{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T04:59:54Z","timestamp":1791262794348,"version":"4.1.0"},"reference-count":24,"publisher":"American Society of Hematology","issue":"4","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2004,2,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>In follicular lymphoma (FL), genomic polymorphisms corresponding to the expression of valine (V) or phenylalanine (F) at amino acid 158 of Fc\u03b3RIIIa alter the binding affinity of immunoglobulin G1 (IgG1) to the receptor and have been associated with varied responses to rituximab. We examined Fc\u03b3RIIIa polymorphisms of 30 CLL patients with the phenotypes V\/V (n = 6), V\/F (n = 12), and F\/F (n = 12) treated with thrice-weekly rituximab (375 mg\/m2) for 4 weeks to correlate polymorphism type with infusion toxicity and response. Infusion toxicity (grade 3 or greater or hypoxia\/hypotension requiring transient cessation of therapy) was observed equally among the groups (V\/V, 50%; V\/F, 33%; F\/F, 41.6%; P = .78). The response to rituximab was also similar among the different polymorphism phenotypes (V\/V, 33%; V\/F, 41.6%; F\/F, 50%). These data suggest that Fc\u03b3RIIIa polymorphisms are not predictive of response in CLL and that, unlike the case with FL, mechanisms of tumor clearance other than antibody-dependent cellular cytotoxicity may be more important.<\/jats:p>","DOI":"10.1182\/blood-2003-07-2548","type":"journal-article","created":{"date-parts":[[2003,10,20]],"date-time":"2003-10-20T20:22:21Z","timestamp":1066681341000},"page":"1472-1474","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":166,"title":["Fc\u03b3RIIIa and Fc\u03b3RIIa polymorphisms do not predict response to rituximab in B-cell chronic lymphocytic leukemia"],"prefix":"10.1182","volume":"103","author":[{"given":"Sherif S.","family":"Farag","sequence":"first","affiliation":[{"name":"From the Division of Hematology-Oncology and the Department of Biostatistics, Ohio State University, Columbus; the Division of Hematologic Malignancies, Johns Hopkins University, Baltimore, MD; and BioServe Biotechnologies, Laurel, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ian W.","family":"Flinn","sequence":"additional","affiliation":[{"name":"From the Division of Hematology-Oncology and the Department of Biostatistics, Ohio State University, Columbus; the Division of Hematologic Malignancies, Johns Hopkins University, Baltimore, MD; and BioServe Biotechnologies, Laurel, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rama","family":"Modali","sequence":"additional","affiliation":[{"name":"From the Division of Hematology-Oncology and the Department of Biostatistics, Ohio State University, Columbus; the Division of Hematologic Malignancies, Johns Hopkins University, Baltimore, MD; and BioServe Biotechnologies, Laurel, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teresa A.","family":"Lehman","sequence":"additional","affiliation":[{"name":"From the Division of Hematology-Oncology and the Department of Biostatistics, Ohio State University, Columbus; the Division of Hematologic Malignancies, Johns Hopkins University, Baltimore, MD; and BioServe Biotechnologies, Laurel, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donn","family":"Young","sequence":"additional","affiliation":[{"name":"From the Division of Hematology-Oncology and the Department of Biostatistics, Ohio State University, Columbus; the Division of Hematologic Malignancies, Johns Hopkins University, Baltimore, MD; and BioServe Biotechnologies, Laurel, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John C.","family":"Byrd","sequence":"additional","affiliation":[{"name":"From the Division of Hematology-Oncology and the Department of Biostatistics, Ohio State University, Columbus; the Division of Hematologic Malignancies, Johns Hopkins University, Baltimore, MD; and BioServe Biotechnologies, Laurel, MD."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"234","reference":[{"key":"2020021221412801600_REF1","doi-asserted-by":"crossref","unstructured":"Maloney DG, Grillo-Lopez AJ, Bodkin DJ, et al. 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The mechanism of tumor cell clearance by rituximab in vivo in patients with B-cell chronic lymphocytic leukemia: evidence of caspase activation and apoptosis induction. Blood. 2002;99: 1038-1043.","DOI":"10.1182\/blood.V99.3.1038"},{"key":"2020021221412801600_REF20","doi-asserted-by":"crossref","unstructured":"Cheson BD, Bennett JM, Grever M, et al. National Cancer Institute-sponsored Working Group guidelines for chronic lymphocytic leukemia: revised guidelines for diagnosis and treatment. Blood. 1996;87: 4990-4997.","DOI":"10.1182\/blood.V87.12.4990.bloodjournal87124990"},{"key":"2020021221412801600_REF21","doi-asserted-by":"crossref","unstructured":"Harris NL, Jaffe ES, Diebold J, et al. World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues: report of the Clinical Advisory Committee meeting-Airlie House, Virginia, November 1997. 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