Abstract
Chemotherapy and targeted therapy remain the cornerstone of treatment of locally advanced and metastatic non-small cells lung cancer (NSCLC). Given the intrinsic chemoresistance of tumor cells, new treatment options have been developped. The knowledge of the molecular mechanisms of tumor biology, and signal transduction pathways activating cancer cells led to the identification of a new targeted therapy such as Crizotinib. The small molecule Crizotinib is a selective inhibitor of the receptor tyrosine kinase ALK (anaplastic lymphoma kinase) and its oncogenic variants (ALK fusion gene and some mutations of ALK). Phases I and II trials showed the efficacy of Crizotinib in the treatment of locally advanced and metastatic NSCLC expressing ALK. Thereafter, randomized Phase III trial confirmed the significant superiority of Crizotinib versus standard chemotherapy in terms of progression free survival and objective response with good tolerance; therefore, it has been approved by the Food and Drug Administration (FDA) as the standard treatment for locally advanced and metastatic ALK-positive NSCLC.
Highlights
Crizotinib is a new targeted molecule [1,2]
The Crizotinib has been tested in patients with metastatic non-small cell lung cancer (NSCLC), the tumor which has a genetic defect on chromosome 2, resulting in the fusion of two genes, ALK and EML4 [7,8,9]
The study profile 1007 is the first Phase III randomized trial comparing crizotinib with standard chemotherapy in patients with locally advanced or metastatic ALK positive NSCLC, having demonstrated a benefit of Crizotinib in progression-free survival (PFS) compared with 2nd line chemotherapy; pemetrexed or docetaxel, and Crizotinb have become the standard 2nd line treatment, in patietns with ALK positive NSCLC
Summary
Crizotinib is a new targeted molecule [1,2]. It has been shown to be effective in the treatment of ALK-positive locally advanced and metastatic non-small cell lung cancer (NSCLC) [3,4], in adenocarcinoma subtype [5]. The Crizotinib has been tested in patients with metastatic NSCLC, the tumor which has a genetic defect on chromosome 2, resulting in the fusion of two genes, ALK and EML4 (echinoderm microtubule-associated proteinlike 4) [7,8,9]. This DNA rearrangement leads to the production of ALK protein which enhances cancer cells proliferation. In patients with locally advanced and metastatic NSCLC expressing ALK, Phase I and II trials showed highly objective responses and acceptable tolerability with crizotinib [4,5] This opens the new era of personalized therapeutic treatment
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