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International Journal of Endocrinology
Volume 2015, Article ID 765406, 6 pages
http://dx.doi.org/10.1155/2015/765406
Research Article

Are Thyroid Hormone and Tumor Cell Proliferation in Human Breast Cancers Positive for HER2 Associated?

1Department of Pharmacology, University of Athens, 75 Mikras Asias Avenue, Goudi, 11527 Athens, Greece
2Second Department of Internal Medicine, Hippokration Hospital, School of Medicine, University of Athens, 11527 Athens, Greece
3First Department of Medical Oncology, “Saint Savvas” Anticancer Hospital, 11522 Athens, Greece

Received 27 November 2014; Accepted 11 January 2015

Academic Editor: Alexander Schreiber

Copyright © 2015 Iordanis Mourouzis et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective. This study investigated whether thyroid hormone (TH) levels are correlated to cell proliferation (Ki67), in euthyroid breast cancer patients. Design and Methods. 86 newly diagnosed breast cancer patients with estrogen receptor (ER) positive tumors, who referred for surgery, were included in the study. Results. FT3, FT4, and TSH were within normal range. No correlation was seen between Ki67 and FT3 (, ), FT4 (, ), or TSH (, ) in all patients studied. However, subgroup analysis showed that, in HER2(+) patients, a negative correlation existed between FT3 levels and Ki67 ( and ) but not between Ki67 and FT4 ( and ) or TSH ( and ). In HER2(−) patients, there was no significant correlation between Ki67 and FT3 (, ), FT4 (, ), or TSH (, ). Phospho-p44/total p44 ERK levels were found to be increased by 2-fold in HER2(+) versus HER2(−) tumors. No difference was detected in phospho-p42/total p42 ERK levels. Conclusions. TH profile is not altered in patients with newly diagnosed breast cancer. However, FT3 levels, even within normal range, are negatively correlated with cell proliferation in HER2(+) breast cancer tumors. This response may be due to the interaction between ERK and TH signaling.