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Michael Mingzhao Xing, M.D., Ph.D.

Photo of Dr. Michael Mingzhao Xing, M.D., Ph.D.

Professor of Medicine

Male

Languages: English, Chinese

Expertise: Endocrine Diseases, Endocrinology, Hyperthyroidism, Hypothyroidism, Thyroid Cancer, Thyroid Diseases, Thyroid Nodules

Research Interests: Thyroid Cancer; Thyroid Nodules

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Locations

Johns Hopkins Outpatient Center
Appointment Phone: 410-955-9270

601 N. Caroline St.
Baltimore, MD 21287 map
Phone: 410-502-6888
Fax: 410-367-2042

The Johns Hopkins Hospital
Appointment Phone: 410-955-9270

600 N. Wolfe Street
Sheikh Zayed Tower Suite 333
Baltimore, MD 21287 map
Phone: 410-502-6888
Fax: 410-367-2042

Background

Michael Mingzhao Xing, M.D., Ph.D., is tenured Professor of Medicine, Oncology, Pathology, and Cellular & Molecular Medicine, Director of the Johns Hopkins Thyroid Tumor Center, and Chief of the Laboratory for Cellular and Molecular Thyroid Research at the Johns Hopkins University School of Medicine.

He previously received medical training at the Second Military Medical University in Shanghai, China and Ph.D. training at Case Western Reserve University in Cleveland, Ohio, USA. He received medical residency training at Greater Baltimore Medical Center and clinical endocrinology fellowship training at Johns Hopkins Hospital in Baltimore, Maryland, USA. American board-certified in Internal Medicine and Endocrinology & Metabolism, for the last nearly two decades, Dr. Xing has been working at Johns Hopkins Hospital as an endocrine subspecialty consultant and teaching attending while directing a thyroid research laboratory as a physician scientist there.

His main clinical and research interests are in thyroid diseases, particularly thyroid tumor. Supported by the American Cancer Society and continuous NIH R0-1 grants, his laboratory has been studying molecular, genetic, and epigenetic mechanisms of thyroid cancer and their clinical translation.

He has >170 publications in various prestigious journals, such as JCEM, Clinical Cancer Research, Cancer Research, Journal of Clinical Investigation, Journal of National Cancer Institute, Journal of Clinical Oncology, JAMA Oncology, Lancet, JAMA, Nature Reviews Cancer, and Endocrine Reviews.

He holds/co-holds eight USA patents on such thyroid research contributions as initial discovery and clinical characterization of the BRAF V600E and TERT promoter mutations in thyroid cancer and initial demonstration of targeting BRAF/MEK to restore thyroid gene expression and radioiodine uptake for radioiodine treatment of thyroid cancer.  His work has had a profound impact on today's molecular-based management of thyroid tumor and is consistently among world's top 1% citations in the thyroid field (received >15,000 citations, with >1,500 IF).  He received the 2006 Maryland Innovator Award, the 2013 British Endocrine Society's Endocrine-Related Cancer Research Award, the 2014 Chinese Endocrine Society's Zhu Xianyi (???) Award, the 2016 American Thyroid Association's Paul Starr Award, and the Johns Hopkins' 2017 Paul W Ladenson Thyroid Award. He has been consistently recognized among the "World's Top 10 Thyroid Cancer Scholar Experts" by Expertscape and "America's Top Doctors" by US News & World Reports and other professional recognition entities.

He has been a standing or frequent ad hoc member on grant committees of NIH and other world's institutions and served several leadership roles at the American Thyroid Association, including the Research Committee Chair, Associate Editor of the journal Thyroid, and Scientific Chair of the 2016-2017 ATA Annual Meeting Program Committee.

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Titles

  • Professor of Medicine
  • Professor of Oncology
  • Professor of Pathology

Education

Degrees

  • MD, Second Military Medical University (1984)

Residencies

  • Greater Baltimore Medical Center / Internal Medicine (2000)

Fellowships

  • University of California San Diego School of Medicine / Pharmacology (1997)
  • Johns Hopkins University School of Medicine / Endocrinology and Metabolism (2003)

Board Certifications

  • American Board of Internal Medicine / Endocrinology/Diabetes/Metabolism (2003)
  • American Board of Internal Medicine / Internal Medicine (2000)

Research & Publications

Clinical Trial Keywords

Thyroid Cancer, novel therapeutic agents, diagnostic and prognostic molecular markers

Selected Publications

Liu R, Zhang T, Zhu G, Xing M. Regulation of mutant TERT by BRAF V600E/MAP kinase pathway through FOS/GABP in human cancer. Nat Commun. 2018;9(1):579. doi: 10.1038/s41467-018-03033-1.

Shen X, Zhu G, Liu R, Viola D, Elisei R, Puxeddu E, Fugazzola L, Colombo C, Jarzab B, Czarniecka A, Lam AK, Mian C, Vianello F, Yip L, Riesco-Eizaguirre G, Santisteban P, O'Neill CJ, Sywak MS, Clifton-Bligh R, Bendlova B, Sýkorová V, Xing M. Patient age-associated mortality risk is differentiated by BRAF V600E status in papillary thyroid cancer. J Clin Oncol. 2018;36(5):438-445

Xing M, Liu R, Liu X, Murugan AK, Zhu g, Zeiger MA, Pai S, Bishop J. BRAF V600E and TERT promoter mutations cooperatively identify the most aggressive papillary thyroid cancer with highest recurrence. J Clin Oncol 2014;32:2718-2726.

Xing M, Alzahrani AS, Carson KA, Viola D, Elisei R, Bendlova B,Yip L, Mian C, Vianello F, Tuttle RM, Robenshtok E, Fagin JA, Puxeddu E, Fugazzola L, Czarniecka A, Jarzab B, O'Neill CJ, Sywak MS, Lam AK, Riesco-Eizaguirre C, Santisteban P, Nakayama H, Tufano RP, Pai SI, Zeiger MA, Westra WH, Clark DP, Clifton-Bligh R, Sidransky D, Ladenson PW, Sykorova V. Association between BRAF V600E mutation and mortality in patients with papillary thyroid cancer. JAMA 2013; 309: 1493-1501.

Xing M. Molecular pathogenesis and mechanisms of thyroid cancer. Nat Rev Cancer 2013; 13: 184-199.

Patient Ratings & Comments

The Patient Rating score is an average of all responses to physician related questions on the national CG-CAHPS Medical Practice patient experience survey through Press Ganey. Responses are measured on a scale of 1 to 5, with 5 being the best score. Comments are also gathered from our CG-CAHPS Medical Practice Survey through Press Ganey and displayed in their entirety. Patients are de-identified for confidentiality and patient privacy.

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