M Duvic, J C Cather
Journal: Dermatologic clinics 2000;18(1):147-56
PMID: 10626120
Improved therapy for CTCL will depend on a better understanding of the pathogenesis of this disease at a molecular level. It is clear that the T cells in MF and CTCL do not undergo normal programmed cell death and have prolonged lifespans. Skin flora or other antigens may stimulate the initial proliferation, offering another approach to change the course of the disease. There has been tremendous interest in biological response modifiers, and the first targeted fusion toxin to activated T cells has been approved for CTCL. New retinoids with increased selectivity and decreased side effects are being tested for this disease. In summary, the treatment of CTCL should continue to improve and should be focused on strategies that preserve the immune function in these patients.
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