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1 2, and 3.1% (31 of 1007) in CHEK2 or another breast cancer gene.
2 ined, but <10% were shared with E2-regulated breast cancer genes.
3 aining knock-in or knockout mutations in key breast cancer genes.
4 o 2000 was sequenced for known and candidate breast cancer genes.
5 affect genomic regions containing well-known breast-cancer genes.
6  identification of additional low-penetrance breast-cancer genes.
7 ely than other women to inherit mutations in breast-cancer genes.
8 monstrated selective cytotoxic effect toward breast cancer gene 1 ( BRCA1)-deficient cells compared t
9                                              Breast cancer gene 1 (BRCA1) deficient cells not only ar
10                                              Breast cancer gene 1 (BRCA1) mutations predispose women
11 us region of the 1863 residue early onset of breast cancer gene 1 (BRCA1) nuclear protein contains a
12   The carboxyl-terminal domain (BRCT) of the Breast Cancer Gene 1 (BRCA1) protein is an evolutionaril
13 tes binding sites for pairs of BRCT repeats (breast cancer gene 1 [BRCA1] C terminal repeats) in the
14 ing S phase, which recruits Brc1 through its breast cancer gene 1 protein (BRCA1) C-terminal (BRCT) d
15                                   The Brca1 (breast cancer gene 1) tumor suppressor protein is phosph
16 ercome these limitations by hypersensitizing BReast CAncer genes 1/2 (BRCA1/2) mutant cells to PARPi.
17 rotein-protein interaction (PPI) mediated by breast-cancer-gene 1 C-terminal (BRCT) is an attractive
18 omologous recombination (HR) deficiency upon Breast Cancer Gene 2 (BRCA2) loss arises from defects in
19 4%) carried a pathogenic mutation in another breast cancer gene (29 in CHEK2, and 1 each in BRIP1 and
20 he fact that 5 FA genes are in fact familial breast cancer genes and FA gene mutations are found freq
21 actors; however, the discovery of additional breast cancer genes and genes contributing to racial dis
22 veral panel genes as high- and moderate-risk breast cancer genes and provides estimates of breast can
23  genetic interaction analyses of top mutated breast cancer genes and the proteomics interactome data
24 gamma transcription factor regulates luminal breast cancer genes, and loss of TFAP2C induces epitheli
25 pplication in cancer gene diagnostics (BRCA1 breast cancer gene) are investigated.
26 and dosage-insensitive genes, including many breast cancer genes as well as sporadic copy-number aber
27                   A minority of cancers have breast cancer gene (BRCA) mutations that confer sensitiv
28               ALC1 loss reduced viability of breast cancer gene (BRCA)-mutant cells and enhanced sens
29 RPis) have changed the treatment paradigm in breast cancer gene (BRCA)-mutant high-grade serous ovari
30 the RNA-DNA helicase senataxin (SETX) or the breast cancer gene BRCA1 (refs.
31 uble-stranded DNA (dsDNA), a sequence of the breast cancer gene BRCA1.
32 gnostic applications in clinical analysis of breast cancer gene BRCA1.
33 e screen for a known polymorphic site in the breast cancer gene BRCA1.
34 ion of adenine and guanine (185delAG) in the breast cancer gene BRCA1.
35  brc-1 and brd-1, the orthologs of the human breast cancer genes BRCA1 and BARD1, respectively.
36 tivity of tumors deficient in the hereditary breast cancer genes BRCA1 and BRCA2 (BRCA).
37 ons have a high penetrance, for example, the breast cancer genes BRCA1 and BRCA2.
38 higher than expected rate of mutation in the breast-cancer gene BRCA1.
39       A second, recently identified familial breast cancer gene, BRCA2, accounts for a proportion of
40                                          The breast cancer gene, BRCA2, is essential for viability, y
41                        The second hereditary breast cancer gene, BRCA2, was recently isolated.
42 ofiles, enumeration of copy numbers of eight breast cancer genes by multicolor fluorescence in situ h
43 ter exclusion of BRCA1, BRCA2, and syndromic breast cancer genes (CDH1, PTEN, and TP53), observed pat
44                                          The Breast Cancer Gene Database (BCGD) is a compendium of mo
45 investigate long-range interactions at three breast cancer gene deserts mapping to 2q35, 8q24.21, and
46 r PALB2 with a pathogenic variant in another breast cancer gene equated to supporting evidence agains
47                                              Breast cancer gene expression analysis correlated estrog
48                                      Luminal breast cancer gene expression and proliferation are driv
49                           We apply BicMix to breast cancer gene expression data and to gene expressio
50                                  Analysis of breast cancer gene expression data indicates that HOTAIR
51 d utility of this method, we applied it to a breast cancer gene expression dataset and tested its abi
52 ation experiments using multiple independent breast cancer gene expression datasets and PPI networks.
53 rom public data repositories a collection of breast cancer gene expression datasets with over 7000 pa
54 well to The Cancer Genome Atlas and to other breast cancer gene expression datasets without the need
55     Through integrative analysis of clinical breast cancer gene expression datasets, cell line models
56 essenger RNA (mRNA) profiling of transfected breast cancer gene expression in a living cell is demons
57 ented and performed a large meta-analysis of breast cancer gene expression profiles from 223 datasets
58 d STAT3 cooperate to regulate the basal-like breast cancer gene expression program and provides the b
59 rturbations driving most of the variation in breast cancer gene expression.
60                      Experiments using three breast cancer gene-expression datasets (i.e., GSE2034, G
61                           Furthermore, other breast cancer genes generally are not evaluated.
62 and rearrangements affecting the most common breast cancer genes, including PIK3CA, TP53, PTEN, BRCA2
63 ogenic mutation in BRCA1 or BRCA2 or another breast cancer gene is not known.
64 te that the products of BRCA1, neu, and erbB breast cancer genes participate in a common or shared si
65 nt Analysis and Tumor Subtyping in High-Risk Breast-Cancer Gene Pedigrees, Study of Shared Genomic Se
66 urbation of BC-associated enhancers disrupts breast cancer gene programs.
67                                 We created a breast cancer gene regulatory network comprising transcr
68 nds identified as inversely connected to the breast cancer gene signatures, 14 of them are known anti
69            Identification of high-penetrance breast cancer genes such as Brca1 has been accomplished
70 d expression of a previously uncharacterized breast cancer gene that encodes a secreted protein desig
71 ceptor was expressed in both the ovarian and breast cancers, genes that are coregulated with the estr
72 e that EpCAM is a potential novel target for breast cancer gene therapy and offer insights into the m
73 ess the value of EpCAM as a novel target for breast cancer gene therapy, we performed real-time rever
74                                          The breast cancer gene trinucleotide-repeat-containing 9 (TN
75 nds was sequenced for 23 known and candidate breast cancer genes using BROCA, a targeted multiplexed