alk inhibitors, a pharmaceutical perspective

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ID: 242582
2012
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Abstract
In 2007, the ALK tyrosine kinase, already known to be translocated and activated in Anaplastic Large Cell Lymphoma, and a few other rare cancers, was described as a potential therapeutic target for a subset of non small-cell lung cancer (NSCLC) patients. Clinical proof of concept, culminating in the recent approval by the FDA of the Pfizer drug Xalkori (crizotinib, formerly known as PF-02341066) followed in record time. The drug was approved together with a companion diagnostic, the Vysis ALK Break Apart FISH Probe Kit (Abbott Molecular, Inc.) for detection of eligible patients. This remarkable example of the coming of age of personalized medicine in cancer therapy is hopefully only an auspice of things to come in this rapidly developing field. Perhaps unsurprisingly, however, the appearance of clinical acquired resistance to crizotinib has already been observed early on in clinical testing, with the identification of several ALK secondary point mutations which diminish drug efficacy, and which open the way for development of second-generation inhibitors. It is also emerging that acquired resistance to crizotinib may also occur through ALK-independent mechanisms, which still need to be elucidated in detail.
Reference Key
egalvani2012frontiersalk Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Arturo eGalvani;Elena eArdini
Journal international journal of heat and technology
Year 2012
DOI
10.3389/fonc.2012.00017
URL
http://journal.frontiersin.org/Journal/10.3389/fonc.2012.00017/full
Keywords
resistance neuroblastoma Oncology alk including cancer and carcinogens tumors imtneoplasms

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