Targeting the aryl hydrocarbon receptor/polyamine biosynthesis axis of evil for cancer therapy
Robert A. Casero Jr.
Department of Oncology, Johns Hopkins University School of Medicine, and the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, Baltimore, Maryland, USA.
Address correspondence to: Robert A. Casero Jr., Department of Oncology, Johns Hopkins University School of Medicine and the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, 1650 Orleans Street, Room 551, Baltimore, Maryland 21231, USA. Phone: 410.955.8580; Email: rcasero@jhmi.edu.
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First published September 10, 2018 - More info
J Clin Invest. 2018;128(10):4254–4256. https://doi.org/10.1172/JCI123266.
Copyright © 2018, American Society for Clinical Investigation
The polyamine metabolic pathway has been considered a rational target for antineoplastic therapy since it was discovered that polyamines are absolute requirements for tumor initiation, growth, and, in some instances, survival. Although several promising preclinical studies have demonstrated the critical nature of polyamines for tumor growth, the clinical success of agents targeting polyamine metabolism have been lacking. In the accompanying article, Bianchi-Smiraglia et al. identify both a new target and new drug that inhibits polyamine biosynthesis, reduces intracellular polyamines, and inhibits the growth of several models of human multiple myeloma. These results are both intriguing and provide promise for moving such a strategy to the clinic.
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