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Updated: May 20, 2026
Murine Model of CD40-activation of B cells
Published on: March 5, 2010
CD20 gene deletion causes a CD20-negative relapse in diffuse large B-cell lymphoma
Tsuyoshi Nakamaki1, Kunihiko Fukuchi, Hidetoshi Nakashima
1Division of Hematology, Department of Medicine, Showa University School of Medicine, Tokyo, Japan. nakamaki@med.showa-u.ac.jp
Abstract:
In diffuse large B-cell lymphoma (DLBCL), a CD20-negative relapse is clinically significant because it is associated with chemo-refractory phenotypes and loss of a therapeutic target. The alteration of the CD20 gene is reported as infrequent in CD20-negative relapse in B-cell lymphoma. We established a DLBCL cell line with loss of CD20 expression (SD07) from a patient at CD20-negative relapse. She was initially diagnosed with CD20-positive DLBCL and received repeated immuno-chemotherapy that included rituximab. SD07, which has an immunoglobulin κ rearrangement identical to that of lymphoma cells at CD20-negative relapse, showed homozygous deletion of the CD20 gene with loss of the copy number of 11q12. SD07 is the first case in which it is proven that the loss of CD20 expression in relapsed DLBCL is the result of deletion of the CD20 gene. Deletion of the CD20 gene is a molecular mechanism of CD20-negative relapse in a subset of DLBCL.
Insights
CD20-negative relapse in diffuse large B-cell lymphoma (DLBCL) is linked to poor outcomes. This study identifies CD20 gene deletion as a key mechanism causing this relapse, impacting therapeutic targets.
Area of Science:
- Oncology
- Hematology
- Molecular Biology
Background:
- CD20-negative relapse in diffuse large B-cell lymphoma (DLBCL) presents significant clinical challenges, often correlating with chemo-refractory disease.
- Loss of CD20 expression limits the efficacy of rituximab-based immunotherapies.
Observation:
- A novel DLBCL cell line (SD07) was established from a patient experiencing CD20-negative relapse after extensive immunochemotherapy, including rituximab.
- The SD07 cell line exhibited identical immunoglobulin kappa rearrangement to the patient's relapsed lymphoma cells, confirming its origin.
Findings:
- SD07 cells demonstrated a homozygous deletion of the CD20 gene, associated with a loss of the 11q12 copy number.
- This is the first documented case definitively proving that CD20 gene deletion is the molecular cause of CD20-negative relapse in a subset of DLBCL.
Implications:
- CD20 gene deletion represents a key molecular mechanism contributing to CD20-negative relapse in specific DLBCL cases.
- Understanding this mechanism is crucial for developing alternative therapeutic strategies for patients with chemo-refractory, CD20-negative DLBCL.
