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Mechanisms of Action of Arsenic Trioxide¹

Lady Davis Institute for Medical Research and Sir Mortimer B. Davis-Jewish General Hospital, McGill University, Montreal H3T 1E2, Quebec, Canada [W. H. M., H. M. S.]; Ingenix, Basking Ridge, New Jersey 07920 [J. S. L.]; Cell Therapeutics, Inc., Seattle, Washington 89119 [J. S.]; and Rochelle Belfer Chemotherapy Foundation Laboratory, Mt. Sinai School of Medicine, New York, New York 10029 [S. W.]

Arsenic trioxide has shown substantial efficacy in treating both newly diagnosed and relapsedpatients with acute promyelocytic leukemia (APL). As a single agent, it induces complete remissions, causing few adverse effects and only minimal myelosuppression. These successes have prompted investigations to elucidate the mechanisms of action underlying these clinical responses. Substantial data show that arsenic trioxide produces remissions in patients with APL at least in part through a mechanism that results in the degradation of the aberrant PML-retinoic acid receptor fusion protein. Studies have also investigated concerns about the toxicity and potential carcinogenicity of long-term exposure to environmental arsenic. Arsenic apparently affects numerous intracellular signal transduction pathways and causes many alterations in cellular function. These actions of arsenic may result in the induction of apoptosis, the inhibition of growth and angiogenesis, and the promotion of differentiation. Such effects have been observed in cultured cell lines and animal models, as well as clinical studies. Because arsenic affects so many cellular and physiological pathways, a wide variety of malignancies, including both hematologic cancer and solid tumors derived from several tissue types, may be susceptible to therapy with arsenic trioxide. These multiple actions of arsenic trioxide also highlight the need for additional mechanistic studies to determine which actions mediate the diverse biological effects of this agent. This information will be critical to realizing the potential for synergy between arsenic trioxide and other chemotherapeutic agents, thus providing enhanced benefit in cancer therapy.

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