Mark W. Jackson joined the Department of Pathology and the Case Comprehensive Cancer Center in the fall of 2007. He received a Bachelor’s degree from Kent State University in 1996, and a Ph.D. from Wright State University (Boonshoft School of Medicine) in 2001. After completing his Ph.D., Dr. Jackson joined the lab of Dr. George Stark at the Cleveland Clinic as a postdoctoral fellow. In addition to the research described below, Dr. Jackson is actively involved in training our next generation of cancer researchers, serving as the Director of the Cancer Biology Training Program, Director of NCI-funded training grants (Cancer Biology T32 and an undergraduate summer training program R25), and the Associate Director of Training and Education in the Case Comprehensive Cancer Center.
We have developed a forward genetics approach named VBIM (validation-based insertional mutagenesis). Using the VBIM approach, we identified FAM83B as a novel transforming oncogene. Interestingly, FAM83B is one of eight members of a previously uncharacterized protein family (FAM83). We have studied the oncogenic role of the FAM83 proteins in a variety of cancers and are continuing to define the molecular interactions between the FAM83 proteins and EGFR/RAS signaling effectors, leading to their hyperactivation in cancer. Our findings suggest that the FAM83 proteins provide vital new targets for therapeutic intervention that may significantly impact an oncologist's ability to treat cancer.
We continue to refine the VBIM strategy, and are currently searching for novel effectors that promote resistance to immune checkpoint inhibitors (anti-PD-L1 and anti-CTLA4) in vivo. Our studies will identify a list of candidate genes that can identify patients that may or may not respond to checkpoint blockade, as well provide a foundation for how to target the identified resistance genes/programs to ultimately induce long-term, durable responses.
Finally, we are studying the molecular antagonism between tumor microenvironmental cytokines Oncostatin M and Interferon-beta in regulating cancer cell plasticity, including epithelial-mesenchymal plasticity and cancer stem cell reprogramming). As we define how Oncostatin M and Interferons antagonize one another, we can develop novel therapeutic approaches to shift the balance towards active Interferon signaling and away from Oncostatin M signaling, with the goal of improving outcomes for patients with metastatic TNBC