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Imiquimod in mycosis fungoides
M Covadonga Martínez-González1, M Magdalena Verea-Hernando, M Teresa Yebra-Pimentel
1Dept of Dermatology, Juan Canalejo Hospital, C/ Sir John Moore S/N. 15001, La Coruña (Spain). covadie@yahoo.es
Insights
Topical imiquimod cream effectively treated early-stage mycosis fungoides (MF) in patients resistant to other therapies. Combination therapy with systemic interferon-alpha-2a showed a rapid, complete response in MF.
Area of Science:
- Dermatology
- Immunology
- Oncology
Background:
- Mycosis fungoides (MF) is a type of cutaneous T-cell lymphoma (CTCL) with limited treatment options for resistant cases.
- Imiquimod, an immunomodulator, stimulates cytokine production, including interferon-alpha (INF-alpha).
Observation:
- Topical imiquimod 5% cream was applied to four patients with treatment-resistant early-stage MF (IA and IIB).
- One patient received imiquimod combined with systemic INFalpha-2a.
Findings:
- Complete clinical clearance of MF lesions was observed in all four patients.
- Histopathological clearance was complete in three patients and partial in one.
- The patient receiving combination therapy showed a rapid and complete response, unlike previous treatment with systemic INFalpha-2a alone.
Implications:
- Topical imiquimod demonstrates potential as an effective monotherapy for early-stage MF.
- Combination therapy with systemic immunomodulators may offer synergistic benefits for refractory MF.
- Further research into imiquimod's role in CTCL treatment is warranted.
Abstract:
Imiquimod is a topically active imidazoquinoline immunomodulator agent. It works as an indirect antiviral and antitumoral and stimulates the production of INF-alpha and various other cytokines. We assayed topical imiquimod in treating early stages of mycosis fungoides. We applied imiquimod 5% cream in four patients with multi-treatment resistant plaques of MF (stages IA and IIB). We applied it on one patient in association with systemic INFalpha-2a. We observed a complete clinical clearance of the lesions in all four patients. In three cases we achieved a complete histopathological clearance and in one case a partial histopathological clearance. The patient treated with imiquimod and systemic INFalpha-2a showed the most spectacular improvement with a rapid total response. We ascribe this improvement to a synergic effect of imiquimod and systemic INFalpha-2a treatment. Before the introduction of imiquimod, this patient had been treated for 2 years with systemic INFalpha-2a alone, without any evidence of clinical response. Imiquimod could be an effective therapy for early-stage disease of CTCL, used alone or in combination with systemic immunomodulatory therapy.
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