Thyroid Cancer and COVID-19: Prospects for Therapeutic Approaches and Drug Development

Abstract

Thyroid cancer is the most prevalent endocrine malignancy and the reported incidence of thyroid cancer has continued to increase in recent years. Since 2019, coronavirus disease 2019 (COVID-19) has been spreading worldwide in a global pandemic. COVID-19 aggravates primary illnesses and affects disease management; relevant changes include delayed diagnosis and treatment. The thyroid is an endocrine organ that is susceptible to autoimmune attack; thus, thyroid cancer after COVID-19 has gradually attracted attention. Whether COVID-19 affects the diagnosis and treatment of thyroid cancer has also attracted the attention of many researchers. This review examines the literature regarding the influence of COVID-19 on the pathogenesis, diagnosis, and treatment of thyroid cancer; it also focuses on drug therapies to promote research into strategies for improving therapy and management in thyroid cancer patients with COVID-19.

Keywords: COVID-19; drug target; immunotherapy; multikinase inhibitors; thyroid cancer.

Figure 1

Molecular pathogenesis and therapeutic drug targets of thyroid cancer. The molecular pathogenesis of thyroid cancer mainly involves the imbalance of two classical signaling pathways: mitogen-activated protein kinase (MAPK) (right) and phosphatidylinositol-3 kinase (PI3K)/Akt (left). Ras can transmit receptor tyrosine kinase (RTK) signals to these two pathways. Common mutations in MAPK pathway include RET-PTC and NTPK rearrangement, RAS and BRAF mutations. Common changes in PI3K pathway include RAS mutation, PTEN mutation or deletion, PIK3CA mutation or amplification and AKT1 mutation. Inhibitor drugs that block these signals are also depicted.

Figure 2

Infection process of SARS-CoV-2. SARS-CoV-2 infection involves two crucial steps: the initial recognition of the receptor angiotensin-converting enzyme 2 (ACE2) via S protein and then the effective fusion of the cell membrane via transmembrane protease serine 2 (TMPRSS2). Both ACE2 and TMPRSS22 are highly expressed in the thyroid.