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Anaplastic large cell lymphoma: twenty-five years of discovery.

Authors
  • 1
  • 1 Department of Pathology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78229-3900, USA. [email protected]
Type
Published Article
Journal
Archives of Pathology & Laboratory Medicine
1543-2165
Publisher
Archives of Pathology and Laboratory Medicine
Publication Date
Volume
135
Issue
1
Pages
19–43
Identifiers
DOI: 10.1043/2010-0507-RAR.1
PMID: 21204709
Source
Medline
License
Unknown

Abstract

Based on immunostaining for activation antigen CD30 and the presence of dysregulation of the anaplastic lymphoma kinase gene (2p23), the diagnosis of ALCL has become relatively straightforward for most patients. Major strides have been made during the last decade in our understanding of the complex pathogenesis of ALCL. Constitutive NPM-ALK signaling has been shown to drive oncogenesis via an intricate network of redundant and interacting pathways that regulate cell proliferation, cell fate, and cytoskeletal modeling. Nevertheless, pathomechanistic, therapeutic, and diagnostic challenges remain that should be resolved as we embark on the next generation of discovery.

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