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Polymorphism of the CD30 Promoter Microsatellite Repressive Element Is Associated with Development of Primary Cutaneous Lymphoproliferative Disorders

¹ Laboratory for Cancer Medicine, The Western Australian Institute for Medical Research, ² Centre for Medical Research, and ³ School of Biomedical and Chemical Sciences, The University of Western Australia, Perth, Western Australia, Australia and ⁴ Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts

Requests for reprints: Lawrence Abraham, Laboratory for Cancer Medicine, The Western Australian Institute for Medical Research and Centre for Medical Research, The University of Western Australia, Level 6, MRF Building, 50 Rear Murray Street, Perth, Western Australia, Australia. Phone: 61-08-92240363; Fax: 61-08-92240322. E-mail: mfranchi{at}cyllene.uwa.edu.au

Lymphomatoid papulosis is a preneoplastic cutaneous lymphoproliferative disorder characterized by overexpression of CD30, a member of the tumor necrosis factor receptor superfamily. CD30 signaling is known to have an effect on the growth and survival of lymphoid cells. Therefore, we hypothesized that the development of lymphomatoid papulosis and progression to an associated neoplasm such as cutaneous and systemic anaplastic large cell lymphoma may reflect an underlying genetic defect. In this study, we determined that two allelic forms of the CD30 promoter microsatellite repressive element, designated 30M377 and 30M362, are associated with the development of lymphomatoid papulosis and CD30+ lymphomas in lymphomatoid papulosis patients, respectively. These findings suggest that allele-specific differences in the control of CD30 transcription may determine the pathogenesis of the spectrum of CD30+ cutaneous lymphoproliferative disorders.