Design of new drugs for medullary thyroid carcinoma

Abstract

Medullary thyroid carcinoma (MTC) is one of the common malignant endocrine tumors, which seriously affects human health. Although surgical resection offers a potentially curative therapeutic option to some MTC patients, most patients do not benefit from it due to the difficulty to access the tumors and tumor metastasis. The survival rate of MTC patients has improved with the recent advances in the research, which has improved our understanding of the molecular mechanism underlying MTC and enabled the development and approval of novel targeted drugs. In this article, we reviewed the molecular mechanisms related to MTC progression and the principle for the design of molecular targeted drugs, and proposed some future directions for prospective studies exploring targeted drugs for MTC.

Targeted Therapy in Thyroid Cancer

“…By identifying and targeting these specific abnormalities, we can effectively inhibit tumor growth and improve patient outcomes. 8 Follicular cells transform into different types of TC after undergoing certain mutations as depicted in Figure 2C. In papillary thyroid carcinoma, 30-70% have BRAF V600E mutation, and 7% have translocation of RET/PTC.…”

“…The mechanisms underlying combined therapies that include immunemediated checkpoint barriers against Pd1 or Pdl1 prevent PDL1 and PDL2 from reducing each other's inhibiting properties in the tumor microenvironment. 8 As a result, blocking the PD1 axis increases the strength of T cells' anticancer response and the expansion of natural killers (NK).…”

“…It has also been demonstrated that VEGF blockade reverses immune deficiency in the cancerous milieu by encouraging the maturity of dendritic and limiting the interaction of suppressor T cells, macrophages, and suppressor cells of myeloid origin. 8 Radiation therapy, BRAF and MEK inhibition, and certain RET inhibitors increase the triggering of major histocompatibility complex type I (MHCI) and/or the expression of antigens. The immune-suppressive cytokines and VEGF production can be reduced by targeting the BRAF-MAPK cascade.…”