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, John C. Byrd

Research output: Contribution to journalArticle

64 Scopus citations

Abstract

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 FcγR 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.

Original languageEnglish (US)
Pages (from-to)289-291
Number of pages3
JournalBlood
Volume105
Issue number1
DOIs
StatePublished - Jan 1 2005

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ASJC Scopus subject areas

  • Biochemistry
  • Immunology
  • Hematology
  • Cell Biology

Cite this

Lin, T. S., Flinn, I. W., Modali, R., Lehman, T. A., Webb, J., Waymer, S., Moran, M. E., Lucas, M. S., Farag, S. S., & Byrd, J. C. (2005). FCGR3A and FCGR2A polymorphisms may not correlate with response to alemtuzumab in chronic lymphocytic leukemia. Blood, 105(1), 289-291. https://doi.org/10.1182/blood-2004-02-0651