Eastman A, Perez RP New targets and challenges in the molecular therapeutics of cancer. Br J Clin Pharmacol 2006 Jul; 62(1):5-14 PMID: 16842374 [PubMed - indexed for MEDLINE]
Armand R, Channon JY, Kintner J, White KA, Miselis KA, Perez RP, Lewis LD The effects of ethidium bromide induced loss of mitochondrial DNA on mitochondrial phenotype and ultrastructure in a human leukemia T-cell line (MOLT-4 cells). Toxicol Appl Pharmacol 2004 Apr 1; 196(1):68-79 PMID: 15050409 [PubMed - indexed for MEDLINE]
Burke LP, Lewis LD, Perez RP Ubiquinone does not rescue acute myeloid leukemia cells from growth inhibition by statins. Leukemia 2003 Jan; 17(1):267-8 PMID: 12529692 [PubMed - indexed for MEDLINE]
Dr Perez focuses on receptor-kinase/MAP-kinase signaling as a therapeutic target and predictor of response to anticancer therapy, and on early-phase clinical trials of molecular targeted anticancer drugs.
Dr. Perez received his B.S. from Kent State University, Kent, OH and his M.D. from the Northeastern Ohio Universities College of Medicine, Rootstown, OH in May 1985. He performed internship and residency in internal medicine at the Michael Reese Hospital and Medical Center, Chicago, an affiliated teaching hospital of the University of Chicago, from 1985 - 1988. From 1988 - 1992, he was a research fellow in medical oncology at the Fox Chase Cancer Center, Philadelphia, PA. In 1992, he joined the faculty at the Roswell Park Cancer Institute and State University of New York at Buffalo as an assistant professor of medicine. There, he was actively involved in the conduct of phase I trials and also established an independent laboratory focused on cellular and molecular mechanisms of platinum cytotoxicity. He joined the faculty at Dartmouth in February 1998. Currently, he directs the Norris Cotton Cancer Center phase I clinical trials program (jointly with Lionel Lewis, M.D.) and a translational laboratory.
Dr. Perez' laboratory focuses on bax and on receptor-kinase/MAP-kinase signaling, as specific targets and as determinants of sensitivity for anticancer agents. Current work on bax involves characterization (quantitation, localization, biologic effects) of a novel splice variant that kills cells despite deletion of a domain previously thought to be required for apoptosis. The other basic laboratory focus involves SPRY2, an endogenous inhibitor of receptor-kinase/MAP-kinase signaling. Work in both areas interfaces with large clinical projects to define genomic and/or proteomic biomarkers for sensitivity to anticancer therapy. Specifically, we are analyzing tumor specimens and clinical outcomes from over 300 women with advanced-stage ovarian cancer enrolled on nationwide Gynecologic Oncology Group (GOG) therapeutic trials, and from patients with high-risk locoregional melanoma treated at Dartmouth. Finally, laboratory projects interface with the translational phase I trials program, where drugs targeting specific signal transduction pathways (atorvastatin, H-ras antisense oligonucleotides, farnesyltransferase inhibitors, etc.) are being evaluated for safety and for molecular proof-of-principle in cancer patients.
Grant Information:
CA131820 “Inhibition of S14 by Conjugated Linoleic Acid in Advanced Solid Tumor Patients.” This trial test the molecular hypothesis that Conjugated Linoleic Acid inhibits lipogenesis in tumor cells at clinically-tolerable doses.
CA141083 “SPRY2 predicts survival post-chemotherapy in advanced ovarian cancer” This project seeks to determine whether SPRY2 protein expression in tumor predicts the survival of women with advanced ovarian cancer following treatment with conventional chemotherapy.