Research paper 367 Incidence rates of acute promyelocytic leukemia among Hispanics, blacks, Asians, and non-Hispanic whites in the United States Matthew J. Matasar a,b , Ellen K. Ritchie b,c , Nathan Consedine d , Carol Magai d and Alfred I. Neugut a,b,c Despite significant improvements in the prognosis of acute promyelocytic leukemia brought about by therapeutic advances, understanding of the epidemiology of acute promyelocytic leukemia remains limited. Earlier reports have suggested that Hispanics may have an increased incidence of acute promyelocytic leukemia, but no systematic analysis of national data has yet been reported. We performed a retrospective cohort study, using data from the Surveillance, Epidemiology, and End Results (SEER) Program of the National Cancer Institute from 1992–2001 in order to compare leukemia incidence rates as a function of race and ethnicity. We identified 709 cases of acute promyelocytic leukemia and analyzed incidence rates by race and sex. Hispanics were not found to have greater lifetime incidence rates than whites, with an incidence relative rate (IRR) of 0.86 that of whites (P = 0.17). The age distribution among Hispanics was significantly different from non-Hispanic whites, with greater incidence rates for children ages 1–19 years (IRR = 1.9, P = 0.02) and adult ages 20–44 years (IRR = 1.6, P = 0.004). Blacks had lower lifetime incidence rates than non-Hispanic whites (IRR = 0.75, P = 0.04), Hispanics (IRR = 0.64, P = 0.007), and Asians (IRR = 0.67, P = 0.03). Asians did not differ from non-Hispanic whites in lifetime or age-specific incidence rates. These results indicate that while US Hispanics do not have greater lifetime incidence rates of acute promyelocytic leukemia, blacks have lower incidence rates of acute promyelocytic leukemia than Hispanics, non-Hispanic whites, and Asians. European Journal of Cancer Prevention 15:367–370  c 2006 Lippincott Williams & Wilkins. European Journal of Cancer Prevention 2006, 15:367–370 Keywords: acute, ethnic groups, leukemia, promyelocytic, Surveillance, Epidemiology, and End Results program a Department of Epidemiology, Mailman School of Public Health, b Department of Medicine, c Herbert Irving Comprehensive Cancer Center, College of Physicians and Surgeons, Columbia University, New York and d Long Island University, Brooklyn, New York, USA Correspondence to Dr. Alfred I. Neugut, Department of Epidemiology, Mailman School of Public Health, 722 West 168th Street, R725, New York, NY 10032, USA Tel: + 1 212 305 9414; fax: + 1 212 305 9413; e-mail: ain1@columbia.edu Sponsorship: M.J.M. is supported by a T-32 post-doctoral fellowship (CA09529), and A.I.N. is the recipient of a K05 award (CA89155) from the National Cancer Institute. A.I.N., N.C. and C.M. are the recipients of a U54 award (CA101388) from the National Cancer Institute. Received 10 October 2005 Accepted 14 November 2005 Introduction Acute promyelocytic leukemia (APL) is one of the most common subtypes of acute myeloid leukemia (AML). It is characterized by unique morphological characteristics of myeloblasts (M3 in the French–American–British classification) and the presence of the t(15;17) transloca- tion, resulting in the fusion of PML and RARa (Grimwade and Enver, 2004). APL also has distinctive clinical characteristics, including its association with the coagulo- pathy of disseminated intravascular coagulation and clinical responsiveness to unique agents. Indeed, APL is the first disease for which molecularly targeted therapies, in the form of all-trans-retinoic acid and arsenic trioxide, improved survival dramatically (Tallman et al., 1997, 2002; Soignet et al., 1998; Fang et al., 2002; Shen et al., 2004). Current understanding of the etiological factors for APL remains limited, however. Approximately 5% of cases are second malignancies following treatment with chemo- therapy and/or radiotherapy; no specific class of agents has emerged as singularly likely to cause APL (Pulsoni et al., 2002; Beaumont et al., 2003). Other uncommon exposures, such as the psoriasis drug bimolane, have been associated with an elevated risk of APL (Xue et al., 1992), but the vast majority of cases remain unexplained (Douer, 2003). The role of genetic contribution to risk has not been determined, but remains an area of active research. Interest in genetic predisposition has been fueled in part by studies of ethnic differences in the incidence rates of APL. Specifically, APL is believed by many to be over- represented among patients of Hispanic origin. Observa- tional studies have found a greater percentage of AML cases consisting of the APL subtype among Hispanics than among non-Hispanics in Los Angeles (Keung et al., 1994; Douer et al., 1996); these findings have been echoed by investigators from diverse settings, including Puebla, Mexico (Ruiz-Arguelles, 1997); Lima, Peru 0959-8278  c 2006 Lippincott Williams & Wilkins Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.