A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.
about
Cancer pharmacogenomics: strategies and challengesTargeting the epigenome in lung cancer: expanding approaches to epigenetic therapyIntrinsic resistance to EGFR tyrosine kinase inhibitors in advanced non-small-cell lung cancer with activating EGFR mutationsRegulation of Bim in Health and DiseaseThe latest therapeutic strategies after resistance to first generation epidermal growth factor receptor tyrosine kinase inhibitors (EGFR TKIs) in patients with non-small cell lung cancer (NSCLC)The BCL2 Family: Key Mediators of the Apoptotic Response to Targeted Anticancer TherapeuticsTumor heterogeneity and resistance to EGFR-targeted therapy in advanced nonsmall cell lung cancer: challenges and perspectivesApoptotic agentsTargeted therapies in development for non-small cell lung cancerPharmacogenomics of chemotherapeutic susceptibility and toxicityHigh throughput sequencing approaches to mutation discovery in the mouseCIViC databaseMechanisms of Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance and Strategies to Overcome Resistance in Lung AdenocarcinomaAberrant splicing and drug resistance in AMLBH3-only proteins: a 20-year stock-takeSecondary mutations as mediators of resistance to targeted therapy in leukemiaNF-κB-activating complex engaged in response to EGFR oncogene inhibition drives tumor cell survival and residual disease in lung cancerHigh-resolution mutational profiling suggests the genetic validity of glioblastoma patient-derived pre-clinical modelsMulti-agent chemotherapy overcomes glucocorticoid resistance conferred by a BIM deletion polymorphism in pediatric acute lymphoblastic leukemiaTransforming growth factor β signaling overcomes dasatinib resistance in lung cancerEfficacy and safety of dasatinib versus imatinib in the East Asian subpopulation of the DASISION trial of newly diagnosed chronic myeloid leukemia in chronic phase.The BCL2 inhibitor ABT-199 significantly enhances imatinib-induced cell death in chronic myeloid leukemia progenitorsExploratory cohort study and meta-analysis of BIM deletion polymorphism in patients with epidermal growth factor receptor-mutant non-small-cell lung cancer treated with epidermal growth factor receptor tyrosine kinase inhibitorsCD200-positive cancer associated fibroblasts augment the sensitivity of Epidermal Growth Factor Receptor mutation-positive lung adenocarcinomas to EGFR Tyrosine kinase inhibitors.ERBB receptors: from oncogene discovery to basic science to mechanism-based cancer therapeutics.Oncogenic mutations in intestinal adenomas regulate Bim-mediated apoptosis induced by TGF-βSystems biology approaches to develop innovative strategies for lung cancer therapy.The quest to overcome resistance to EGFR-targeted therapies in cancer.Establishment of a Novel Method for Screening Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance Mutations in Lung CancerCRIPTO1 expression in EGFR-mutant NSCLC elicits intrinsic EGFR-inhibitor resistance.Impact of the Bim Deletion Polymorphism on Survival Among Patients With Completely Resected Non-Small-Cell Lung CarcinomaBim polymorphisms: influence on function and response to treatment in children with acute lymphoblastic leukemia.Clinical significance of BIM deletion polymorphism in non-small-cell lung cancer with epidermal growth factor receptor mutation.The virus-induced protein APOBEC3G inhibits anoikis by activation of Akt kinase in pancreatic cancer cells.Downregulated microRNA-148b in circulating PBMCs in chronic myeloid leukemia patients with undetectable minimal residual disease: a possible biomarker to discontinue imatinib safely.Pulmonary adenocarcinoma: implications of the recent advances in molecular biology, treatment and the IASLC/ATS/ERS classification.The MAPK pathway across different malignancies: a new perspective.Emerging treatment for advanced lung cancer with EGFR mutation.Colorectal cancer stem cells and their implications for novel anticancer therapy.Improving but inferior survival in patients with chronic lymphocytic leukemia in taiwan: a population-based study, 1990-2004.
P2860
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P2860
A common BIM deletion polymorphism mediates intrinsic resistance and inferior responses to tyrosine kinase inhibitors in cancer.
description
2012 nî lūn-bûn
@nan
2012 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի մարտին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@ast
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@en
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@nl
type
label
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@ast
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@en
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@nl
altLabel
A common BIM deletion polymorp ...... ne kinase inhibitors in cancer
@en
prefLabel
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@ast
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@en
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@nl
P2093
P2860
P50
P3181
P356
P1433
P1476
A common BIM deletion polymorp ...... e kinase inhibitors in cancer.
@en
P2093
Ai Leen Ang
Atif Shahab
Audrey S M Teo
Balram Chowbay
Charles T H Chuah
Chia-Tien Chang
Daniel S W Tan
Dianne Poh
Eng Huat Tan
Gee Fung How
P2860
P2888
P3181
P356
10.1038/NM.2713
P407
P577
2012-03-18T00:00:00Z
P5875
P6179
1028536763