| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
1 Herbert Irving Comprehensive Cancer Center and 2 Department of Medicine, Columbia University Medical Center, New York, New York
Requests for reprints: I. Bernard Weinstein, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, HHSC-1509, 701 West 168th Street, New York, NY 10032-2704. Phone: 212-305-6921; Fax: 212-305-6889; E-mail: ibw1{at}columbia.edu.
Cancer cells contain multiple genetic and epigenetic abnormalities. Despite this complexity, their growth and survival can often be impaired by the inactivation of a single oncogene. This phenomenon, called "oncogene addiction," provides a rationale for molecular targeted therapy. The efficacy of this strategy requires novel methods, including integrative genomics and systems biology, to identify the state of oncogene addiction (i.e., the "Achilles heel") in specific cancers. Combination therapy may also be required to prevent the escape of cancers from a given state of oncogene addiction. [Cancer Res 2008;68(9):3077–80]
Reviews |
1 Herbert Irving Comprehensive Cancer Center and 2 Department of Medicine, Columbia University Medical Center, New York, New York
Requests for reprints: I. Bernard Weinstein, Herbert Irving Comprehensive Cancer Center, Columbia University Medical Center, HHSC-1509, 701 West 168th Street, New York, NY 10032-2704. Phone: 212-305-6921; Fax: 212-305-6889; E-mail: ibw1{at}columbia.edu.
Cancer cells contain multiple genetic and epigenetic abnormalities. Despite this complexity, their growth and survival can often be impaired by the inactivation of a single oncogene. This phenomenon, called "oncogene addiction," provides a rationale for molecular targeted therapy. The efficacy of this strategy requires novel methods, including integrative genomics and systems biology, to identify the state of oncogene addiction (i.e., the "Achilles heel") in specific cancers. Combination therapy may also be required to prevent the escape of cancers from a given state of oncogene addiction. [Cancer Res 2008;68(9):3077–80]
Department of Medicine and Oncology, Stanford University, Stanford, California
This article has been cited by other articles:
|
|
 |
|
  B. Dai, X. F. Zhao, P. Hagner, P. Shapiro, K. Mazan-Mamczarz, S. Zhao, Y. Natkunam, and R. B. Gartenhaus Extracellular Signal-Regulated Kinase Positively Regulates the Oncogenic Activity of MCT-1 in Diffuse Large B-Cell Lymphoma Cancer Res., October 1, 2009; 69(19): 7835 - 7843. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A Woyach and M. H Shah New therapeutic advances in the management of progressive thyroid cancer Endocr. Relat. Cancer, September 1, 2009; 16(3): 715 - 731. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. M. Reilly Aiming for a Direct Hit: Combining Molecular Imaging with Targeted Cancer Therapy J. Nucl. Med., July 1, 2009; 50(7): 1017 - 1019. [Full Text] [PDF]
|
|
|
|
|
|
D. Raina, R. Ahmad, M. D. Joshi, L. Yin, Z. Wu, T. Kawano, B. Vasir, D. Avigan, S. Kharbanda, and D. Kufe Direct Targeting of the Mucin 1 Oncoprotein Blocks Survival and Tumorigenicity of Human Breast Carcinoma Cells Cancer Res., June 15, 2009; 69(12): 5133 - 5141. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. Brambilla and A. Gazdar Pathogenesis of lung cancer signalling pathways: roadmap for therapies Eur. Respir. J., June 1, 2009; 33(6): 1485 - 1497. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. F. Jabbar, L. Abrams, A. Glick, and P. F. Lambert Persistence of High-Grade Cervical Dysplasia and Cervical Cancer Requires the Continuous Expression of the Human Papillomavirus Type 16 E7 Oncogene Cancer Res., May 15, 2009; 69(10): 4407 - 4414. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Chen, W. G. Wierda, S. Chubb, R. E. Hawtin, J. A. Fox, M. J. Keating, V. Gandhi, and W. Plunkett Mechanism of action of SNS-032, a novel cyclin-dependent kinase inhibitor, in chronic lymphocytic leukemia Blood, May 7, 2009; 113(19): 4637 - 4645. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. L. Gabai, J. A. Yaglom, T. Waldman, and M. Y. Sherman Heat Shock Protein Hsp72 Controls Oncogene-Induced Senescence Pathways in Cancer Cells Mol. Cell. Biol., January 15, 2009; 29(2): 559 - 569. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. Banerji Heat Shock Protein 90 as a Drug Target: Some Like It Hot Clin. Cancer Res., January 1, 2009; 15(1): 9 - 14. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z. S. Boyd, Q. J. Wu, C. O'Brien, J. Spoerke, H. Savage, P. J. Fielder, L. Amler, Y. Yan, and M. R. Lackner Proteomic analysis of breast cancer molecular subtypes and biomarkers of response to targeted kinase inhibitors using reverse-phase protein microarrays Mol. Cancer Ther., December 1, 2008; 7(12): 3695 - 3706. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. A. Loeb and C. C. Harris Advances in Chemical Carcinogenesis: A Historical Review and Prospective Cancer Res., September 1, 2008; 68(17): 6863 - 6872. [Full Text] [PDF]
|
|
|
|
 |
|
 G. C. Prendergast From Sturm und Drang to Zebrafish Cancer Reviews Online Content, June 1, 2008; 2008(6): 11 - 11. [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Cancer Research | Clinical Cancer Research |
| Cancer Epidemiology Biomarkers & Prevention | Molecular Cancer Therapeutics |
| Molecular Cancer Research | Cancer Prevention Research |
| Cancer Prevention Journals Portal | Cancer Reviews Online |
| Annual Meeting Education Book | Meeting Abstracts Online |
