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Phenotypic transformation of CD52pos to CD52neg leukemic T cells as a mechanism for resistance to CAMPATH-1H

Abstract

Immunotherapy utilizing CAMPATH-1H for patients with chemotherapy-refractory chronic lymphocytic leukemia has yielded encouraging results with many reports of complete remission. Here we report the outcome of two patients with CD4-positive T cell prolymphocytic leukemia treated with CAMPATH-1H. Both patients responded rapidly to treatment and subsequently developed CD4 lymphopenia. One patient remained in complete remission after 14 weeks of treatment. Serial peripheral blood flow cytometry revealed that the CD52 antigen was present throughout treatment. The other patient who was initially CD52-positive, became CD52-negative after 6 weeks of treatment, and developed progressive symptoms of T cell prolymphocytic leukemia. Immunotherapy was stopped, chemotherapy proved futile, and the patient died. This change in phenotype from CD52-positive to -negative during CAMPATH-1H therapy points out a need to develop strategies for maintaining antigenic expression during monoclonal antibody therapy.

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Acknowledgements

This work was supported in part by a grant from the Marshfield Medical Research Foundation and funds from Millennium and ILEX Partners, Cambridge, MA, USA. We would like to thank Esoterix Oncology for its continued assistance on the interpretation of these cases, and acknowledge support provided by the Marshfield Medical Research and Education Foundation through the assistance of Graig Eldred and Alice Stargardt for manuscript preparation.

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Birhiray, R., Shaw, G., Guldan, S. et al. Phenotypic transformation of CD52pos to CD52neg leukemic T cells as a mechanism for resistance to CAMPATH-1H. Leukemia 16, 861–864 (2002). https://doi.org/10.1038/sj.leu.2402471

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