Molecular on/off switch

Cancer genomics approaches employ high-throughput technologies to identify the complete catalog of somatic alterations that characterize the genome, transcriptome and epigenome of cohorts of tumor samples. Discover the latest research using such technologies in this feed.

Molecular on/off switch

Abstract

References

Gain-of-function mutations of c-kit in human gastrointestinal stromal tumors

Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia

Clinical resistance to STI-571 cancer therapy caused by BCR-ABL gene mutation or amplification

Cancer. Addiction to oncogenes--the Achilles heal of cancer

A tyrosine kinase created by fusion of the PDGFRA and FIP1L1 genes as a therapeutic target of imatinib in idiopathic hypereosinophilic syndrome

Multi-institutional randomized phase II trial of gefitinib for previously treated patients with advanced non-small-cell lung cancer (The IDEAL 1 Trial) [corrected

Gastrointestinal stromal tumors (GIST): a model for molecule-based diagnosis and treatment of solid tumors

Efficacy of gefitinib, an inhibitor of the epidermal growth factor receptor tyrosine kinase, in symptomatic patients with non-small cell lung cancer: a randomized trial

A new mutation in the KIT ATP pocket causes acquired resistance to imatinib in a gastrointestinal stromal tumor patient

Determinants of tumor response and survival with erlotinib in patients with non--small-cell lung cancer

EGFR mutation and resistance of non-small-cell lung cancer to gefitinib

Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain

Irreversible inhibitors of the EGF receptor may circumvent acquired resistance to gefitinib

Citations

The quest to overcome resistance to EGFR-targeted therapies in cancer

Rational, biologically based treatment of EGFR-mutant non-small-cell lung cancer

Survival and death signals can predict tumor response to therapy after oncogene inactivation.

Mechanisms of Resistance to Epidermal Growth Factor Receptor Inhibitors and Novel Therapeutic Strategies to Overcome Resistance in NSCLC Patients.

Combined Inactivation of MYC and K-Ras oncogenes reverses tumorigenesis in lung adenocarcinomas and lymphomas.

A subset of lung adenocarcinomas and atypical adenomatous hyperplasia-associated foci are genotypically related: an EGFR, HER2, and K-ras mutational analysis

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