David S. Rickman   Associate Professor of Research in Pathology and Laboratory Medicine

The focus of Dr. Rickman’s lab is to elucidate the role of key oncogenic transcription factors in the biology of prostate cancer with an emphasis on the role of ETS family members and N-Myc in gene regulation and response to treatment. His lab has shown that Aurora-A and N-Myc associate with and stabilize each other in neuroendocrine prostate cancer (NEPC) and generated mechanistic data showing that N-Myc over-expression is associated pro-metastatic, dedifferentiation and Polycomb Repressive Complex deregulated genes (Beltran H, Rickman DS et al., Cancer Discovery 2011; Dardenne E., Beltran, et al. Cancer Cell, 2016, Berger A, Brady N., et al. J. Clinical Investigation 2019). The Rickman lab has developed multiple pre-clinical models over-expressing N-Myc (isogenic cell lines, xenografts, genetically engineered mice and organoid cultures) of NEPC and transitioning CRPC to NEPC in order to determine the molecular features driving these cancer entities. Most recently, his lab has also analyzed epigenetic modifications along with the N-Myc transcriptome, cistrome and chromatin-bound interactome by performing ChIP-seq, RNA-seq and RIME in a combination of mouse models, human prostate cancer cell lines, and NEPC patient-derived organoids and found that the expression of MYCN in CRPC and NEPC patients correlates with reduced overall survival, that the N-Myc cistrome is androgen-dependent and drives a transcriptional program leading to epithelial plasticity and the acquisition of clinically relevant neuronal lineage markers. Interestingly, histone marks specifically associated with lineage-defining genes are epigenetically reprogrammed by N-Myc.


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full name

  • David S. Rickman

primary email

  • dsr2005@med.cornell.edu