Case Western Reserve University School of Medicine, MD / Case Western Reserve University School of Graduate Studies, PhD (Biochemistry)
Whitehead Institute for Biomedical Research (Cancer Biology)
Dimaras H, J Zhao, T Corson, D Cobrinik, F Munier, D Abramson, C Shields, G Chantada, F Njuguna, A White, and B Gallie. (2015) Retinoblastoma. Nature Reviews Disease Primers 1: 1-22.
Cobrinik D. (2015) Retinoblastoma Progression. EBioMedicine, 2:623-4.
Xu, XL, HP Singh, L Wang, D Qi, BK Poulos, DH Abramson, SC Jhanwar, and D Cobrinik. (2014) Rb suppresses human cone precursor-derived retinoblastoma tumors. Nature 514:385-8. PMID: 25252974.
Wang, H, F Bauzon, P Ji, XL Xu, D Sun, J Locker, RS Sellers, K Nakayama, KI Nakayama, D Cobrinik, and L Zhu. (2010) Skp2 is required for survival of aberrantly proliferating Rb1-deficient cells and for tumorigenesis in Rb1+/- mice. Nature Genetics 42: 82-8. PMID: 19966802.
Xu, XL, Y Fang, TC Lee, D Forrest, C Gregory-Evans, D Almeida, A Liu, SC Jhanwar, DH Abramson, and D Cobrinik. (2009) Retinoblastoma has properties of a cone precursor tumor and depends upon cone-specific MDM2 signaling. Cell 137: 1018-31. PMID: 19524506.
Lee, TC, D Almeida, N Claros, DH Abramson, and D Cobrinik. (2006) Cell cycle-specific and cell type-specific expression of Rb in the developing human retina. Invest Ophthal Vis Sci 47: 5590-98. PMID: 17122153.
Retinoblastoma is a childhood eye cancer that develops in response to mutations in the RB1 tumor suppressor gene. While RB1 regulates proliferation in many cell types, only cells within the retina routinely form cancers when RB1 function is lost. Our research aims to characterize the cell type-specific signaling pathways that collaborate with RB1 inactivation, as a means to identify therapeutic targets for retinoblastoma and other cancers.
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