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

Research

Research interests

Dr. Xing is a M.D./Ph.D. physician scientist and Professor of Medicine and Oncology.  He is the Co-Director for research of the Johns Hopkins Thyroid Tumor Center and Chief of the Laboratory for Cellular and Molecular Thyroid Research.   His research interest is mainly in thyroid tumors, particularly their genetic and epigenetic alterations, such as gene mutation and methylation, and related aberrant molecular signaling.  His study involves both sporadic and familial thyroid cancers.   His team has been particularly interested in exploring the molecular derangements associated with genetic and epigenetic alterations in the RAS/RAF/MAP kinase and the PI3K/Akt pathways.  Examples include BRAF, Ras, PIK3CA, and receptor tyrosine kinase mutations and amplifications, and mutation and aberrant methylation of tumor suppressor and thyroid-specific genes.   Being also an active clinical endocrinologist, Dr. Xing makes vigorous effort in leading his team to translate laboratory findings into the clinic.   His team is particularly interested in testing the therapeutic potential of targeting novel molecular abnormalities and identifying novel diagnostic and prognostic molecular markers for thyroid cancer.   Dr. Xing’s research has been supported by grant funding from the National Institute of Health, the American Cancer Society, and other funding sources.

Recent publications 

  •Genetic alterations in the phosphoinositide 3-kinase/Akt signaling pathway confer sensitivity of thyroid cancer cells to therapeutic targeting of Akt and mammalian target of rapamycin

•Induction of thyroid gene expression and radioiodine uptake in melanoma cells: novel therapeutic implications

•BRAF mutation testing of thyroid fine-needle aspiration biopsy specimens for preoperative risk stratification in papillary thyroid cancer

•Association of PTEN gene methylation with genetic alterations in the phosphatidylinositol 3-kinase/AKT signaling pathway in thyroid tumors

•Highly prevalent genetic alterations in receptor tyrosine kinases and phosphatidylinositol 3-kinase/akt and mitogen-activated protein kinase pathways in anaplastic and follicular thyroid cancers

•BRAF V600E Maintains Proliferation, Transformation and Tumorigenicity of BRAF-Mutant Papillary Thyroid Cancer Cells

•Suppression of BRAF/MEK/MAP kinase pathway restores expression of iodide-metabolizing genes in thyroid cells expressing the V600E BRAF mutant

•Genetic alterations and their relationship in the phosphatidylinositol 3-kinase/Akt pathway in thyroid cancer

•Absence of germline mutations in genes within the MAP kinase pathway in familial non-medullary thyroid cancer

•Association of aberrant methylation of tumor suppressor genes with tumor aggressiveness and BRAF mutation in papillary thyroid cancer

•Detection of serum deoxyribonucleic acid methylation markers: a novel diagnostic tool for thyroid cancer

•BRAF mutation predicts a poorer clinical prognosis for papillary thyroid cancer

•Uncommon mutation, but common amplifications, of the PIK3CA gene in thyroid tumors

•Detection of BRAF mutation on fine needle aspiration biopsy specimens: a new diagnostic tool for papillary thyroid cancer

•Early occurrence of RASSF1A hypermethylation and its mutual exclusion with BRAF mutation in thyroid tumorigenesis

•Methylation of the thyroid-stimulating hormone receptor gene in epithelial thyroid tumors: a marker of malignancy and a cause of gene silencing

•BRAF mutation in papillary thyroid carcinoma

•Liu Z, Liu DX, Bojdani E, El-Naggar AK, Vasko V, Xing M. IQGAP1 Plays an Important Role in the Invasiveness of Thyroid Cancer. Clin Cancer Res. 2010 Oct 19. [Epub ahead of print]

•Liu D, Xing J, Trink B, Xing M. BRAF mutation-selective inhibition of thyroid cancer cells by the novel MEK inhibitor RDEA119 and genetic-potentiated synergism with the mTORinhibitor temsirolimus. Int J Cancer. 2010 Mar 5. [Epub ahead of print]

•Xing M. Prognostic utility of BRAF mutation in papillary thyroid cancer. Mol Cell Endocrinol. 2010 May 28;321(1):86-93

 

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