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 Blood, 1 January 2005, Vol. 105, No. 1, pp. 289-291.
Prepublished online as a Blood First Edition Paper on June 24, 2004; DOI 10.1182/blood-2004-02-0651.

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NEOPLASIA

FCGR3A and FCGR2A polymorphisms may not correlate with response to alemtuzumab in chronic lymphocytic leukemia

Thomas S. Lin, Ian W. Flinn, Rama Modali, Teresa A. Lehman, Jennifer Webb, Sharon Waymer, Mollie E. Moran, Margaret S. Lucas, Sherif S. Farag, and John C. Byrd

From the Department of Medicine, Division of Hematology-Oncology, and the Department of Pharmacy, Division of Medicinal Chemistry, The Ohio State University, Columbus; the Department of Oncology, Division of Hematologic Malignancies, Johns Hopkins University, Baltimore, MD; and BioServe Biotechnologies, Laurel, MD.

The in vivo mechanism of action of alemtuzumab (anti-CD52; Campath-1H) remains unclear. With rituximab, FCGR3A and FCGR2A high-affinity polymorphisms have been associated with clinical response in lymphoma but not in CLL, suggesting potential divergent mechanisms of action between these 2 diseases. Herein, we examined FCGR3A (V/V, n = 4; V/F, n = 10; F/F, n = 19) and FCGR2A (A/A, n = 5; H/A, n = 22; H/H, n = 6) polymorphisms in 36 patients with relapsed CLL who were treated with thrice-weekly alemtuzumab for 12 weeks to assess the potential influence these high-affinity Fc{gamma}R receptor polymorphisms had on response to alemtuzumab. Response to alemtuzumab was similar regardless of FCGR3A polymorphism (V/V, 25%; V/F, 40%; F/F, 32%) or FCGR2A polymorphism (A/A, 40%; H/A, 32%; H/H, 33%). These findings indicate that FCGR3A and FCGR2A polymorphisms may not predict response to alemtuzumab in CLL. Future studies examining larger cohorts of alemtuzumab-treated patients with CLL will be required to definitively determine the predictive value of specific FCGR polymorphisms to treatment response. (Blood. 2005;105:289-291)


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