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Research

Future directions and current projects

The main research focus of the Unit of Laboratory Animal Pathology lies in investigating the link between PDGFRB and lymphoma generation and dissemination. To this end we have generated mouse strains lacking the PDGFRB in the NPM-ALK model and dissect the contribution of PDGFRB to a malignant lymphoma phenotype by in vivo and in vitro methods.

  1. The interplay between tumor cells and tumor stroma
  2. The epigenetic component of lymphoma development
  3. The influence of DNA damage response and apoptosis to tumor progression

References

  1. Kadin, M. E. Ki-1/CD30+ (anaplastic) large-cell lymphoma: maturation of a clinicopathologic entity with prospects of effective therapy. J. Clin. Oncol.12, 884‑7 (1994).
  2. Stein, H. et al. CD30(+) anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features. Blood96, 3681‑95 (2000).
  3. Morris, S. W. et al. Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin’s lymphoma. Science263, 1281‑4 (1994).
  4. Mathas, S. et al. Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B. EMBO J.21, 4104‑13 (2002).
  5. Staber, P. B. et al. The oncoprotein NPM-ALK of anaplastic large-cell lymphoma induces JUNB transcription via ERK1/2 and JunB translation via mTOR signaling. Blood110, 3374‑83 (2007).
  6. Laimer, D. et al. PDGFR blockade is a rational and effective therapy for NPM-ALK–driven lymphomas. Nat. Med.18, 1699‑1704 (2012).