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

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....

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Bibliographic Details
Published in:Blood 2005-01, Vol.105 (1), p.289-291
Main Authors: Lin, Thomas S., Flinn, Ian W., Modali, Rama, Lehman, Teresa A., Webb, Jennifer, Waymer, Sharon, Moran, Mollie E., Lucas, Margaret S., Farag, Sherif S., Byrd, John C.
Format: Article
Language:English
Subjects:
Adult
Aged
Alemtuzumab
Antibodies, Monoclonal - therapeutic use
Antibodies, Monoclonal, Humanized
Antibodies, Neoplasm - therapeutic use
Antineoplastic agents
Biological and medical sciences
Female
Hematologic and hematopoietic diseases
Humans
Immunotherapy
Leukemia, Lymphocytic, Chronic, B-Cell - drug therapy
Leukemia, Lymphocytic, Chronic, B-Cell - genetics
Leukemia, Lymphocytic, Chronic, B-Cell - immunology
Leukemia, Lymphocytic, Chronic, B-Cell - pathology
Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis
Male
Medical sciences
Middle Aged
Neoplasm Staging
Pharmacology. Drug treatments
Polymorphism, Genetic - genetics
Receptors, IgG - genetics
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Summary: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. (Blood. 2005;105:289-291)
ISSN:0006-4971
1528-0020
DOI:10.1182/blood-2004-02-0651