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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]
Complete surgical resection and/or radiation therapy are used to treat primary cutaneous anaplastic large cell lymphoma as a single lesion; the majority of patients experience total remission. [7] While radiation of the primary lesion and the surrounding lymph nodes has been advised for patients whose local lymph nodes are involved, adding ...
Activin A receptor, type I (ACVR1) is a protein which in humans is encoded by the ACVR1 gene; it is also known as ALK-2 (activin receptor-like kinase-2). [5] ACVR1 has been linked to the 2q23-24 region of the genome. [ 6 ]
ALK+ large B-cell lymphoma is a type of lymphoma. [ 1 ] [ 2 ] : 378 It was first reported in 1997. [ 2 ] : 378 [ 3 ] [ 4 ] It is a rare, aggressive large B-cell process that shows ALK expression.
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