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This Article Full Text Full Text (PDF) All Versions of this Article: ERC-08-0325v1 16/4/1273    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Bi, Y.-f. Articles by Ning, G. PubMed PubMed Citation Articles by Bi, Y.-f. Articles by Ning, G.

¹ Department of Endocrinology and Metabolism, Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases
² State Key Laboratory of Medical Genomics
³ , Shanghai Key Laboratory for Endocrine Tumors
⁴ Department of Thoracic Surgery, Ruijin Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, People's Republic of China

(Correspondence should be addressed to G Ning at Department of Endocrinology and Metabolism, Shanghai Institute of Endocrine and Metabolic Diseases, Shanghai Clinical Center for Endocrine and Metabolic Diseases, Ruijin Hospital Affiliated to Shanghai Jiao-Tong University School of Medicine, 197 Ruijin 2nd Road, Shanghai 200025, People's Republic of China; Email: guangning{at}medmail.com.cn)

^* (Y-f Bi and R-x Liu contributed equally to this work)

Although there has been increased knowledge about the molecular biology of neuroendocrine tumors (NETs), little is known about thymic carcinoids and even less about those with excessive hormone disorders, such as ectopic ACTH syndrome. This study was designed to gain insights into the molecular networks underlying the tumorigenesis of thymic carcinoids with ACTH secretion. By an approach integrating cDNA microarray and methods of computational biology, we compare gene expression profile between ACTH-producing thymic carcinoids and the normal thymus. In total, there are 63 biological categories increased and 108 decreased in thymic carcinoids. Cell proliferation was stimulated, which may explain the relatively uncontrolled cell growth of the tumor. Dysregulation of the Notch-signaling pathway was likely to be underlying the neuroendocrine features of this type of tumors. Moreover, inhibition of immunity and increased neuropeptide signaling molecules (POMC and its sorting molecule CPE) made the clinical manifestation reasonable and thus validated the array data. In conclusion, thymic carcinoids have a distinct gene expression pattern from the normal thymus, and they are characterized by deregulations of a series of biofunctions, which may be involved in the development of NETs. Hence, this study has provided not only a detailed comprehension of the molecular pathogenesis of thymic carcinoids with ectopic ACTH syndrome, but also a road map to approach thymic NETs at the system level.