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Blood, 15 November 2005, Vol. 106, No. 10, pp. 3380-3382. Prepublished online as a Blood First Edition Paper on August 2, 2005; DOI 10.1182/blood-2005-01-0335. This Article Full Text (PDF) All Versions of this Article: 2005-01-0335v1 106/10/3380    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Mone, A. Articles by Porcu, P. Search for Related Content PubMed PubMed Citation Articles by Mone, A. Articles by Porcu, P. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 27, 2005 Accepted July 19, 2005 Durable hematological complete response and suppression of HTLV-1 viral load following alemtuzumab in AZT/IFN-refractory adult T-cell leukemia Andrew Mone, Shannon Puhalla, Susan Whitman, Robert Baiocchi, Julio Cruz, Tamara Vukosavljevic, Amy Banks, Charles F Eisenbeis, John C Byrd, Michael A Caligiuri, and Pierluigi Porcu* Division of Hematology-Oncology, Department of Internal Medicine, The Comprehensive Cancer Center, Ohio State University, Columbus, Ohio, USA Division of Dermatopathology, Department of Pathology, Ohio State University, Columbus, Ohio, USA * Corresponding author; email: porcu-1{at}medctr.osu.edu. Adult T-cell leukemia (ATL) is a highly chemoresistant and usually fatal T-cell malignancy due to the human T-cell lymphotropic virus (HTLV)-1. After chemotherapy failure, antiretrovirals and interferon-alpha (IFN) produce brief responses followed by progression and death. More effective agents and new approaches to detect and treat minimal residual disease are needed. ATL cells express CD52, the target of the antibody alemtuzumab, which is active in a preclinical model of ATL and is cytotoxic for p53-deficient cells. A patient with refractory chronic ATL in transformation achieved a 1-year(+) complete hematological response following 12 weeks of outpatient subcutaneous alemtuzumab. Persistent suppression of HTLV-1 viral load, even at recovery of T-cells, post-alemtuzumab, and efficient in vitro complement-mediated cytotoxicity of primary ATL cells with mutated p53 were observed. The unprecedented response and the profound suppression of HTLV-1 viral load observed in this patient suggest that further clinical investigation of alemtuzumab in ATL is warranted. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: C. A. Pise-Masison, M. Radonovich, K. Dohoney, J. C. Morris, D. O'Mahony, M.-J. Lee, J. Trepel, T. A. Waldmann, J. E. Janik, and J. N. Brady Gene expression profiling of ATL patients: compilation of disease-related genes and evidence for TCF4 involvement in BIRC5 gene expression and cell viability Blood, April 23, 2009; 113(17): 4016 - 4026. [Abstract] [Full Text] [PDF] E Matutes Adult T-cell leukaemia/lymphoma J. Clin. Pathol., December 1, 2007; 60(12): 1373 - 1377. [Abstract] [Full Text] [PDF] A. Datta, M. Bellon, U. Sinha-Datta, A. Bazarbachi, Y. Lepelletier, D. Canioni, T. A. Waldmann, O. Hermine, and C. Nicot Persistent inhibition of telomerase reprograms adult T-cell leukemia to p53-dependent senescence Blood, August 1, 2006; 108(3): 1021 - 1029. [Abstract] [Full Text] [PDF]

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