Research Topics
Species | MICHAEL XINGSummaryAffiliation: Johns Hopkins University Country: USA Publications
Research Grants
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Detail Information
Publications
Association between BRAF V600E mutation and mortality in patients with papillary thyroid cancerMingzhao Xing
Laboratory for Cellular and Molecular Thyroid Research, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
JAMA 309:1493-501. 2013..BRAF V600E is a prominent oncogene in papillary thyroid cancer (PTC), but its role in PTC-related patient mortality has not been established...- Molecular pathogenesis and mechanisms of thyroid cancerMingzhao Xing
Laboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
Nat Rev Cancer 13:184-99. 2013.... 
Single nucleotide polymorphism rs17849071 G/T in the PIK3CA gene is inversely associated with follicular thyroid cancer and PIK3CA amplificationJeffrey C Xing
Department of Otolaryngology Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD, USA
PLoS ONE 7:e49192. 2012..Thus, the present study uncovers an interesting phenomenon that rs17849071G/T is protective against FTC possibly through preventing PIK3CA amplifications...- Oxidative stress: a new risk factor for thyroid cancerMingzhao Xing
Laboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Endocr Relat Cancer 19:C7-11. 2012..These interesting possibilities deserve further studies... - The Akt inhibitor MK2206 synergizes, but perifosine antagonizes, the BRAF(V600E) inhibitor PLX4032 and the MEK1/2 inhibitor AZD6244 in the inhibition of thyroid cancer cellsRuixin Liu
Laboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 97:E173-82. 2012.... 
The T1799A BRAF mutation is not a germline mutation in familial nonmedullary thyroid cancerMingzhao Xing
Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
Clin Endocrinol (Oxf) 63:263-6. 2005..As the somatic T1799A BRAF mutation is highly prevalent in papillary thyroid cancer, the aim was to test whether this mutation was a susceptibility mutation for FNMTC...- Recent advances in molecular biology of thyroid cancer and their clinical implicationsMingzhao Xing
Department of Medicine and Oncology, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Otolaryngol Clin North Am 41:1135-46, ix. 2008..These exciting advances provide unprecedented opportunities for the development of molecular-based novel diagnostic, prognostic, and therapeutic strategies for thyroid cancer... - BRAF mutation predicts a poorer clinical prognosis for papillary thyroid cancerMingzhao Xing
Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 90:6373-9. 2005..Use of BRAF mutation in papillary thyroid cancer (PTC) has the potential to improve risk stratification of this cancer... - Gene methylation in thyroid tumorigenesisMingzhao Xing
Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, MD 21287, USA
Endocrinology 148:948-53. 2007..Future studies need to emphasize the mechanistic aspects of these two types of epigenetic alterations to uncover new molecular mechanisms in thyroid tumorigenesis and to provide novel therapeutic targets for thyroid cancer... - BRAF mutation in papillary thyroid cancer: pathogenic role, molecular bases, and clinical implicationsMingzhao Xing
Division of Endocrinology and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Endocr Rev 28:742-62. 2007..With these advances, it has become clearer that BRAF mutation will likely have significant impact on the clinical management of PTC... - BRAF mutation in thyroid cancerM Xing
Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, 1830 E Monument St Suite 333 Baltimore, MD 21287, USA
Endocr Relat Cancer 12:245-62. 2005..This newly discovered BRAF mutation may prove to have an important impact on thyroid cancer in the clinic... - BRAF mutation testing of thyroid fine-needle aspiration biopsy specimens for preoperative risk stratification in papillary thyroid cancerMingzhao Xing
Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
J Clin Oncol 27:2977-82. 2009..This study investigated the utility of BRAF mutation testing of thyroid fine-needle aspiration biopsy (FNAB) specimens for preoperative risk stratification in papillary thyroid cancer (PTC)... - Prognostic utility of BRAF mutation in papillary thyroid cancerMingzhao Xing
Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, MD 21287, United States
Mol Cell Endocrinol 321:86-93. 2010..Use of this unique molecular marker, in conjunction with conventional clinicopathological risk factors, to assist the prognostication of PTC is likely to improve the efficiency of contemporary management of thyroid cancer... - Genetic alterations in the phosphatidylinositol-3 kinase/Akt pathway in thyroid cancerMingzhao Xing
Laboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Thyroid 20:697-706. 2010..As the drivers of this process, many genetic alterations activating the PI3K/Akt pathway have been identified in thyroid cancer in recent years... - Detection of BRAF mutation on fine needle aspiration biopsy specimens: a new diagnostic tool for papillary thyroid cancerMingzhao Xing
Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 89:2867-72. 2004..Thus, we have demonstrated the usefulness of BRAF mutation detection on FNAB specimens that can help diagnose and identify those PTC patients who may need more aggressive surgical treatment and vigilant clinical monitoring... - BRAF T1796A transversion mutation in various thyroid neoplasmsM Xing
Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
J Clin Endocrinol Metab 89:1365-8. 2004.... - BRAF V600E maintains proliferation, transformation, and tumorigenicity of BRAF-mutant papillary thyroid cancer cellsDingxie Liu
Division of Endocrinology and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
J Clin Endocrinol Metab 92:2264-71. 2007..Although the BRAF V600E mutant can initiate the formation of papillary thyroid cancer (PTC), it is unclear whether it is required to maintain cell proliferation, transformation, and tumor growth of BRAF mutation-harboring PTC... - Potent inhibition of thyroid cancer cells by the MEK inhibitor PD0325901 and its potentiation by suppression of the PI3K and NF-kappaB pathwaysDingxie Liu
Division of Endocrinology and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine, 1830 E Monument Street, Baltimore, MD 21287, USA
Thyroid 18:853-64. 2008..The objective of this study was to use a potent new-generation MEK inhibitor PD0325901 to further investigate the therapeutic potential of specifically targeting MEK in the MAP kinase pathway for thyroid cancer... - Inhibitory effects of the mitogen-activated protein kinase kinase inhibitor CI-1040 on the proliferation and tumor growth of thyroid cancer cells with BRAF or RAS mutationsDingxie Liu
Division of Endocrinology and Metabolism Department of Medicine, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 92:4686-95. 2007..Targeting MAPK kinase (MEK) in the MAPK pathway is a potentially effective therapeutic strategy for thyroid cancer... - Association of aberrant methylation of tumor suppressor genes with tumor aggressiveness and BRAF mutation in papillary thyroid cancerShuiying Hu
Department of Medicine, Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Int J Cancer 119:2322-9. 2006..These results suggest that aberrant methylation and hence silencing of TIMP3, SLC5A8, DAPK and RARbeta2, in association with BRAF mutation, may be an important step in PTC tumorigenesis and progression... - Hypermethylation of the DNA mismatch repair gene hMLH1 and its association with lymph node metastasis and T1799A BRAF mutation in patients with papillary thyroid cancerHaixia Guan
Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Cancer 113:247-55. 2008..It remains to be investigated whether the aberrant methylation of DNA repair genes plays a pathogenic role in BRAF mutation-promoted tumorigenesis of papillary thyroid cancer (PTC)... - Early occurrence of RASSF1A hypermethylation and its mutual exclusion with BRAF mutation in thyroid tumorigenesisMingzhao Xing
Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Cancer Res 64:1664-8. 2004.... - Association of PTEN gene methylation with genetic alterations in the phosphatidylinositol 3-kinase/AKT signaling pathway in thyroid tumorsPeng Hou
Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Cancer 113:2440-7. 2008..Epigenetic silencing of the PTEN gene, a negative regulator of the PI3K/AKT pathway, also occurs in thyroid tumors, but its relationship with genetic alterations in this pathway is unclear... - Association of the T1799A BRAF mutation with tumor extrathyroidal invasion, higher peripheral platelet counts, and over-expression of platelet-derived growth factor-B in papillary thyroid cancerYangang Wang
Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Endocr Relat Cancer 15:183-90. 2008..The data suggest that the BRAF T1799A mutation is associated with aggressive pathological outcomes of PTC in which high platelet counts and increased PDGF production may play a role... - 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 rapamycinDingxie Liu
Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Cancer Res 69:7311-9. 2009..This genotype-based targeting of the PI3K/Akt pathway using Akt and mTOR inhibitors may offer an effective therapeutic strategy for thyroid cancer and warrants further studies... - Selective growth inhibition in BRAF mutant thyroid cancer by the mitogen-activated protein kinase kinase 1/2 inhibitor AZD6244Douglas W Ball
Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Johns Hopkins University School of Medicine, 1650 Orleans Street, Room 553, Baltimore, Maryland 21231 1000, USA
J Clin Endocrinol Metab 92:4712-8. 2007..MAPK kinase (MEK), immediately downstream of BRAF, is a promising target for ras-raf-MEK-ERK pathway inhibition... - High prevalence and mutual exclusivity of genetic alterations in the phosphatidylinositol-3-kinase/akt pathway in thyroid tumorsYangang Wang
Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
J Clin Endocrinol Metab 92:2387-90. 2007..Genetic alterations in the phosphatidylinositol-3-kinase (PI3K)/Akt pathway and their role in thyroid tumor pathogenesis in Chinese people remain undefined... - Suppression of BRAF/MEK/MAP kinase pathway restores expression of iodide-metabolizing genes in thyroid cells expressing the V600E BRAF mutantDingxie Liu
Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Clin Cancer Res 13:1341-9. 2007.... - BRAF mutation in papillary thyroid carcinomaYoram Cohen
Division of Head and Neck Cancer Research, Department of Otolaryngology Head and Neck Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21205 2196, USA
J Natl Cancer Inst 95:625-7. 2003..Our data suggest that activating BRAF mutations may be an important event in the development of papillary thyroid cancer... - Uncommon mutation, but common amplifications, of the PIK3CA gene in thyroid tumorsGuojun Wu
Department of Otolaryngology Head and Neck Surgery, The Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 90:4688-93. 2005..As in many other human cancers, overactivation of the phosphotidylinositol 3-kinase (PI3K)/Akt signaling pathway occurs frequently in thyroid cancer, but the mechanism is not completely clear... - Somatic mutation and gain of copy number of PIK3CA in human breast cancerGuojun Wu
Department of Otolaryngology Head and Neck Surgery, Head and Neck Cancer Research Division, Johns Hopkins University School of Medicine, Baltimore, MD, USA
Breast Cancer Res 7:R609-16. 2005..Even though PIK3CA amplification and somatic mutation have been reported previously in various kinds of human cancers, the genetic change in PIK3CA in human breast cancer has not been clearly identified... - Induction of thyroid gene expression and radioiodine uptake in thyroid cancer cells by targeting major signaling pathwaysPeng Hou
Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 95:820-8. 2010..Further studies are warranted to test this therapeutic potential in restoring radioiodine avidity of thyroid cancer cells for effective ablation treatment... - Tumor-specific changes in mtDNA content in human cancerElizabeth Mambo
Department of Otolaryngology-Head and Neck Surgery, Head and Neck Cancer Research Division, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
Int J Cancer 116:920-4. 2005..Our findings suggest that mtDNA content can be used as a molecular diagnostic tool to help identify genetic abnormalities in human tumors... - DeltaNp63alpha up-regulates the Hsp70 gene in human cancerGuojun Wu
Department of Otolaryngology-Head and Neck Surgery, Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, 720 Rutland Avenue, Baltimore, MD 21205-2196, USA
Cancer Res 65:758-66. 2005..Our study provides strong evidence for the physiologic association between DeltaNp63alpha and hsp70 in human cancer, thus further supporting the oncogenic potential of DeltaNp63alpha... - Mitochondrial DNA alterations in thyroid cancerBetty C Tong
Department of Surgery, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
J Surg Oncol 82:170-3. 2003..This mutation rate is lower than the reported rate of alteration in tumors of epithelial origin, and shows no relationship to histologic grade... - High prevalence and possible de novo formation of BRAF mutation in metastasized papillary thyroid cancer in lymph nodesVasily Vasko
Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 90:5265-9. 2005..The role of the T1799A BRAF mutation in lymph node metastasis of papillary thyroid cancer (PTC) is not clear... - Association of high iodine intake with the T1799A BRAF mutation in papillary thyroid cancerHaixia Guan
Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 94:1612-7. 2009..Epidemiological studies have indicated that high iodine intake might be a risk factor for papillary thyroid cancer (PTC), which commonly harbors the oncogenic T1799A BRAF mutation... - Detection of serum deoxyribonucleic acid methylation markers: a novel diagnostic tool for thyroid cancerShuiying Hu
Division of Endocrinology and Metabolism, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 91:98-104. 2006..CONCLUSIONS: We have demonstrated the potential usefulness of serum DNA methylation markers as a novel tool for differential diagnosis of solid thyroid nodules and thyroid cancer recurrence monitoring... - Lack of mutations in the thyroid hormone receptor (TR) alpha and beta genes but frequent hypermethylation of the TRbeta gene in differentiated thyroid tumorsBiju Joseph
Division of Endocrinology and Metabolism, Department of Meidcine, The Johns Hopkins University School of Medicine, 813 Hunterian Street, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 92:4766-70. 2007..It remains inconclusive whether mutations in thyroid hormone receptor (TR) genes naturally occur in thyroid cancer and whether these genes could be suppressors of this cancer... - Genetic alterations and their relationship in the phosphatidylinositol 3-kinase/Akt pathway in thyroid cancerPeng Hou
Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland 21287, USA
Clin Cancer Res 13:1161-70. 2007..To investigate the overall occurrence and relationship of genetic alterations in the phosphatidylinositol 3-kinase (PI3K)/Akt pathway in thyroid tumors and explore the scope of this pathway as a therapeutic target for thyroid cancer... - Highly prevalent genetic alterations in receptor tyrosine kinases and phosphatidylinositol 3-kinase/akt and mitogen-activated protein kinase pathways in anaplastic and follicular thyroid cancersZhi Liu
Division of Endocrinology and Metabolism, Department of Pathology, The Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 93:3106-16. 2008.... - Identification and functional characterization of isocitrate dehydrogenase 1 (IDH1) mutations in thyroid cancerAvaniyapuram Kannan Murugan
Laboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, USA
Biochem Biophys Res Commun 393:555-9. 2010..Thus, functionally relevant IDH1 mutations can also occur in thyroid cancer, particularly ATC, suggesting a potential tumorigenic role of the IDH1 system that could represent a new therapeutic target for thyroid cancer... - Methylation of the thyroid-stimulating hormone receptor gene in epithelial thyroid tumors: a marker of malignancy and a cause of gene silencingMingzhao Xing
Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Cancer Res 63:2316-21. 2003..We propose that methylation of TSHR may provide a novel diagnostic marker of malignancy and a basis for potential use of demethylating agents in conjunction with TSH-promoted radioiodine therapy for epithelial thyroid cancers... - Hypermethylation of the Pendred syndrome gene SLC26A4 is an early event in thyroid tumorigenesisMingzhao Xing
Division of Endocrinology and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA
Cancer Res 63:2312-5. 2003..SLC26A4 gene methylation in benign adenomas and the relatively well-differentiated WRO cell line suggest that this alteration is an early event in thyroid tumorigenesis... - The Akt-specific inhibitor MK2206 selectively inhibits thyroid cancer cells harboring mutations that can activate the PI3K/Akt pathwayRuixin Liu
Laboratory for Cellular and Molecular Thyroid Research, Division of Endocrinology and Metabolism, The Johns Hopkins University School of Medicine, 1830 East Monument Street, Suite 333, Baltimore, Maryland 21287, USA
J Clin Endocrinol Metab 96:E577-85. 2011..The phosphoinositide 3-kinase (PI3K)/Akt pathway is widely postulated to be an effective therapeutic target in thyroid cancer... - Induction of thyroid gene expression and radioiodine uptake in melanoma cells: novel therapeutic implicationsPeng Hou
Division of Endocrinology and Metabolism, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA
PLoS ONE 4:e6200. 2009....
Research Grants
- Genetic and Epigenetic Alterations in Thyroid TumorsMICHAEL XING; Fiscal Year: 2007..We expect to discover important molecular information on the mechanisms of PTC pathogenesis and novel therapeutic targets for this most common endocrine cancer. ..
- Molecular Events in the PI3K/Akt Pathway in Thyroid CancerMICHAEL MINGZHAO XING; Fiscal Year: 2010....
- Genetic & Epigenetic Events in Papillary Thyroid CancerMICHAEL MINGZHAO XING; Fiscal Year: 2010..We expect to discover important molecular information on the mechanisms of PTC pathogenesis and novel therapeutic targets for this most common endocrine cancer. ..