Genetic alterations in differentiated thyroid cancers.
Differentiated thyroid cancers are the predominant malignancies of the thyroid. Due to advances in the understanding of the activation of the cell proliferation pathway at a molecular level, multiple genetic alterations have been linked to the development of thyroid carcinogenesis. Although the genetic alterations can be categorized into 7 categories, the BRAF mutation, RET/PTC, Pax8/PPARGamma, and dysfunctional Fas pathway have been most commonly described. Each of the gene alterations can ultimately result in cancer development, invasion and/or metastasis. This article provides a detailed review of the altered cell proliferation pathway activations found in thyroid carcinogenesis. The molecular targets that may be disrupted by therapeutic agents during the abnormal proliferation are also summarized.
Salehian
Behrouz
B
Department of Diabetes, Endocrinology and Metabolism, City of Hope National Medical Center, Duarte, CA 91010-3000, USA. bsalehian@coh.org
Liu
Zhong
Z
D006801:Humans; D009154:Mutation; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D047495:PPAR gamma / Q000235:genetics; D048493:Proto-Oncogene Proteins B-raf / Q000235:genetics; D051096:Proto-Oncogene Proteins c-ret / Q000235:genetics; D011988:Receptors, Thyroid Hormone / Q000235:genetics; D015398:Signal Transduction; D013964:Thyroid Neoplasms / Q000235:genetics* / Q000473:pathology; D019014:fas Receptor / Q000502:physiology
D047495:PPAR gamma; D011988:Receptors, Thyroid Hormone; D019014:fas Receptor; D051096:Proto-Oncogene Proteins c-ret; C099282:RET protein, human; C482119:BRAF protein, human; D048493:Proto-Oncogene Proteins B-raf