< Brochure Homepage | Faculty Index | Pathology Homepage

Email ademarz@jhmi.edu
Phone (410) 614-5686

Related Websites
DeMarzo Laboratory

Tissue Microarray Core

Brady Urological Institute

Angelo M. DeMarzo, M.D., Ph.D.

Primary Appointment in Pathology
Secondary Appointments in Oncology and Urology
Member; Graduate Program in Pathobiology

We study the molecular pathogenesis of prostate cancer development and progression including:

i) studies of etiological factors including the role of inflammation; and
ii) the molecular alterations responsible for driving the development of neoplastic precursors (prostatic intraepithelial neoplasia – PIN) as well as disease progression.

We study how MYC oncogene overexpression leads to PIN and prostate cancer and how MYC cooperates with PTEN loss in disease progression. We employ a number of molecular pathology techniques to human tissues as well mouse models, and, molecular techniques to cell culture systems.

We collaborate extensively with a number of other investigators as well as research team consisting of basic scientists/molecular biologists, epidemiologists, bioinformaticists, medical oncologists and urologists.


Nelson, W.G., De Marzo, A.M., and Isaacs, W.B. Mechanisms of disease. The molecular pathogenesis of prostate cancer: a new role for inflammation? New Eng. J. Med., 349:366-81, 2003.

De Marzo AM, Platz EA, Sutcliffe S, Xu J, Grönberg H, Drake CG, Nakai Y, Isaacs WB, Nelson WG. Inflammation in prostate carcinogenesis. Nat Rev Cancer. 2007;7:256-69.

Koh CM, Gurel B, Sutcliffe S, Aryee MJ, Schultz D, Iwata T, Uemura M, Zeller KI, Anele U, Zheng Q, Hicks JL, Nelson WG, Dang CV, Yegnasubramanian S, De Marzo AM. Alterations in nucleolar structure and gene expression programs in prostatic neoplasia are driven by the MYC oncogene. Am J Pathol. 2011 Apr;178(4):1824-34.

Xu J, Hicks JL, Park BH, Humphreys E, Partin AW, Han M, Netto GJ, Isaacs WB, De Marzo AM. PTEN protein loss by immunostaining: analytic validation and prognostic indicator for a high risk surgical cohort of prostate cancer patients. Clin Cancer Res. 2011; 17:6563-73.

Sfanos KS, Canene-Adams K, Hempel H, Yu SH, Simons BW, Schaeffer AJ, Schaeffer EM, Nelson WG, De Marzo AM. Bacterial Prostatitis Enhances 2-Amino-1-Methyl-6-Phenylimidazo[4,5-b]Pyridine (PhIP)-Induced Cancer at Multiple Sites. Cancer Prev Res. 2015; 8:683-92.

Haffner MC, Weier C, Xu M, Vaghasia A, Gürel B, Gümüşkaya B, Esopi DM, Fedor H, Tan HL, Kulac I, Hicks J, Isaacs WB, Lotan TL, Nelson WG, Yegnasubramanian S, De Marzo AM. Molecular evidence that invasive adenocarcinoma can mimic prostatic intraepithelial neoplasia (PIN) and intraductal carcinoma through retrograde glandular colonization. J Pathol. 2015 Aug 31. doi: 10.1002/path.4628.

Hubbard GK, Mutton LN, Khalilia M, McMullin RP, Hicks JL, Bianchi-Frias D, Horn LA, Kulac I, Moubarek MS, Nelson PS, Yegnasubramanian S, De Marzo AM, and Bieberich CJ. Combined MYC activation and Pten loss are sufficient to create genomic instability and lethal metastatic prostate cancer. Can Res, 2015, In Press


Copyright © 2017 Johns Hopkins University. All Rights Reserved