ALK

Anaplastic large-cell lymphomas (ALCLs) are a subtype of the high-grade non-Hodgkin's family of lymphomas with distinct morphology, immunophenotype, and prognosis. ALCLs are postulated to arise from T-cells and, in rare cases, can also exhibit a B cell phenotype. ALCL presents as a systemic disease afflicting skin, bone, soft tissues, and other organs, with or without the involvement of lymph nodes. ALCL can be subdivided into at least two subtypes, characterized by the presence or absence of chromosomal rearrangements between the anaplastic lymphoma kinase (ALK) gene locus and various fusion partners such as nucleophosmin (NPM). NPM-ALK has constitutive tyrosine kinase activity and has been shown to transform various hematopoietic cell types in vitro and support tumor formation in vivo[1].
A small inversion within chromosome 2p results in the formation of a fusion gene comprising portions of the echinoderm microtubule-associated protein-like 4 (EML4) gene and the anaplastic lymphoma kinase (ALK) gene, and seems to be the cause of non-small-cell lung cancer (NSCLC) cells. The EML4–ALK fusion transcript is detected in approx. 7% of NSCLC patients[2].

Oncogene Fusion Proteins listed: ALKBCR-ABL


[1] A.V. Galkin et al. Identification of NVP-TAE684, a potent, selective, and efficacious inhibitor of NPM-ALK. Proc. Natl. Acad. Sci. USA 2007, 104 (1), 270-275.
[2] M. Soda et al. Identification of the transformingEML4-ALK fusion gene in non-small-cell lung cancer. Nature. 2007, 448, 561-566.

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1660 PF 02341066 c-MET Inhibitor; NPM-ALK inhibitor €80.00

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