Genomes and Genes
Affiliation: Memorial Sloan-Kettering Cancer Center
- Molecular pathology of thyroid cancer: diagnostic and clinical implicationsJames A Fagin
Department of Medicine and Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY 10021, USA
Best Pract Res Clin Endocrinol Metab 22:955-69. 2008..Based on preclinical evidence, mutations of genes encoding certain kinases may also predict response to specific tyrosine kinase inhibitors, although this has not yet been explored systematically in clinical trials...
- Frequent Somatic TERT Promoter Mutations in Thyroid Cancer: Higher Prevalence in Advanced Forms of the DiseaseIñigo Landa
MD, Memorial Sloan Kettering Cancer Center, 1275 York Avenue, Box 296, Zuckerman Building, ZRC 504, New York, New York 10065
J Clin Endocrinol Metab 98:E1562-6. 2013..Acquisition of a TERT promoter mutation could extend survival of BRAF- or RAS-driven clones and enable accumulation of additional genetic defects leading to disease progression. ..
- Genome-wide analysis of Pax8 binding provides new insights into thyroid functionsSergio Ruiz-Llorente
Instituto de Investigaciones Biomedicas Alberto Sols, Consejo Superior de Investigaciones Cientificas CSIC y Universidad Autonoma de Madrid UAM, c Arturo Duperier 4, Madrid 28029, Spain
BMC Genomics 13:147. 2012..of thyroid cells, we obtained transcriptional profiles of Pax8-silenced PCCl3 thyroid cells using whole genome expression arrays and integrated these signals with global cis-regulatory sequencing studies performed by ChIP-Seq analysis..
- GLP-1 receptor agonists and the thyroid: C-cell effects in mice are mediated via the GLP-1 receptor and not associated with RET activationLars Wichmann Madsen
Novo Nordisk A S, Novo Alle, DK 2880, Bagsvaerd, Denmark
Endocrinology 153:1538-47. 2012..These observations are consistent with effects of GLP-1R agonists on rodent C cells being mediated via mammalian target of rapamycin activation in a RET- and MAPK-independent manner...
- Molecular, morphologic, and outcome analysis of thyroid carcinomas according to degree of extrathyroid extensionMichael Rivera
Department of Pathology, Memorial Sloan Kettering Cancer Center, 1275 York Ave, New York, NY 10065, USA
Thyroid 20:1085-93. 2010..Our objective was to analyze ETE at the molecular and histologic levels and assess the effect of its extent on outcome...
- ONCOGENIC EVENTS IN THYROID NEOPLASIAJames Fagin; Fiscal Year: 2007..This would be consistent with the notion that Ras mutation, in thyroid cells induce a "mutator" phenotype, and are thus more likely to undergo phenotypic progression. ..
- MOLECULAR PATHOPHYSIOLOGY OF THYROID CELL GROWTHJames Fagin; Fiscal Year: 2004..Activation of PLC-gamma can cause activation of PKC-epsilon, and this may possibly be involved in apoptosis. ..
- MOLECULAR PATHOPHYSIOLOGY OF THYROID CELL GROWTHJames Fagin; Fiscal Year: 2007....
- Paracrine IGF/GFBP Interactions In VivoJames Fagin; Fiscal Year: 2007..abstract_text> ..
- ONCOGENIC EVENTS IN THYROID NEOPLASIAJames A Fagin; Fiscal Year: 2010..This will help us decide what key genetic abnormalities to focus on as we develop specific treatments for patients with the most advanced forms of the disease. ..
- MOLECULAR PATHOPHYSIOLOGY OF THYROID CELL GROWTHJames Fagin; Fiscal Year: 1999....
- PARACRINE IGF/IGFBP INTERACTIONS IN VIVOJames Fagin; Fiscal Year: 2002..He will also study the effects of crossing these mice will the IGF transgenic mice to study the impact of co-expression on phenotype. ..
- ONCOGENIC EVENTS IN THYROID NEOPLASIAJames Fagin; Fiscal Year: 2001..Finally, the role of mutations of PKC alpha in the control of thyroid-differentiated gene expression will be studied. ..
- MOLECULAR PATHOPHYSIOLOGY OF THYROID CELL GROWTHJames A Fagin; Fiscal Year: 2010....