Psoralen Plus Long-Wave UV-A (PUVA) and Bexarotene Therapy

McGinnis, Karen S.; Shapiro, Michael B.; Vittorio, Carmela C.; Rook, Alain H.; Junkins‐Hopkins, Jacqueline M.

doi:10.1001/archderm.139.6.771

Cited by 45 publications

(7 citation statements)

References 8 publications

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“…Response duration was over 5 months and reached even 3 years in one patient. What can be interesting, these observations confirm the efficacy of PUVA in MF/SS also in systemic disease [ 54 – 56 ]. Unfortunately, there have been also several reports, mainly in SS, of rapid worsening of disease after implementation of bexarotene.…”

Section: Rexinoid In Cutaneous T-cell Lymphomassupporting

confidence: 71%

Oral retinoids and rexinoids in cutaneous T-cell lymphomas

Sokołowska‐Wojdyło¹,

Ługowska-Umer²,

Maciejewska-Radomska³

2013

pdia

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Retinoids are biologically active derivatives of vitamin A modulating cell proliferation, differentiation, apoptosis and altering the immune response. They have been used for years in therapy of cutaneous T-cell lymphomas (CTCL) but the exact mechanism of retinoids’ action is unclear. It is based on the presence of specific receptors’ families, mediating the biological effects of retinoids on the tumor cells: retinoic acid receptor (RAR) and retinoic X receptor (RXR). Orally administrated bexarotene, the first synthetic selective RXR retinoid, was revealed to be active against the cutaneous manifestation of CTCL. The toxicity profile caused by bexarotene seems to be more limited to laboratory values and better tolerated than classical retinoids, but generally associated with more severe grades of toxicity. Both selective retinoic acid receptor- and retinoic X receptor-mediated retinoids have modest objective response rates and, therefore, most likely will have limited impact as monotherapeutic agents. However, the immunomodulatory effects of RAR and RXR retinoids provide a rational basis for using retinoids in combination with other biologic immune response modifiers, phototherapy and radiotherapy. The authors reviewed the literature on the results of the use of retinoids and rexinoids in patients with mycosis fungoides and Sézary syndrome.

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Section: Rexinoid In Cutaneous T-cell Lymphomassupporting

confidence: 71%

Oral retinoids and rexinoids in cutaneous T-cell lymphomas

Sokołowska‐Wojdyło¹,

Ługowska-Umer²,

Maciejewska-Radomska³

2013

pdia

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“…More recently, bexarotene, a new retinoid that binds to the nuclear retinoid × receptor ( R × R ), has been specifically developed for the treatment of MF (50). The drug has shown efficacy as monotherapy in randomized clinical trials and an increasing number of case series and smaller studies indicate that its combination with PUVA might be safe and feasible (51–58). In general, however, the questions as to whether any PUVA combination is superior to PUVA alone in terms of clinically relevant endpoints (e.g.…”

Section: Puvamentioning

confidence: 99%

Phototherapy of mycosis fungoides

Trautinger

2011

Photoderm Photoimm Photomed

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SummaryBackground/purpose: Among the primary cutaneous T-cell lymphomas, mycosis fungoides (MF) is the most common disease entity. Recently, an improved understanding of the pathology, clinical presentation, and prognosis of MF has lead to the development of new and practically useful classification and staging systems. In most patients, MF presents with patches and plaques and remains confined to the skin for years and decades, making it an ideal target for phototherapy. However, treatment schedules vary widely and this review describes the current knowledge about phototherapy of MF focusing mainly on narrow-and broadband UVB and 8-methoxypsoralen plus UVA, its indications, practical aspects, and clinical outcome. Methods: Review and summary of the pertinent literature. Results and conclusions: Since 1976, when the first report on phototherapy for MF was published, sufficient evidence has accumulated to make narrowband UVB and PUVA safe and effective treatment options for early stages of the disease. In refractory cases or more advanced stages, combination of phototherapy with systemic treatments including mainly interferons and retinoids might be valuable. Additional research is required to further define the optimal treatment schedules and the role of maintenance.

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“…However, almost all patients eventually experience a tumour relapse . Advanced stages of CTCLs are treated with combinations of PUVA with interferon alpha, retinoids, glucocorticosteroids, alemtuzumab, chemotherapy, extracorporeal photopheresis, or total skin electron beam irradiation . All treatments lead to partial or total remission, but curative modalities have proven elusive, for which reason the development of new therapies is imperative.…”

Section: Introductionmentioning

confidence: 99%

The antihistamines clemastine and desloratadine inhibit STAT3 and c‐Myc activities and induce apoptosis in cutaneous T‐cell lymphoma cell lines

Döbbeling

Waeckerle-Men

Zabel

et al. 2013

Experimental Dermatology

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Mycosis fungoides and its leukaemic counterpart Sézary syndrome are the most frequent cutaneous T-cell lymphomas (CTCL), and there is no cure for these diseases. We evaluated the effect of clinically approved antihistamines on the growth of CTCL cell lines. CTCL cell lines as well as blood lymphocytes from patients with Sézary syndrome were cultured with antihistamines, and the cell were analysed for proliferation, apoptosis and expression of programmed death molecules and transcription factors. The two antihistamines clemastine and desloratadine, currently used for symptom alleviation in allergy, induced potent reduction of the activities of the constitutively active transcription factors c-Myc, STAT3, STAT5a and STAT5b in mycosis fungoides and Sézary syndrome cell lines. This inhibition was followed by apoptosis and cell death, especially in the Sézary syndrome-derived cell line Hut78 that also showed increased expression of the programmed death-1 (PD-1) after clemastine treatment. In lymphocytes isolated from Sézary syndrome patients, the CD4-positive fraction underwent apoptosis after clemastine treatment, while CD4-negative lymphocytes were little affected. Because both c-Myc and STAT transcription factors are highly expressed in proliferating tumours, their inhibition by clemastine, desloratadine and other inhibitors could complement established chemotherapies not only for cutaneous T-cell lymphomas but perhaps also other cancers.

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Psoralen Plus Long-Wave UV-A (PUVA) and Bexarotene Therapy

Cited by 45 publications

References 8 publications

Oral retinoids and rexinoids in cutaneous T-cell lymphomas

Oral retinoids and rexinoids in cutaneous T-cell lymphomas

Phototherapy of mycosis fungoides

The antihistamines clemastine and desloratadine inhibit STAT3 and c‐Myc activities and induce apoptosis in cutaneous T‐cell lymphoma cell lines

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