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Expression of anaplastic lymphoma kinase, tyrosine-phosphorylated STAT3, and associated factors in pediatric anaplastic large cell lymphoma: A report from the children's oncology group.

Nasr MR, Laver JH, Chang M, Hutchison RE

Department of Pathology, State University of New York Upstate Medical University, Syracuse, NY 13210, USA.

In anaplastic large cell lymphoma (ALCL), anaplastic lymphoma kinase (ALK) activates (phosphorylates) signal transducer and activator of transcription 3 (STAT3) with subsequent cytoplasmic expression, in some cases, of survivin and tissue inhibitor of metalloprotease 1 (TIMP1). These are inhibitors of apoptosis and negative prognostic factors. CD56 is also a negative prognostic marker in ALCL. We assayed 40 cases of predominantly ALK+ pediatric ALCL for pSTAT3, survivin, TIMP1, and CD56 using immunohistochemical analysis. The patients were derived from a Pediatric Oncology Group treatment protocol that showed 72% event-free survival at 4 years for ALCL. The results show that in advanced-stage pediatric ALCL, although most tumors express ALK and a majority show activated STAT3, cytoplasmic localization of survivin and TIMP1 is not frequent, nor is expression of CD56. This may help, in part, explain the relatively good prognosis of pediatric ALCL.

Published 18 April 2007 in Am J Clin Pathol, 127(5): 770-8.
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