Jak3 contributes to the activation of ALK and Stat3 in ALK + anaplastic large cell lymphoma. Response.
Research output: Contribution to journal › Letter › Research
A polemic in response to Amin et al. (Lab. Investigation, 2006, 86, 417-419) is presented. In a study, Amin et al. reported that Jak3 is phys. assocd. with ALK and contributes to ALK and Stat3 activation in ALK + anaplastic large cell lymphoma (ALCL) cells, based on the observation that the WHI compds. inhibit tyrosine phosphorylation of NPM/ALK. However, another study showed that the WHI compds. inhibit NPM/ALK enzymic activity using two different methods, and that Jak3 participation is not crit. for Stat3 activation by NPM/ALK. In this study, the NPM/ALK-expressing cells are significantly much more affected by the WHI compds. in regard to their growth, proliferation, cell cycle progression, viability, and Stat3 phosphorylation. Several tyrosine kinases including certain growth factor receptors, src, and bcr/abl, are capable of activating Stat3 seemingly directly and independently of Jaks. Activation of Stat3 by NPM/ALK independently of Jak3 and, apparently, of other members of the Jak/Tyk family, is consistent with such alternative mechanism of Stat3 activation. [on SciFinder(R)]
|Number of pages||2|
|Publication status||Published - 2006|
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CAPLUS AN 2006:265835(Journal)
- anaplastic large T cell lymphoma Stat3 Jak3 ALK protein