La Creis R. Kidd, Ph.D., M.P.H.

Associate Professor; Our Highest Potential Endowed Chair in Cancer Research

Department of Pharmacology and Toxicology

CTRB 306 502–852–3465


Ph.D., Toxicology, Massachusetts Institute of Technology (1997)

M.P.H., Epidemiology and Biostatistics, Johns Hopkins University (2001)

Research Areas and Projects

Dr. Kidd’s research focuses on the utilization of state of the art bioinformatics tools to identify and validate genetic susceptibilities related to cancer risk and poor disease prognosis (i.e., high tumor grade/stage, disease/biochemical recurrence).  Although Dr. Kidd is intrigued by major cancer malignancies, a majority of her work has centered on prostate cancer.  Her earlier work focused on complex interactions among xenobiotic metabolism, DNA repair, oxidative stress-related genes, and angiogenesis in relation to prostate and breast cancer outcomes.  She was a lead author on the first study on the role of genomic anomalies in the chemokine ligand 5 (CCL5) and chemokine receptor 5 (CCR5) associated genetic alterations in prostate cancer risk among men of African and Caribbean Descent (Hered Cancer Clin Pract. 2012 Nov 20; 10(1): 16).  A majority of her work focuses on understanding the role genetic plays in high cancer incidence and mortality rates among underserved populations.  She has 3 patents for important prostate cancer predictors from her population-based studies (61/240089, 61/313,595, 61/655,243). Dr. Kidd was a significant contributor of a multi-center genome wide study for genetic susceptibility genes for prostate cancer among men of African and European descent.

Recently, Dr. Kidd’s lab demonstrated the up-regulation of one particular miRNA, miR-186-5p in metastatic prostate cancer cell lines and serum from prostate cancer patients. Her lab also demonstrated a decrease in cell proliferation, colony formation and cell invasion in miR-186 depleted metastatic prostate cancer cell lines.  Based on pre-clinical studies, the decrease in cell invasion may be related to an up-regulation of AKAP12 following the repression of miR-186 in metastatic prostate cancer cell lines.  Presumably, AKAP12, a tumor suppressor gene, inhibits pAkt, which in turn suppresses beta-catenin, a gene essential for cell invasion, epithelial mesenchymal transition and chemo-sensitivity.  It is her hope that her research findings will lead to the discovery of therapeutic targets for the effective treatment of aggressive and lethal forms of cancer.  Such efforts will help to reduce the burden of this disease among cancer patients and their families.