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Anaplastic lymphoma kinase (ALK) was originally discovered in 1994 [5] [7] in anaplastic large-cell lymphoma (ALCL) cells. ALCL is caused by a (2;5)(p23:q35) chromosomal translocation that generates the fusion protein NPM-ALK, in which the kinase domain of ALK is fused to the amino-terminal part of the nucleophosmin (NPM) protein.
ALK inhibitors are anti-cancer drugs that act on tumours with variations of anaplastic lymphoma kinase (ALK) such as an EML4-ALK translocation. [1] They fall under the category of tyrosine kinase inhibitors , which work by inhibiting proteins involved in the abnormal growth of tumour cells.
ALK, i.e. anaplastic lymphoma kinase, is a protein product of the ALK gene located on chromosome 2. In ALK-positive ALCL, a portion of the ALK gene has merged with another site on the same or different chromosome to form a chimeric gene consisting of part of the new site and part of the ALK gene coding for ALK's activity. [4]
ALK, i.e. anaplastic lymphoma kinase (also termed protein kinase B), is produced by the ALK gene. [21] In IMT, the ALK gene has merged with a gene located at another site on the same or different chromosome to form a chimeric gene consisting of a part of the new gene and a part of the ALK gene coding for ALK's activity. [22]
Ensartinib is an Anaplastic lymphoma kinase (ALK) inhibitor used as the salt ensartinib hydrochloride. [1] It is taken by mouth. [1] The most common adverse reactions include rash, musculoskeletal pain, constipation, cough, pruritis, nausea, edema, pyrexia, and fatigue. [2] Ensartinib was approved for medical use in the United States in ...
In August 2011, the US Food and Drug Administration (FDA) approved crizotinib to treat certain late-stage (locally advanced or metastatic) non-small cell lung cancers that express the abnormal anaplastic lymphoma kinase (ALK) gene. [4] Approval required a companion molecular test for the EML4-ALK fusion.
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