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• W2012135986 abstract "The fusion protein, nucleophosmin-anaplastic lymphoma kinase (NPM-ALK), results from the chromosome translocation t(2;5)(p23;q25) and is present in 50–70 percent of anaplastic large-cell lymphomas (ALCLs). NPM-ALK is a constitutively activated kinase that transforms cells through stimulating several mitogenic signaling pathways. To examine if the NPM-ALK is a potential therapeutic target in ALCL, we used siRNA to specifically downregulate the expression of the NPM-ALK in ALCL cell lines. In this report, we demonstrated viability loss in t(2;5)-positive ALCL cell lines, SUDHL-1 and Karpas 299 cells, but not in lymphoma cell lines without the chromosome translocation, Jurkat and Granta 519 cells. Further study demonstrated that the downregulation of NPM-ALK resulted in decreased cell proliferation and increased cell apoptosis. When used in combination with chemotherapeutic agents, such as doxorubicin, the inhibition of the NPM-ALK augments the chemosensitivity of the tumor cells. These results revealed the importance of continuous expression of NPM-ALK in maintaining the growth of ALCL cells. Our data also suggested that the repression of the fusion gene might be a potential novel therapeutic strategy for NPM-ALK positive ALCLs." @default.
• W2012135986 created "2016-06-24" @default.
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• W2012135986 date "2007-01-01" @default.
• W2012135986 modified "2023-09-23" @default.
• W2012135986 title "Downregulation of NPM-ALK by siRNA Causes Anaplastic Large Cell Lymphoma Cell Growth Inhibition and Augments the Anti Cancer Effects of Chemotherapy In Vitro" @default.
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• W2012135986 doi "https://doi.org/10.1080/07357900701206372" @default.
• W2012135986 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17612934" @default.
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