Dr. Zaika is an established cancer scientist with a long-standing track record of innovative clinical and basic science research. He has developed multiple research collaborations nationally and internationally. His laboratory works tightly with basic science (Cancer Biology, Cell biology, Microbiology, and Statistics/Bioinformatics) and clinical (Pharmacology, Pathology, Surgery, and Gastroenterology) departments on two intertwined objectives: to better understand the mechanisms of carcinogenesis and to develop novel strategies for cancer prevention and treatment. He has made important contributions to these areas of research. His laboratory also provides unique training experiences in cancer science, specifically on gastric and esophageal tumors. Dr. Zaika leads an independent research program that is funded by the VA and NIH/NCI. His main research interests are in cancer biology, molecular signaling, and host-pathogen interactions. Dr. Zaika’s research utilizes various animal models, ex-vivo techniques, and human tissues as tools for studies of tumor development and progression. For discovery and translational research, his laboratory employs single cell RNA seq, ChiP seq, MALDI-TOF MS, CyTOF and other approaches. He has been successful in identifying the molecular links between gastroesophageal reflux/esophageal adenocarcinoma and DNA damage/protein adducts in the esophagus. His studies have also revealed the complex interactions between H. pylori pathogen and host p53/p14ARF tumor suppressors, discovering novel targets for upper GI cancer prevention and control. His pioneering work on protein adducts in the esophagus has demonstrated, for the first time, that peroxidation of lipids caused by gastroesophageal reflux, which is a principal cause of Barrett’s esophagus and esophageal adenocarcinoma, leads to accumulation of isolevuglandins-protein adducts that covalently modify cellular proteins causing carcinogenic alterations. This innovative work opens new opportunities for prevention and treatment of esophageal cancer with a new class of drugs termed isoLG scavengers. Zaika lab has also made significant contributions to our understanding of the molecular mechanisms underlying the development and progression of gastric cancer caused by Helicobacter pylori infection that is the strongest known risk factor for gastric cancer. The groundbreaking work from his lab has shown that tumorigenic variants of H. pylori alter mRNA splicing of p53 tumor suppressor producing short inhibitory isoforms of p53 protein, thereby facilitating progression of gastric cancer. He was also the first who describe proteasomal degradation of p14ARF tumor suppressor by H. pylori, as a bacterial mechanism responsible for inactivation of the oncogenic stress response, a pivotal cellular pathway, that protects human cells against cancerogenic transformation. As a professor of Surgery, Biochemistry and Molecular Biology, Dr. Zaika oversees the research development, mentors...