Ignet

Gene Pair Information

Gene Pair: BRCA1, RAD51

Related Sentences

#	PMID	Sentence
1	9515792	We sought to identify novel genes associated with cis-diamminedichloroplatinum(II) (CDDP) resistance, and by differential display analysis, we found that the human breast and ovarian cancer susceptibility gene BRCA1 was overexpressed in CDDP-resistant MCF-7 cells.
2	9515792	A recent report that BRCA1 and human Rad51 colocalize in S-phase cells suggests a role for BRCA1 in DNA damage repair.
3	9679245	Germline mutations in either the BRCA1 or the BRCA2 gene are responsible for the majority of hereditary breast cancers.
4	9679245	The proposition that BRCA1 might play a role as a caretaker of the genome was first put forward by the demonstration that, in mitotic and meiotic cells, BRCA1 can interact with Rad51, which plays a major role in repair and/or recombination processes.
5	9679245	From there, a fair body of observations have converged to support the concept that BRCA1 and BRCA2 play a role in monitoring and/or repairing DNA lesions.
6	9679245	Understanding the precise biochemical function of BRCA1 and BRCA2 should provide a basis for early diagnosis and prevention in women carrying a predisposition to breast cancer.
7	10197592	BRCA1, BRCA2, and Rad51 operate in a common DNA damage response pathway.
8	10197592	The two major hereditary breast cancer susceptibility genes, BRCA1 and BRCA2, are associated with early-onset breast and/or ovarian cancer and encode products that each interact with the product of the eukaryotic RecA homologue, hRad51.
9	10197592	We have recently found that BRCA1 and BRCA2 coexist in a common biochemical complex.
10	10197592	Thus, BRCA1 and BRCA2 participate in a common DNA damage response pathway associated with the activation of homologous recombination and double-strand break repair.
11	10197592	The BRCA1/BRCA2 complex may function in postreplicational repair processes activated during the DNA synthesis stage of the cell cycle.
12	10919664	The rationale underlying this hypothesis is derived from the clues provided by family breast cancer syndromes, in which susceptibility genes, including p53, ATM, BRCA1 and BRCA2, are involved within the common functional pathway of DSB-related checkpoint/ repair.
13	10919664	Support for our hypothesis comes from the observations that: (a) the extent of DSB-initiated CIN in tumors significantly increased as tumors progressed to poorer grades or later stages; (b) in the sequential steps toward CIN, the loci of p53 and ATM, the key checkpoint genes against DSB, were lost at the earliest stage; and (c) many loci identified to be important in breast tumorigenesis were the genomic sites possibly harboring the genes involved in DSB-related checkpoint/repair (including RAD51, RAD52, and BRCA1) or CIN (including FA-A, FA-D, and WRN), and a higher number of these loci showing LOH was significantly associated with increased level of DSB-initiated CIN (P < 0.0001).
14	11093813	BRCA1 is part of a multiprotein complex, which also contains the recombination factor Rad51.
15	11093813	Here we describe that in contrast to BRCA1, histological grading of sporadic invasive ductal breast cancer significantly correlates with over-expression of wild-type Rad51.
16	11093813	These data suggest that in addition to the absence of the tumour-suppressor protein BRCA1, over-expression of wild-type Rad51 also contributes to the pathogenesis of a significant percentage of sporadic breast cancers and that other mechanisms than mutations must be responsible for this altered expression.
17	11406561	The protein products of the hereditary breast cancer susceptibility genes, BRCA1 and BRCA2, interact with the Rad51 protein, a central component of homologous repair pathways.
18	33637776	BKM120 sensitizes BRCA-proficient triple negative breast cancer cells to olaparib through regulating FOXM1 and Exo1 expression.
19	33637776	Poly (ADP-ribose) polymerase (PARP) inhibitors offer a significant clinical benefit for triple-negative breast cancers (TNBCs) with BRCA1/2 mutation.
20	33637776	Phosphoinositide 3-kinase (PI3K) inhibition sensitizes BRCA-proficient TNBC to PARP inhibition, which broadens the indication of PARP inhibitors.
21	33637776	Previously researches have reported that PI3K inhibition induced the defect of homologous recombination (HR) mediated repair by downregulating the expression of BRCA1/2 and Rad51.
22	33637776	Herein, we focused on DNA damage, DNA single-strand breaks (SSBs) repair and DNA double-strand breaks (DSBs) repair three aspects to investigate the mechanism of dual PI3K and PARP inhibition in DNA damage response.
23	33637776	We found that dual PI3K and PARP inhibition with BKM120 and olaparib significantly reduced the proliferation of BRCA-proficient TNBC cell lines MDA-MB-231 and MDA231-LM2.
24	33637776	Olaparib resulted in concomitant gain of PARP1, forkhead box M1 (FOXM1) and Exonuclease 1 (Exo1) while inhibited the activity of PARP.
25	33637776	BKM120 downregulated the expression of PARP1 and PARP2 to assist olaparib in blocking PARP mediated repair of DNA SSBs.
26	33637776	Meanwhile, BKM120 inhibited the expression of BRAC1/2 and Rad51/52 to block HR mediated repair through the PI3K/Akt/NFκB/c-Myc signaling pathway and PI3K/Akt/ FOXM1/Exo1 signaling pathway.
27	33637776	FOXM1 and Exo1 are novel therapeutic targets that serves important roles in DNA damage response.
28	38087035	While the expression of the BRCA1 and BRCA2 was upregulated, the expression of the ATM (p < 0.001), RAD51 (p < 0.001), and KU70 (p < 0.001) was downregulated in dose-treated BC-SCs (p < 0.001) to the qPCR results.