Role of FGR2 in thyroid tumor progression and their involement in the correlation between thyroid cancer and melanoma
P. Grilli, C. DErcole, S. Federici, A. Giannella, S. Ceccarelli & C. Marchese
Thyroid cancer is the most common endocrine malignancy. It is known that cancer progression involve dysregulation of growth factors (FGFs) and their receptors (FGFRs) have been identified. In thyroid tumors. In particular, FGFR1 and FGFR3 are expressed in most well differenziated tumors, FGFR4 is predominantly expressed in aggressive tumor types and cells lines, while FGFR2 is the only receptor consistently detected in normal human thyroid tissue and its expression is downmodulated in thyroid cancers and carcinoma cells lines.
The study is conduced on a series of 7963 patient undergoing t.t. in the Department of Surgical Science, Policlinico Umberto I, Sapienza University of Rome, from 1996 to 2011of these patients 1391 had a diagnosis of thyroid cancer.The aim of the study is the evaluation of a possible correlation between FGFR2 expression and progression/prognosis of thyroid cancer, analyzing FGFR2 downregulation in normal thyrocytes, in term of proliferation, differentiation, apoptosis and expression of tumoral markers.
Recent studies have identified an association between cutaneous malignant and thyroid carcinoma. Molecular studies show that TSHR is expressed by cutaneous melanocytic lesions, with higher expression in malignant and premalignant lesions, and that cultured melanoma cells, but not melanocytes, are induced to proliferate by TSH; this suggests that hypothyroidism may promote the development and progression of melanoma.
We will set up a retrospective analysis of FGFR2 expression in patients with thyroid carcinoma that have successively developed a melanoma or vice versa, in order to identify differences in FGFR2 expression in double positive patients versus patients affected by only thyroid cancer or melanoma.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector