Anaplastic Lymphoma Kinase ( Alk ) Essay

Anaplastic Lymphoma Kinase ( Alk ) Essay

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Anaplastic lymphoma kinase (ALK) gene rearrangements represent the primary oncogenic driver in 3–5% of patients with nonsmall cell lung cancers (NSCLCs), with echinoderm microtubule-associated protein-like 4 (EML4) gene being the most frequent translocation partner [1-3]. ALK inhibitor crizotinib has been associated with over 60% response rate in ALK-rearranged advanced NSCLCs [4, 5], as shown by multicenter clinical trials [6, 7]. In these clinical trials, ALK status was determined by fluorescence in situ hybridization (FISH) using the Vysis break-apart probe set (Abbott Molecular, Des Plaines, Ill), which is the only diagnostic assay licensed by the United States Food and Drug Administration (FDA) to date [3, 8, 9].
In addition to the percentage of cells with ALK rearrangements, the break-apart FISH assay also provides information on the ALK gene copy number per cell. In contrast to the rarity of ALK gene rearrangement, ALK gene copy number gain (CNG) is a relatively common finding in NSCLCs, with a reported incidence of up to 63% [10, 11]. CNG is divided into two categories: low copy numbers with a mean copy number of 3–5 are usually due to polysomy status, whereas high copy numbers with over 6 copies per cell are due to ALK gene amplification. The incidence rate of CNG is significantly higher in NSCLC without ALK rearrangement than that in NSCLC with ALK rearrangement [12]. Very few previous studies with conflicting results have been reported on the biological roles of ALK CNG [12-15]. The clinical significance of ALK CNG is unclear, and it is unknown whether patients with combined ALK translocation and CNG respond differently to ALK inhibitor. Herein, we reported a case of pulmonary adenocarcinoma that demonstrated combined ...


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...confers resistance to crizotinib [26]. The sensitivity of the tumor to ALK inhibitor in this case is at least comparable, or even superior, to that in previously reported cases of ALK-positive tumors, which were reported to have a median progression-free survival of 8–10 months [4, 5, 7, 9]. This indicates that ALK gene CNG due to polysomy status does not affect, and may increase the tumor’s sensitivity to ALK inhibitors. De novo ALK CNG in combination with ALK translocations might lead to a different outcome in response to ALK tyrosine kinase inhibitors with compared with acquired ALK CNG. Therefore, patients with ALK CNG in addition to ALK translocation may gain additional benefits from ALK inhibitor therapy. More cases with combined ALK CNG and translocation and their treatment responses to ALK inhibitors are needed to further evaluate its clinical significance.

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