Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer. - sprookjes - yvandenbroek - TriplyDB

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

http://www.wikidata.org/entity/Q33552870

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Prognostic and predictive significance of MYC and KRAS alterations in breast cancer from women treated with neoadjuvant chemotherapy.Ets-1 is a transcriptional mediator of oncogenic nitric oxide signaling in estrogen receptor-negative breast cancer.Activation of MAPK pathways due to DUSP4 loss promotes cancer stem cell-like phenotypes in basal-like breast cancer Genome-wide DNA methylome analysis reveals epigenetically dysregulated non-coding RNAs in human breast cancer.Spectrum of EGFR gene copy number changes and KRAS gene mutation status in Korean triple negative breast cancer patients.Update on the molecular profile of the MDA-MB-453 cell line as a model for apocrine breast carcinoma studies Analysis of PIK3CA Mutations and Activation Pathways in Triple Negative Breast Cancer.An essential role of metalloprotease-disintegrin ADAM12 in triple-negative breast cancer The combinatorial activation of the PI3K and Ras/MAPK pathways is sufficient for aggressive tumor formation, while individual pathway activation supports cell persistence.Profiling of residual breast cancers after neoadjuvant chemotherapy identifies DUSP4 deficiency as a mechanism of drug resistance miR-564 acts as a dual inhibitor of PI3K and MAPK signaling networks and inhibits proliferation and invasion in breast cancer.Anti-EGFR monoclonal antibodies and EGFR tyrosine kinase inhibitors as combination therapy for triple-negative breast cancer.Acinar cell plasticity and development of pancreatic ductal adenocarcinoma.IL-2- or IL-15-activated NK cells enhance Cetuximab-mediated activity against triple-negative breast cancer in xenografts and in breast cancer patients.Evolution of the predictive markers amphiregulin and epiregulin mRNAs during long-term cetuximab treatment of KRAS wild-type tumor cells.Stem cell property epithelial-to-mesenchymal transition is a core transcriptional network for predicting cetuximab (Erbitux™) efficacy in KRAS wild-type tumor cells.Low-grade fibromatosis-like spindle cell carcinomas of the breast are molecularly exiguous.Rare oncogenic mutations of predictive markers for targeted therapy in triple-negative breast cancer.Involvement of multiple cellular pathways in regulating resistance to tamoxifen in BIK-suppressed MCF-7 cells.Effects of PTEN Loss and Activated KRAS Overexpression on Mechanical Properties of Breast Epithelial Cells.Computational Structural Biology of -nitrosylation of Cancer Targets

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P2860

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

http://www.wikidata.org/entity/Q33552870

description

2010 nî lūn-bûn

@nan

2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի ապրիլին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

@yue

2010年論文

@zh-hant

2010年論文

@zh-hk

2010年論文

@zh-mo

2010年論文

@zh-tw

2010年论文

@wuu

name

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@ast

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@en

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@nl

type

label

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@ast

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@en

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@nl

prefLabel

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@ast

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@en

Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

@nl

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Lack of evidence for KRAS oncogenic mutations in triple-negative breast cancer.

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Alfonso Sánchez-Muñoz

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Elena Gallego

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Emilio Alba

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Luís G Pérez-Rivas

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Luís Vicioso

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Nuria Ribelles

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Vanessa de Luque

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P2860

Expression of cytokeratins 17 and 5 identifies a group of breast carcinomas with poor clinical outcome

Metaplastic breast carcinomas exhibit EGFR, but not HER2, gene amplification and overexpression: immunohistochemical and chromogenic in situ hybridization analysis.

KRAS mutation status is predictive of response to cetuximab therapy in colorectal cancer.

K-ras mutations and benefit from cetuximab in advanced colorectal cancer.

Gene expression patterns of breast carcinomas distinguish tumor subclasses with clinical implications

Gene expression profiling predicts clinical outcome of breast cancer

Molecular portraits of human breast tumours

High frequency of mutations of the PIK3CA gene in human cancers

Cetuximab and chemotherapy as initial treatment for metastatic colorectal cancer

PIK3CA mutations correlate with hormone receptors, node metastasis, and ERBB2, and are mutually exclusive with PTEN loss in human breast carcinoma

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