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Medicine - Mitsiades Lab

Houston, Texas

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Medicine - Mitsiades Lab
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Nicholas Mitsiades, M.D., Ph.D.

Nicholas MitsiadesAssistant Professor
Departments of Medicine and Molecular and Cellular Biology
Baylor College of Medicine
Caroline Wiess Law Scholar
Dan L. Duncan Scholar

Education and scientific background

Dr Mitsiades is a physician-scientist specialized in the treatment of endocrine malignancies. He completed his clinical training in Internal Medicine at the Beth Israel Deaconess Medical Center/ Harvard Medical School in Boston, MA, followed by clinical training in Endocrinology, Diabetes and Metabolism (also at Harvard Medical School in Boston, MA) and then in Medical Oncology at Memorial Sloan-Kettering Cancer Center in New York.

He also has a strong background in molecular biology and translational therapeutics, with training at the intramural program of the National Cancer Institute in Bethesda, MD (1996-1999) as a Fogarty fellow, followed by research work at Harvard Medical School (1999-2003, Massachusetts General Hospital and Dana Farber Cancer Institute, Boston, MA), elucidating the signaling pathways mediating the anticancer activity of novel targeted therapies and identifying of clinically relevant biomarkers associated with tumor cell sensitivity in order to allow for appropriate patient selection and stratification prior to enrollment in a clinical trial. His research at the Dana Farber Cancer Institute led to several seminal publications that advanced the preclinical development of proteasome inhibitors, histone deacetylase inhibitors and Hsp90 inhibitors as targeted anticancer therapies. Based on his preclinical data, he proposed rationally designed, clinically applicable drug combinations, that have since been proven to be safe and effective in subsequent clinical trials and now are standard clinical practice in Oncology, improving outcomes for people with cancer.

Appointments, Awards and Grants

  • In 2010, he joined BCM as an assistant professor in the Departments of Medicine and Molecular and Cellular Biology at Baylor College of Medicine.
  • In 2011, he was selected as BCM's third Caroline Wiess Law Scholar.
  • In 2013, he was awarded the Molecular and Cellular Biology Faculty Award for Excellence in Research.
  • He is also a member of the NCI-designated Dan L. Duncan Cancer Center at BCM and a Duncan Scholar.
  • His work has also been funded by the Conquer Cancer Foundation of the American Society of Clinical Oncology, the American Association for Cancer Research, the American Society of Hematology, the Prostate Cancer Foundation, the Multiple Myeloma Research Foundation and the Helis Medical Research Foundation.

Ongoing research

Dr Mitsiades’ research interests include the development of novel anticancer approaches by:

  • Exploring and targeting the mechanisms involved in hormonal regulation of cancer (in particular of prostate cancer by androgen, and of breast cancer by estrogen).
  • Identifying clinically applicable inhibitors of the expression and/or function of steroid receptor coactivators (which are key pleiotropic coactivators of transcription factors and other proteins necessary for cancer cell proliferation and survival signaling).
  • Investigating the mechanisms involved in the anticancer activity of the diabetes drug metformin and the lipid-lowering drugs HMG-CoA reductase inhibitors (statins).
  • Targeting the signaling pathways triggered by somatic mutations in the G protein α subunits Gαq and Gα11 (encoded by the genes GNAQ and GNA11, respectively) in uveal melanomas.
  • Exploring novel therapies for thyroid cancer.

Selected publications

  • Mitsiades N. A Road Map to Comprehensive Androgen Receptor Axis Targeting for Castration-Resistant Prostate Cancer. Cancer Res. 2013 Jul 25. [Epub ahead of print]
  • Geng C, He B, Xu L, Barbieri CE, Eedunuri VK, Chew SA, Zimmermann M, Bond R, Shou J, Li C, Blattner M, Lonard DM, Demichelis F, Coarfa C, Rubin MA, Zhou P, O'Malley BW, Mitsiades N. Prostate cancer-associated mutations in speckle-type POZ protein (SPOP) regulate steroid receptor coactivator 3 protein turnover. Proc Natl Acad Sci U S A. 2013 Apr 4. [Epub ahead of print]
  • Bedoya DJ, Mitsiades N. Clinical appraisal of abiraterone in the treatment of metastatic prostatic cancer: patient considerations, novel opportunities, and future directions. Onco Targets Ther. 2013;6:9-18. doi: 10.2147/OTT.S24941. Epub 2013 Jan 3.
  • Mitsiades N, Sung CC, Schultz N, Danila DC, He B, Eedunuri VK, Fleisher M, Sander C, Sawyers CL, Scher HI. Distinct patterns of dysregulated expression of enzymes involved in androgen synthesis and metabolism in metastatic prostate cancer tumors. Cancer Res. 2012 Dec 1;72(23):6142-52. doi: 10.1158/0008-5472.CAN-12-1335. Epub 2012 Sep 12.
  • Bedoya DJ, Mitsiades N. Abiraterone acetate, a first-in-class CYP17 inhibitor, establishes a new treatment paradigm in castration-resistant prostate cancer. Expert Rev Anticancer Ther. 2012 Jan;12(1):1-3. doi: 10.1586/era.11.196. No abstract available.
  • Mitsiades CS, Mitsiades N, McMullan CJ, Poulaki V, Shringarpure R, et al. Inhibition of the insulin-like growth factor receptor-1 tyrosine kinase activity as a therapeutic strategy for multiple myeloma, other hematologic malignancies and solid tumors. Cancer Cell 2004;5(3):221-30.
  • Mitsiades CS, Mitsiades N, McMullan CJ, Poulaki V, Shringarpure R, Hideshima T, Akiyama M, Chauhan C, Munshi N, Gu X, Bailey C, Joseph M, Libermann TA, Richon VM, Marks PA, Anderson KC. Transcriptional signature of histone deacetylase inhibition in multiple myeloma: biological and clinical implications. Proc Natl Acad Sci U S A 2004; 101(2): 540-5.
  • Mitsiades N, et al. The proteasome inhibitor PS-341 potentiates sensitivity of multiple myeloma cells to conventional chemotherapeutic agents: therapeutic applications. Blood 2003;101(6):2377-80.
  • Mitsiades N, Mitsiades CS, et al. Molecular sequelae of proteasome inhibition in human multiple myeloma cells. Proc Natl Acad Sci U S A. 2002; 99: 14374-14379.
  • Mitsiades N, Mitsiades CS, et al. “Apoptotic signaling induced by immunomodulatory thalidomide analogs (IMiDs) in human multiple myeloma cells: therapeutic implications.” Blood 2002;99(12):4525-30.
  • Mitsiades N, Mitsiades CS, Poulaki V, et al. “Biologic sequelae of NF-κB blockade in multiple myeloma: therapeutic applications” Blood 2002;99(11):4079-86.
  • Mitsiades N, Mitsiades CS, Poulaki V, Anderson KC, Treon SP. Intracellular regulation of TRAIL–induced apoptosis in multiple myeloma cells. Blood 2002; 99(6):162-71.
  • Mitsiades, N, et al. Ewing’s Sarcoma Family Tumors Are Sensitive To Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL) and express death receptor 4 and death receptor 5. Cancer Research 2001;61(6):2704-12.
  • Mitsiades, N, Yu, W, Poulaki, V, et al. Matrix Metalloproteinase-7-mediated cleavage of Fas ligand protects tumor cells from chemotherapeutic drug cytotoxicity. Cancer Research 2001; 61(2):577-581.
  • Mitsiades N, et al. Thyroid carcinoma cells are resistant to Fas-mediated apoptosis but sensitive to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL). Cancer Research 2000;60(15):4122-9.

For additional publications, please click here.

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