Methylprednisolone-rituximab is an effective salvage therapy for patients with relapsed chronic lymphocytic leukemia including those with unfavorable cytogenetic features

Deborah A. Bowen, Timothy G. Call, Greg D. Jenkins, Clive Z. Zent, Susan M. Schwager, Daniel L. Van Dyke, Diane F. Jelinek, Neil E. Kay, Tait D. Shanafelt

Research output: Contribution to journalArticlepeer-review

88 Scopus citations

Abstract

Chronic lymphocytic leukemia (CLL) patients with aggressive molecular characteristics such as deletion of 17p13.1 do not respond to conventional treatments and have a shorter survival. Studies suggest that high-dose methylprednisolone (HDMP) has activity in such patients and combining HDMP with rituximab may enhance efficacy. We identified 37 patients with CLL treated with the HDMP-rituximab who had follow-up at Mayo Clinic. Nine of 27 (33%) had deletion of 17p13.1 and six of 27 (22%) had deletion of 11q22.3. After a median of one cycle of HDMP-rituximab, 29 (78%) patients had an objective response according to the National Cancer Institute CLL Working Group Criteria including five of nine patients with deletion of 17p13.1. Eight (22%) patients had a complete clinical response. Although well tolerated, 11 (29%) patients developed infectious complications before completing one month of therapy. Three-year survival was 41% (95% CI: 26-66%). HDMP-rituximab is an active regimen in patients with relapsed, refractory, and cytogenetically high-risk CLL. Further evaluation of this regimen in controlled trials appears warranted.

Original languageEnglish (US)
Pages (from-to)2412-2417
Number of pages6
JournalLeukemia and Lymphoma
Volume48
Issue number12
DOIs
StatePublished - Dec 2007

Keywords

  • 17P-
  • CLL
  • Methylprednisolone
  • Rituximab
  • Treatment

ASJC Scopus subject areas

  • Hematology
  • Oncology
  • Cancer Research

Fingerprint

Dive into the research topics of 'Methylprednisolone-rituximab is an effective salvage therapy for patients with relapsed chronic lymphocytic leukemia including those with unfavorable cytogenetic features'. Together they form a unique fingerprint.

Cite this