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About the Authors:
Meenu Jain
Affiliation: Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
Lisa Zhang
Affiliation: Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
Myriem Boufraqech
Affiliation: Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
Yi Liu-Chittenden
Affiliation: Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
Kimberly Bussey
Affiliation: Translational Genomic Research Institute, Phoenix, Arizona, United States of America
Michael J. Demeure
Affiliation: Translational Genomic Research Institute, Phoenix, Arizona, United States of America
Xiaolin Wu
Affiliation: Laboratory of Molecular Technology, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland, United States of America
Ling Su
Affiliation: Laboratory of Molecular Technology, SAIC-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, Maryland, United States of America
Karel Pacak
Affiliation: Section on Medical Neuroendocrinology, Eunice Kennedy Shriver National Institute of Child Health, National Institutes of Health, Bethesda, Maryland, United States of America
Constantine A. Stratakis
Affiliation: Section on Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health, National Institutes of Health, Bethesda, Maryland, United States of America
Electron Kebebew
* E-mail: [email protected]
Affiliation: Endocrine Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America
Introduction
Our knowledge of the biologic events that inhibit or promote the metastatic spread of endocrine cancers locally and to distant sites is limited [1]. Understanding the molecular events involved in cancer progression has important implications for identifying targets for therapeutic benefit. Genomic, genetic, and epigenetic approaches have been used to identify changes in genes/pathways, transcription factors, or gene signatures by comparing normal, primary tumors, and/or metastasis. However, these analyses have not often distinguished between promoters, inhibitors, or passenger markers in cancer initiation and progression, and rarely define a specific mechanism for dysregulated gene expression.
Endocrine cancers are a diverse group of malignancies that exhibit the full spectrum of biologic behavior of malignant tumors: indolent growth to rapidly progressive cancers with poor survival. Thus, endocrine cancers represent an excellent model for studying the...