Oncogene addiction: Mouse models and clinical relevance for molecularly targeted therapies
Publication
, Journal Article
Alvarez, JV; Yeh, ES; Feng, Y; Chodosh, LA
January 1, 2012
Cancer results from the dysregulation of pathways controlling the growth, proliferation, differentiation, and survival of tumor cells, as well as fundamental alterations in the manner in which cells interact with their microenvironment (Hanahan and Weinberg 2000). Several lines of evidence suggest that these alterations are due to the accumulation of multiple mutations in oncogenes and tumor suppressor genes that disrupt their normal function or regulation. These mutations provide a selective advantage to the cells in which they occur, leading to their expansion and clinical manifestation as a tumor.
Duke Scholars
Citation
APA
Chicago
ICMJE
MLA
NLM
Alvarez, J. V., Yeh, E. S., Feng, Y., & Chodosh, L. A. (2012). Oncogene addiction: Mouse models and clinical relevance for molecularly targeted therapies, 527–547. https://doi.org/10.1007/978-0-387-69805-2_25
Alvarez, J. V., E. S. Yeh, Y. Feng, and L. A. Chodosh. “Oncogene addiction: Mouse models and clinical relevance for molecularly targeted therapies,” January 1, 2012, 527–47. https://doi.org/10.1007/978-0-387-69805-2_25.
Alvarez JV, Yeh ES, Feng Y, Chodosh LA. Oncogene addiction: Mouse models and clinical relevance for molecularly targeted therapies. 2012 Jan 1;527–47.
Alvarez, J. V., et al. Oncogene addiction: Mouse models and clinical relevance for molecularly targeted therapies. Jan. 2012, pp. 527–47. Scopus, doi:10.1007/978-0-387-69805-2_25.
Alvarez JV, Yeh ES, Feng Y, Chodosh LA. Oncogene addiction: Mouse models and clinical relevance for molecularly targeted therapies. 2012 Jan 1;527–547.