Abstract
SPECIALTY GRAND CHALLENGE article Front. Pharmacol., 20 September 2010Sec. Pharmacology of Anti-Cancer Drugs https://doi.org/10.3389/fphar.2010.00120
Highlights
Imatinib/Gleevec, as an inhibitor of the bcr-abl fusion protein (Druker et al, 2001) and trastuzumab/Herceptin as inhibitor of the human epidermal growth factor receptor 2 (HER2) (Baselga et al, 1998) are two of the very first examples of the development of molecularly targeted therapies
The identification of patients who may benefit from these treatments was guided by the detection of corresponding genetic alterations: the Philadelphia chromosome consistently found in chronic myelogenous leukemia (CML) patients, formed by a reciprocal translocation of DNA leading to a fusion gene between cABL and BCR (Bartram et al, 1983), and the overexpression of HER-2/neu as observed in 20–25% invasive breast cancers (Slamon et al, 1987)
Potentially fatal cardiac toxicity is reported with trastuzumab (Telli et al, 2007) and better tolerated, hematological, and non-hematological toxicities are reported with imatinib (Deininger et al, 2005)
Summary
Imatinib/Gleevec, as an inhibitor of the bcr-abl fusion protein (Druker et al, 2001) and trastuzumab/Herceptin as inhibitor of the human epidermal growth factor receptor 2 (HER2) (Baselga et al, 1998) are two of the very first examples of the development of molecularly targeted therapies. We know today that the disease can find a way to advance despite the treatments: patients with BCR-ABL or HER2-positive cancers can still progress after receiving the above targeting drugs (often despite encouraging first responses).
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