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Hindi Review Article
RAC1b: A New Player in the Scenario of Thyroid Tumorigenesis?
Ana Luisa Silva1*, Márcia Faria1, Liliana Capinha1 and Maria João Bugalho1,2,3
1Research Unit of Molecular Pathobiology, Portugal
2Endocrinology service, Portuguese Oncology Institute of Lisbon Francisco Gentil E.P.E , Lisbon, Portugal
3University Clinic of Endocrinology, NOVA Medical School / Faculty of Medical Sciences, New University of Lisbon, Portugal
- *Corresponding Author:
- Ana Luísa Silva
Molecular Pathobiology Research Unit
Oncology Portuguese Institute of Lisbon Francisco Gentil E.P.E
Rua Professor Lima Basto
1099-023 Lisbon, Portugal
Tel: 35121 7229818
Fax: 351217229895
E-mail: silva.r.analuisa@gmail.com
Received: Nov 27, 2015; Accepted: Mar 10, 2016; Published: Mar 15, 2016
Citation: Silva AL, Faria M, Capinha L, Bugalho MJ (2016) RAC1b: A New Player in the Scenario of Thyroid Tumorigenesis. Adv Mol Diag 1:103.
Copyright: © 2016 Silva AL, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction H2O in any medium, provided the original author and source are credited.
Abstract
Tumor-associated RAC1b overexpression has been recently highlighted as one promising target for therapeutic intervention in pancreatic, breast, colon and lung cancer. Recent data documenting RAC1b overexpression in a subset of papillary thyroid carcinomas, carrying the activating mutation BRAFV600E and associated with an unfavorable outcome, support the inclusion of thyroid cancer to the previous list thus opening new therapeutic avenues to thyroid cancer patients.
Herein, we will focus on the potential of RAC1b, a hyperactive variant of the small GTPase RAC1, as a molecular player in the development of thyroid malignancies.
