© 2005 Oxford University Press
EDITORIAL |
EGFR Gene Mutations: A Call for Global x Global Views of Cancer
Affiliations of authors: Department of Medical Oncology, Dana-Farber Cancer Institute, Departments of Medicine and Pathology, Brigham and Women's Hospital, Departments of Medicine and Pathology, Harvard Medical School, Boston, MA (WRS); Broad Institute of Harvard and the Massachusetts Institute of Technology, Cambridge, MA (MM)
Correspondence to: William R. Sellers, MD, Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA 02115 (e-mail: William_Sellers@dfci.harvard.edu).
| The first 150 words of the full text of this article appear below. |
Successful medical therapy depends largely on penetrating the molecular underpinnings of pathogenic processes. Gradually, we have begun to link pathogenesis to alterations in the genome. The completed human genome sequence coupled with the development of technology capable of high-resolution genome interrogation holds special promise for cancer therapeutics because, unlike most medical illness, cancer presents with a separate genome that can be readily isolated. Thus, comparative analysis of the diseased and normal genomes may in theory identify the pathogenic genome alterations. Indeed, identification of genetic alterations leading to the inactivation of tumor suppressor genes and/or activation of oncogenes has revealed many of the regulatory pathways deregulated during cancer initiation and progression.
Although the development of novel therapeutics based on the discovery of specific genetic lesions (e.g., the p53 mutation) has been difficult recently, a number of therapeutics targeting specific genetic alterations have gained a foothold in the clinic. Successes have included
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