia and contributes to the global spectrum of BRCA1/2 mutations in breast cancer

6. Our findings, using the largest gene panel for Male breast cancer (MBC) patients so far, indicate that BRCA testing (BRCA1 and BRCA2)should be the primary concern for MBC patients.

7. association between family history (FH) of Breast cancer(BC) and ovarian cancer(OC) risks was slightly smaller in magnitude (HR: 0.85, 95% CI: 0.55-1.30; HR: 0.64, 95% CI: 0.34-1.21 for BC-only FH in BRCA1 and BRCA2, respectively; HR: 1.46, 95% CI: 0.80-2.68; HR: 1.49, 95% CI: 0.44-4.02 for OC-only FH in BRCA1 and BRCA2, respectively), indicating that mutation position explains only part of the association.

8. This study reports familial communication in a BRCA1/BRCA2 screening setting... This suggests that universal BRCA screening does not differentially affect communication or the use of familial genetic information

9. The study of BRCA1/2 gene in Southern Mediterranean countries revealed low penetrance recurrent mutations in sporadic and familial breast cancer.

10. Results identified a novel large BRCA2 deletion in 0.9% of the screened Colombian families in addition to 6310delGA and the recurrent 1991del4 mutations. Among unselected breast cancer cases, 1.1% tested positive for BRCA2/3034del4, and 0.4% for BRCA2/1991del4.

11. our study provides novel data on ovarian BRCA1/2 mutation prevalence worldwide, enhances adequate patient selection for family counseling and prevention, and sheds light on the benefits of iPARP treatment.

12. It is possible that mutant BRCA1/2 genes are associated with a reduction in ovarian reserve (review)

13. In 7657 consecutive unselected breast cancer patients without BRCA1/2 mutations.

14. Study show that damage-induced long non-coding RNAs (dilncRNAs) play a role in DNA double-strand breaks (DSBs) repair by homologous recombination (HR) by contributing to the recruitment of the HR proteins BRCA1, BRCA2, and RAD51, without affecting DNA-end resection. BRCA2 directly interacts with RNase H2, mediates its localization to DSBs in the S/G2 cell-cycle phase, and controls DNA:RNA hybrid levels at DSBs.

15. The overall yield of comprehensive BRCA1/2 testing in ethnically diverse high-risk Israeli individuals is 3.3%. This is lower than expected by probability models. A slightly higher rate of BRCA1/2 carriers was seen among ovarian cancer cases. These data should guide BRCA1/2 optimal testing strategy in Israel.

16. The 2 identified likely pathogenic Unclassified variants in BRCA1 and BRCA2 require further verification with clinical evidence.

17. The total number of Ovarian Cancer patients captured was 802; of these, 53 and five families carry 22 mutations in BRCA1/2 genes. Of these, eight mutations were unique to the Arab populations, and five mutations were commonly circulated among Arabs (BRCA1: c.5266dupC, c.5095C>T, c.68_69delAG, and c.4041_4042delAG; BRCA 2 c.1310_1313delAAGA).

18. We conclude that BRCA1 and BRCA2 could be used as clinicopathological biomarkers to evaluate the prognosis of digestive system cancers.

19. Neither the patients tested nor the control subjects showed germline hypermethylation of the BRCA1 and BRCA2 promoter regions analyzed

20. Male carrying BRCA mutations have significantly lower QMAX than healthy men. BRCA1 patients have on average larger prostate glands and higher PSA than BRCA2 patients.

Fruit Fly (Drosophila melanogaster) Breast Cancer 2, Early Onset (BRCA2) Interaktionspartner

1. 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.

2. A mutation in Cyp6d2, a cytochrome P450 gene, when combined with a brca2 mutation, resulted in synergistic hypersensitivity to camptothecin.

3. DNA repair by homologous recombination is dramatically decreased in CG30169 (brca2 homolog) mutants.

Zebrafish Breast Cancer 2, Early Onset (BRCA2) Interaktionspartner

1. the data suggest for the first time that brca2/fancd1 is essential for vertebrate kidney ontogeny.

2. Carcinogenesis in zebrafish with combined mutations in tp53 and brca2 typically requires biallelic mutation or loss of at least one of these genes.

3. The novel role of Brca2 in organizing the vertebrate egg nucleus may provide new insights into the origin of ovarian cancer

4. critical roles for brca2 in ovarian development and tumorigenesis in reproductive tissues

Mouse (Murine) Breast Cancer 2, Early Onset (BRCA2) Interaktionspartner

1. BRCA2-proficient and deficient cells are radiosensitised by HT, indicating that HT does not exclusively act by inhibition of HR.

2. Results suggest that the greater reliance on homology-directed repair (HDR) in the proliferating mammary gland, rather than a specific dependence on breast cancer 2 protein (BRCA2), may increase its susceptibility to tumorigenesis incurred by BRCA2 mutation.

3. The functional consequence of Parp1 heterozygosity on BRCA2 loss is demonstrated by a significant increase in tumorigenesis in Brca2 knockout mice.

4. Data indicate the importance of breast cancer 1 protein (BRCA1)/breast cancer 2 protein (BRCA2) function in cranial neural crest cells (CNCCs) during craniofacial skeletal formation.

5. 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.

6. we describe a genetic approach to examine the functional significance of the interaction between BRCA2 and PALB2 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 and Trp53 heterozygosity .

7. Merit40 mutation exacerbated ICL-induced chromosome instability in the context of concomitant Brca2 deficiency but not in conjunction with Fancd2 mutation.

8. Heterozygous and homozygous Brca2 mutation may lead to dysfunction in T cell populations.

9. 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.

10. we use a genetically engineered mouse model of BRCA2-associated hereditary breast cancer to study drug resistance to several types of chemotherapy and PARP inhibition.

11. BRCA2-mediated sequestration of nuclear RAD51 serves to prevent inappropriate DNA interactions.

12. BRCA2 directly represses the expression of IFN-related genes

13. the models reveal novel aspects of cancer evolution in carriers of germline BRCA2 mutations, provide new insights into the tumour suppressive role of BRCA2

14. 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.

15. Results suggest that cellular levels of Brca2 and Rad51 are mutually dependent on each other, and that low levels of these proteins provide selective pressure for reduction of p53, which permits cell growth

16. BRCA2 accumulates DNA damage, which triggers checkpoint signalling and ARF activation

17. data showed that silencing of BRCA2 promoted cell proliferation, migration and invasion in vitro; data reported here demonstrate that BRCA2 may be a promising therapeutic targets for pancreatic ductal adenocarcinoma progression

18. BRCA2 is required for telomere homeostasis and may be particularly important for the replication of G-rich telomeric lagging strands.

19. Loss of Brca2 function predisposes the exocrine pancreas to profound DNA damage, and the frequency of invasive neoplasia is accentuated by the concomitant deregulation of p53

20. FANCD1/BRCA2 played notably important roles in the repair of TMZ-induced DNA damage.