Addiction to multiple oncogenes can be exploited to prevent the emergence of therapeutic resistance.

Choi, Peter S; Li, Yulin; Felsher, Dean W

Choi, Peter S; Li, Yulin; Felsher, Dean W.

Affiliation

Choi PS; Division of Oncology, Departments of Medicine, Pathology, and Molecular Imaging, Stanford University School of Medicine, Stanford, CA 94305.
Li Y; Division of Oncology, Departments of Medicine, Pathology, and Molecular Imaging, Stanford University School of Medicine, Stanford, CA 94305.
Felsher DW; Division of Oncology, Departments of Medicine, Pathology, and Molecular Imaging, Stanford University School of Medicine, Stanford, CA 94305 dfelsher@stanford.edu.

Proc Natl Acad Sci U S A ; 111(32): E3316-24, 2014 Aug 12.

Article in En | MEDLINE | ID: mdl-25071175

Subject(s)

Drug Resistance, Neoplasm/genetics; Oncogenes; Animals; Apoptosis; Apoptosis Regulatory Proteins/metabolism; Bcl-2-Like Protein 11; Cell Line, Tumor; Genes, myc/drug effects; Lymphoma/drug therapy; Lymphoma/genetics; Lymphoma/metabolism; Membrane Proteins/metabolism; Mice; Mice, SCID; Mice, Transgenic; Mutation; Neoplasm Recurrence, Local/genetics; Neoplasm Recurrence, Local/metabolism; Oncogenes/drug effects; Proto-Oncogene Proteins/metabolism; RNA Splice Sites; bcl-X Protein/metabolism; beta Catenin/antagonists & inhibitors; beta Catenin/genetics; beta Catenin/metabolism

Key words

combination targeted therapy; oncogene addiction; splice site mutations

Fulltext

XML

PubMed Links

Search on Google

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Oncogenes / Drug Resistance, Neoplasm Limits: Animals Language: En Journal: Proc Natl Acad Sci U S A Year: 2014 Type: Article

Fulltext

XML

PubMed Links

Search on Google