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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+ 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.
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.
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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]
Unlike MEITL, ALCL,ALK+ occurs most commonly in young individuals and individuals from Western Countries and most often involves tissue infiltrates of large, anaplastic-appearing T cells which express a fusion gene involving the ALK gene (which encodes Anaplastic lymphoma kinase), [11] but do not express CD3, CD8, or CD56. [7]
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