Abstract
CONTEXT: The impaired ability of thyroid cancer (TC) cells to uptake and concentrate iodine represents a major therapeutic challenge in malignant TC management. This has been reported probably due to reduced or loss of expression of pendrin in thyroid tumors. AIMS: In view of this, we evaluated the pendrin expression in the chemically induced (using N-bis[2-hydroxypropyl] nitrosamine [DHPN]) TC model in Wistar rats. METHODS: Uptake in the thyroid gland was evaluated by positron emission tomography with computed tomography (PET-CT) and scintigraphy imaging. Further histopathology (HP) and immunohistochemistry (IHC) were performed for confirming malignancy. RESULTS: The altered uptake in the thyroid gland was observed by PET-CT and scintigraphy imaging. Significant pathological changes in the thyroid were observed using 2-deoxy-2-(fluorine-18) fluoro-D-glucose PET-CT, technetium-99m pertechnetate imaging, and reduced iodine-131 uptake (n = 4) in DHPN-induced animals compared to control indicative of thyroid cell proliferation. In treated groups, tissue HP revealed hyperplastic follicular to papillary cell proliferation with variable mitotic activity. The malignant nature of the tissue and variable uptake of the tracer were further reconfirmed by IHC. IHC revealed reduced pendrin expression in malignant thyroid tissue. CONCLUSIONS: Hence, nuclear imaging techniques can be of aid in the early identification and evaluation of cellular changes during the early development of tumor models in laboratory animals. In conclusion, our study reveals that pendrin expression plays a vital role in thyroid uptake, and its reduction was observed in TC in a chemically induced TC model.