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PDGFR blockade is a rational and effective therapy for NPM-ALK-driven lymphomas
Daniela Laimer1, Helmut Dolznig, Karoline Kollmann
1Clinical Institute of Pathology, Medical University of Vienna, Vienna, Austria.
Nature Medicine
|October 16, 2012
Summary
JUN and JUNB proteins drive anaplastic large cell lymphoma (ALCL) by regulating PDGFRB. Inhibiting PDGFRB shows promise as a novel therapy for ALCL, improving survival and patient remission.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Anaplastic large cell lymphoma (ALCL) is an aggressive non-Hodgkin's lymphoma.
- ALCL often involves the NPM-ALK oncoprotein, but downstream pathways are not fully understood.
Purpose of the Study:
- To investigate the role of AP-1 family members JUN and JUNB in NPM-ALK-driven lymphomagenesis.
- To identify novel therapeutic targets for ALCL.
Main Methods:
- Utilized a mouse model of NPM-ALK-triggered lymphomagenesis.
- Examined the transcriptional regulation of PDGFRB by JUN and JUNB.
- Assessed the therapeutic efficacy of PDGFRB inhibition in preclinical models and a patient.
Main Results:
- JUN and JUNB promote ALCL development and dissemination via PDGFRB regulation.
- PDGFRB inhibition significantly improved survival in NPM-ALK mice.
- Combined inhibition of PDGFRA and PDGFRB led to complete remission in a refractory ALCL patient.
Conclusions:
- PDGFRB is a novel downstream target of JUN and JUNB in ALCL.
- Targeting PDGFRB represents a potential effective therapeutic strategy for ALCL.
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