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1 gesterone receptors and amplification of the HER2 gene.
2 -361 and MDA-453 cells, which do not exhibit HER2 gene amplification and are relatively resistant to
3 ression in HER2-positive breast cancers with HER2 gene amplification and HER2-low or HER2-negative br
4 used breast cancer cell lines to investigate HER2 gene amplification and modelled a range of differen
5 uggest that mammary tumors that contain both HER2 gene amplification and PIK3CA mutations should be t
6 uency and prognostic impact of heterogeneous HER2 gene amplification and polysomy 17 in patients with
7 ponents of breast cancers with heterogeneous HER2 gene amplification and to define the repertoire of
8 in 108 assessable patients with and without HER2 gene amplification by fluorescence in situ hybridiz
9 f these cases, heterogeneous distribution of HER2 gene amplification can be found, which creates clin
10 study was to determine whether the level of HER2 gene amplification determined by the HER2/CEP17 rat
13 mutations occur primarily in the absence of HER2 gene amplification such that most HER2-mutant tumor
14 hat even driver genetic alterations, such as HER2 gene amplification, can be heterogeneously distribu
16 e use of HER2-blocking agents to tumors with HER2 gene amplification, recent retrospective analyses s
19 tyrosine kinase inhibitor lapatinib against HER2 gene-amplified breast cancers, most patients eventu
21 D1, and increased p27 protein levels in the HER2 gene-amplified BT-474 and SKBR-3 human breast cance
22 factor receptor 2 [HER2] protein expression, HER2 gene and chromosome 17 copy number, hormone recepto
24 meable peptide reduced the expression of the Her2 gene and specifically impaired the growth and viabi
28 hybridization (FISH) result of more than six HER2 gene copies per nucleus or a FISH ratio (HER2 gene
29 g of 0 or 1+, a FISH result of less than 4.0 HER2 gene copies per nucleus, or FISH ratio of less than
30 timal cutoff values for HER2/CEP17 ratio and HER2 gene copy number (GCN) for discriminating positive
32 ation determined by the HER2/CEP17 ratio and HER2 gene copy number could significantly predict some b
33 of 6.11 (95% CI, 2.27 to 21.90) and a median HER2 gene copy number of 11.90 (95% CI, 3.30 to 43.80) w
34 ups according to HER2 FISH ratio and average HER2 gene copy number per tumor cell: group 1 (in situ h
37 rkable similarities of mutations in EGFR and HER2 genes involving tumor type and subtype, mutation ty
42 ER2 gene copies per nucleus or a FISH ratio (HER2 gene signals to chromosome 17 signals) of more than
44 number of 4 to 6, 41 (47.7%) of 86 had their HER2 gene status upgraded from nonamplified to amplified
46 oncurrent RNAi-mediated silencing of FAS and HER2 genes synergistically stimulated apoptotic cell dea
49 is of HER2-related diseases by detecting the HER2 gene with minimal consumption of samples and reagen
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