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Vincenzo Coppola, MD

Assistant Professor

Director, Genetically Engineered Mouse Modeling Core
Department of Cancer Biology and Genetics​

Contact Information


Comprehensive Cancer Center
The Ohio State University Comprehensive Cancer Center
Biomedical Research Tower, Room 988
460 W. 12th Avenue
Columbus, OH 43210
(614) 688 8038 office
(614) 688 5933 fax

Education and Training

1991 Doctoral Degree in Medicine and Surgery (honors), Federico II University, Naples, Italy
1992 Residency (Medical Sciences) University of Naples, Italy
1997 Specialization in Oncology (honors), University of Padua, Italy
2000 Post-doctoral Fellowship in Dr. Lino Tessarollo’s Laboratory at the Center for Cancer Research/National Cancer Institute in Frederick, MD, USA

Positions and Appointments

2010-Present: Director Genetically Engineered Mouse Modeling Shared Resource (GEMMSR) of the Ohio State Comprehensive Cancer Center (OSUCCC)
Assistant Professor, Molecular Virology Immunology and Medical Genetics in the College of Medicine of the Ohio State University
2001-2010: Head, Gene Targeting Facility, Mouse Cancer Genetics Program, Center for Cancer Research/National Cancer Institute in Frederick, MD, USA

Genetically Engineered Mouse Modeling Core

As Director of the GEMMC, I collaborate with Ohio State University Investigators for designing, generation, and development of Mouse Models for human disease.

For more information about the GEMMC, please visit: GEMMC webpage

Research Interests​

Non-oncogenic addictions are defined by the need in cancer cells of proper functionality of genes/pathways that are usually non-mutated or tumorigenic per se. However, cancer cells depend on those functions due their increased level of stress (Solimini et al. Cell, 2007). Targeting non-oncogenic addictions provides powerful anticancer treatments able to cause synthetic lethality (Nagel et al., EMBO Rep, 2016).

The Coppola Lab is studying the biological role of Scorpins (RANBP9 and RANBP10) and IWS1 (Interacting With Spt6 1) on which specific tumors might be heavily relying for their survival. The ultimate goal is to find novel synthetic lethality to treat lung cancer and melanoma.  

Scorpins are a subgroup of Ran Binding Proteins made of RANBP9 and RANBP10, which share high similarities in their protein structure and likely resulted from a gene duplication during evolution. RANBP9 and RANBP10 have functions unrelated to the rest of the RANBPs. In fact, those two proteins do not bind RAN and are not involved in nuclear cytoplasmic shuttling. On the other hand, they are part of macromolecular complexes responding to different types of stress.

Focusing on lung cancer, we have found that RANBP9, in comparison with the normal counterpart, is highly expressed in all different histotypes and its ablation causes increased sensitivity damage and lethality induced by common DNA-damaging agents (Palmieri et al. 2016). In addition, RANBP9 is both a target and a facilitator of ATM signaling, which is decreased when RANBP9 is silenced or ablated. We are currently assessing whether the genetic ablation of RANBP9 affects lung cancer genesis in mice.

The second Scorpin, RANBP10 is highly expressed in melanoma in comparison to other types of cancer (TCGA data). We are currently assessing whether the genetic ablation of RANBP10 affects melanoma genesis in mice.

IWS1 is essential in coupling RNA transcription elongation to splicing and export in conjunction with chromatin modifications acting as signals to regulate RNA processing (ref). IWS1 was found to be essential for cancer cell proliferation and survival (ref). We have recently established that IWS1 is necessary for mouse development since the very first stages after oocyte fertilization (Orlacchio et al., 2018). We are exploring possibilities to target IWS1 in cancers in which is highly expressed (like melanoma and lung cancer for example), without side effects due to cytotoxicity toward normal cells.