Gemtuzumab ozogamicin: one size does not fit all--the case for personalized therapy.

摘要

Increased understanding of the biology of neoplastic transformation is providing us with an ever-increasing array of targets for intervention and drug development, and identification of new molecular subsets within various cancer diagnoses is further refining our choices for therapy. The process of neoplastic change is the culmination of a number of cooperating molecular aberrations, some of which are the driving force behind the process, which make them susceptible to selective drug intervention. Examples include HER-2eu gene amplification in breast cancer and EGFR expression and mutations in non-small-cell lung cancer, making them susceptible to trastuzumab and erlotinib or gefitinib, respectively.1'2 This is also the case in leukemia therapy where the morphologic classifications have been progressively supplanted with cytogenetic and molecular data, with the inclusion of a number of recurring cytogenetic/molecular abnormalities as specific disease subtypes in the WHO classification of myeloid neoplasms. Furthermore, selective inhibitors of the constitutively activated protein products of the better characterized molecular events, such as the internal tandem duplication mutations of the fms-like tyrosine kinase-3 gene are under evaluation.