한빛사 논문
Vaibhav G. Patel MD1, Xiaobo Zhong DrPH2, Bobby Liaw MD1, Douglas Tremblay MD1, Che-Kai Tsao MD1, Matthew D. Galsky MD1, William K. Oh MD1,*
1Division of Hematology and Medical Oncology, Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai
2Department of Population Health and Policy, Icahn School of Medicine at Mount Sinai
*Corresponding author
Abstract
Dear Editors
Currently, there is a paucity of effective treatments to address the remarkably high morbidity and mortality associated with SARS-CoV-2 coronavirus disease-19 (COVID-19). This letter highlights a potential therapeutic strategy based on known biology of SARS-CoV-2 cellular entry and replication.
SARS-CoV-2 relies on surface expression of ACE2 and TMPRSS2 for cellular entry and replication in the respiratory epithelium.1,2 In in vitro and mouse models, TMPRSS2 inhibition limits respiratory cell damage and reduces severity of infection.1,3 TMPRSS2 is commonly expressed in prostate cancer cells and is known to be regulated by androgens.4 Hence, androgen deprivation therapy (ADT) may theoretically reduce TMPRSS2 expression limiting SARS-CoV-2 cellular entry and preventing severe complications from COVID-19. In fact, a recent report from Alimonti and colleagues demonstrated a lower rate of infection in prostate cancer patients on ADT, compared to those not on ADT.5 Herein, we report our observational study of all patients in a single New York City health system with COVID-19 and prostate cancer to determine the impact of ADT on COVID-19 clinical outcomes. To our best knowledge, this is the largest study to report severity of COVID-19 in patients receiving ADT.
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