Benjamin Kirk CanalesBenjamin Kirk Canales, MD, MPH

Assistant Professor, Department of Urology
Investigator, UF Prostate Disease Center


Medical School: Louisiana State University School of Medicine, New Orleans, LA
Residency: University of Minnesota Medical School, Minneapolis, MN
Fellowship: Laparoscopy and Endourology, University of Minnesota, Minneapolis, MN

Dr. Canales performs basic science research in kidney stones. He and his colleagues are testing enzymes with the potential to dissolve kidney stones within the urinary tract. Additionally, they are developing a variety of animal models with kidney stones. Humans who undergo gastric bypass are at increased stone risk, and Dr. Canales is developing an obese animal model to determine why stones form after this procedure. In conjunction with Professor Saeed Khan, Ph.D., they are studying a genetic knock-out mouse that deposits calcium phosphate mineral within their kidneys. These “plaques” look very similar to mineral deposits seen in human kidneys where calcium oxalate stones have been noted to attach and grow. The goal of these projects is to learn about the cellular mechanisms involved in stone formation in the hopes of prevention in human stone formers.

KhanSaeed R. Khan, PhD

Professor, Department of Pathology
Affiliated Professor, Department of Urology
Director, Center for the Study of Lithiasis and Pathological Calcification
Investigator, UF Prostate Disease Center


BS: Agra University, Agra, India
MS: Peshawar University, Peshawar, Pakistan
PhD: University of Florida, Gainesville, Florida

Dr. Khan is involved in examining all aspects of the Kidney Stone Disease using in vitro tissue culture and in vivo laboratory rat models. During development of the disease urinary oxalate is increased and renal epithelial cells come in contact with abnormally high levels of oxalate and calcium oxalate crystals, resulting in localized injury and inflammation. Expression of immediate early genes is induced. Production of urinary macromolecules such as osteopontin and bikunin is increased. Cells are injured. Some go through necrosis and others become apoptotic. Crystal binding to renal epithelial cells is increased. There is also evidence of oxidative stress and lipid peroxidation of cell membranes. Dead cells are sloughed off their basement membranes. Cell membrane fragments are released into the urine where they can promote further crystallization. Aggregation and retention of crystals in the renal tubules initiate the stone formation. There is upregulation and increased production of Monocyte-chemoattractant protein-1, which attracts inflammatory cells to the renal interstitium. Vitamin E and citrate appear to reduce crystal-induced oxidative stress and crystal deposition in the kidneys.

Sergei Kusmartsev, PhDSergei Kusmartsev, PhD

Assistant Professor, Department of Urology
Investigator, UF Prostate Disease Center


PhD: Immunology, Russian Academy of Medical Sciences, Russia
BS: Biophysics, Tomsk State University, Russia

Dr. Kusmartsev studies the mechanisms of tumor-induced immune suppression in urological cancers. Obtained information will allow the definition of specific molecular signatures and mechanisms of tumor-induced immune suppression in genitourinary (GU) cancers. The major goal is to identify the cancer-specific mechanism(s) of immune suppression, which would be important for the development of efficient therapeutic strategies aimed at immune correction in cancer. In addition, he studies the tumor-specific mechanisms of local immune regulation in tumor microenvironment in human kidney, bladder and prostate cancers. Research methods include flow cytometry, gene and protein expression, gene therapy, metabolomics/lipidomics and others.

Dietmar SiemannDietmar W. Siemann, PhD

Professor and Associate Chair for Research, Department of Radiation Oncology
Leader, Experimental Therapeutics Program, University of Florida Shands Cancer Center
Investigator, UF Prostate Disease Center


PhD: University of Toronto, Canada
BS: University of Manitoba, Canada

The tumor microenvironment has long been identified as a major factor influencing treatment resistance of cancer to conventional anticancer therapies. In addition, it is now well recognized that the tumor microenvironment plays a critical role in neoplastic cell initiation, malignant progression, and metastatic spread of tumor cells. However, the very characteristics of the tumor microenvironment that lead to therapy resistance also can provide unique treatment opportunities. A major focus of this laboratory is the development and assessment of novel anticancer treatment strategies. This research emphasizes approaches targeting two critical aspects of cancer growth: the initiation of a tumor blood vessel network, and the secondary spread of cancer cells. Current laboratory projects focus on characterizing the impact of tumor microenvironment on cancer cell function and behavior; exploring targeting strategies directed against critical cancer cell signaling pathways’ developing treatment approaches that impair the tumor blood vessel network; combining biologic targeting strategies with conventional anticancer treatments; identifying and characterizing stem cells in solid tumors; and evaluating therapeutic interventions designed to inhibit the spread of cancer cells. These laboratory investigations utilize a variety of human and rodent preclinical cancer models, with particular emphasis on models of kidney, prostate, colorectal, and breast cancer. The research emphasizes translational medicine in oncology with the ultimate goal of developing and advancing new treatment strategies for the clinical management of cancer.