ECE2018 Poster Presentations: Thyroid Thyroid cancer (88 abstracts)
1Kanagawa Cancer Center, Yokohama, Japan; 2Yokohama City University Medical Center, Yokohama, Japan; 3Yokohama City University School of Medicine, Yokohama, Japan.
Introduction: Angiogenesis is known to play an important role in the development, growth, and metastasis of carcinomas. The vascular endothelial growth factor (VEGF) and VEGF receptor (VEGFR) are major molecules involved in angiogenesis. The VEGF family includes seven members, respectively named VEGF-A (often simply denoted as VEGF), VEGF-B, VEGF-C, VEGF-D, VEGF-E, VEGF-F, and placental growth factor. The VEGFR is a tyrosine kinase receptor with one to three types and is activated by binding to the VEGF. Among these receptors, the VEGFR2 has an important role in angiogenesis. It is suggested that the expression of VEGF correlates with advanced tumor stage in papillary thyroid cancer (PTC). Anaplastic thyroid cancer (ATC) accounts for 2% of all thyroid cancers but is one of the most lethal neoplasms in humans, with a median survival of 46 months. Conventional ATC therapy uses a multimodal approach with radiation therapy and conventional chemotherapy. Some patients survive for a fairly long time after receiving this therapy. A monoclonal antibody against VEGF has been developed for cancer treatment, and its antitumor effect has been reported. The effectiveness of lenvatinib, which mainly inhibits the VEGFR2, has been shown for PTC. Lenvatinib also has significant antitumor effects for ATC and is used in clinical practice. However, few studies report the expression of VEGF or VEGFR in ATC. Here, we studied the expression of VEGFR2 in ATC and the therapeutic effect of lenvatinib on ATC.
Materials and methods: Primary tumors were obtained from 12 patients with ATC (five males, seven females; age range, 6389 years)[Editor1] who underwent surgery or core needle biopsy of a thyroid tumor at the Department of Breast and Endocrine Surgery, Kanagawa Cancer Center, Kanagawa, Japan. The protein expression of VEGFR2 in ATC was analyzed using immunohistochemical analysis. Furthermore, the therapeutic effect of lenvatinib was evaluated in seven patients who underwent the same tissue biopsy and lesion evaluation.
Result: All 12 patients had no expression of VEGFR2. The therapeutic effect of lenvatinib was classified as a partial response in four patients and as a stable disease in three patients.
Conclusion: There was no correlation between the expression of VEGFR2 in ATC tissues and the therapeutic effect of lenvatinib. Further studies are required to improve the overall survival of patients with ATC by investigating clinical predictive factors or new therapeutic target molecules.