IMR Press / FBE / Volume 8 / Issue 1 / DOI: 10.2741/E751

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


The emerging role of CD30 and p53 as novel targets for therapy in anaplastic large cell lymphoma

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1 Department of Pathology and Cytology, Karolinska University Hospital and Karolinska Institute, Radiumhemmet, Stockholm, Sweden SE-17176
2 Department of Hematopathology, The University of Texas MD Anderson Cancer Center, Houston, Texas
3 European Research Initiative on ALK-related malignancies (ERIA), University of Crete Medical School, Heraklion, Crete, Greece
4 Department of Pathology, University of Crete Medical School, Heraklion, Crete, Greece

*Author to whom correspondence should be addressed.


Front. Biosci. (Elite Ed) 2016, 8(1), 61–71;
Published: 1 January 2016

ALK+ anaplastic large cell lymphoma (ALCL). frequently carries the t(2;5).(p23;q35). resulting in expression of NPM-ALK oncogenic kinase, which is capable of activating multiple oncogenic pathways. ALK+ ALCL is also characterized by overexpression of CD30 receptor, a member of the tumor necrosis factor (TNF). receptor superfamily, which has been targeted for therapy using conjugated anti-CD30 antibodies with clinical success. Also, the tumor suppressor p53 is frequently non-mutated in ALK+ ALCL allowing for therapeutic modulation of p53 reactivation in this lymphoma type. Therefore, this review is focused on the role of CD30 receptor and p53 as novel targets for therapy in ALK+ ALCL, and also provides an update on their potential involvement in ALK+ ALCL pathogenesis.

Anaplastic Large Cell Lymphoma
Cell cycle
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