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1 pective Study of Outcomes in Sporadic versus Hereditary breast cancer.
2 astases in sporadic breast cancer but not in hereditary breast cancer.
3 ity genetic disorder Fanconi anemia (FA) and hereditary breast cancer.
4 ffect its structure-function relationship in hereditary breast cancer.
5 A2, are responsible for the vast majority of hereditary breast cancer.
6 f the BRCA2 gene contribute significantly to hereditary breast cancer.
7 yet be found that explain some proportion of hereditary breast cancer.
8 moderate to high penetrant genes involved in hereditary breast cancer.
9 tions in BRCA genes are the leading cause of hereditary breast cancer.
10 tions (BRCA1(+/mut)) have increased risk for hereditary breast cancer.
11 Germline mutations in BRCA2 predispose to hereditary breast cancers.
12 btype in human sporadic and BRCA1-associated hereditary breast cancers.
13 oportion of non BRCA1-, non BRCA2-associated hereditary breast cancers.
14 le for a significant fraction of early-onset hereditary breast cancers.
15 st frequent mutation alleles predisposing to hereditary breast cancer among the Ashkenazim, and sugge
16 lial and stromal cells from 43 patients with hereditary breast cancer and 175 patients with sporadic
17 sible for approximately half of all cases of hereditary breast cancer and almost all cases of combine
18 nactivated by gross gene disruption in BRCA1 hereditary breast cancer and BRCA1-methylated sporadic b
20 basal-like breast cancer but rarely in BRCA2 hereditary breast cancer and non-BRCA1-deficient sporadi
21 mbination with mutations in genes that cause hereditary breast cancer and ovarian cancer like BRCA1,
22 ent options in the management of early-stage hereditary breast cancer and should provide reassurance
23 methods are tested on data sets arising from hereditary breast cancer and small round blue-cell tumor
24 BRCA1 or BRCA2 in a sample of North American hereditary breast cancers and assess the evidence for ad
25 1 (BRCA1) is mutated in approximately 50% of hereditary breast cancers, and its expression is decreas
27 nes later in life suggest that most cases of hereditary breast cancer are not related to cumulative h
29 ssion data sets with multiple classes: (a) a hereditary breast cancer data set with (1) BRCA1-mutatio
30 ient in other DSB repair pathways, including hereditary breast cancers defective in homologous recomb
32 -like subtype, which include the majority of hereditary breast cancers due to mutations in the breast
35 the potential role of RRSO in BRCA-negative hereditary breast cancer families will also be discussed
36 Much of the published work on management of hereditary breast cancer focuses on women with known mut
38 chemosensitivity of tumors deficient in the hereditary breast cancer genes BRCA1 and BRCA2 (BRCA).
41 ever, it is not yet clear what proportion of hereditary breast cancer is explained by BRCA1 and BRCA2
42 6174delT frameshift mutation in BRCA2 in an hereditary breast cancer kindred of Ashkenazi Jewish anc
45 ve, perhaps allowing us to identify cases of hereditary breast cancer on the basis of gene-expression
46 factor important in meiosis, associated with hereditary breast cancer (p = 0.018) and likely represen
48 utations, identified in 189 Northern Finnish hereditary breast cancer patients in parallel sequencing
52 pective Study of Outcomes in Sporadic versus Hereditary breast cancer (POSH) study (n=315, 108 events
55 ks, which is shared with two other high-risk hereditary breast cancer suppressors, BRCA2 and PALB2.
60 tion carrier, family history consistent with hereditary breast cancer syndrome and estimated personal
62 y beneficial in other syndromes, such as the hereditary breast cancer syndromes, hereditary nonpolypo
64 1 and BRCA2 probably explain the majority of hereditary breast cancer that exists in the North Americ
65 also called BACH1/BRIP1 was first linked to hereditary breast cancer through its direct interaction
66 y engineered mouse model of BRCA2-associated hereditary breast cancer to study drug resistance to sev
67 tellite locus (2p25.1) in stromal cells from hereditary breast cancers was associated with mutated TP
68 tations of which contribute significantly to hereditary breast cancer, was not identified in the exis
70 of the clinical or pathological features of hereditary breast cancer with somatic TP53 mutations.
71 mutations in PALB2 are an important cause of hereditary breast cancer, with respect both to the frequ