mycosis fungoides/náusea

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Comparison of Narrowband UV-B With Psoralen-UV-A Phototherapy for Patients With Early-Stage Mycosis Fungoides: A Systematic Review and Meta-analysis.

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Phototherapy is one of the mainstays of treatment for early mycosis fungoides (MF). The most common modalities are psoralen-UV-A (PUVA) and narrowband UV-B (NBUVB).To compare the efficacy and adverse effects of PUVA vs NBUVB in early-stage

Advanced mycosis fungoides: chemotherapy with etoposide, methotrexate, bleomycin, and prednimustine.

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We assessed the efficacy and toxicity of a chemotherapeutic regimen in patients with stage II-IV mycosis fungoides. Eleven previously treated outpatients received etoposide and methotrexate p.o. and bleomycin i.v. every 3 weeks. There was 1 complete remission for 2 months and 7 partial remissions

Treatment of advanced mycosis fungoides and Sézary syndrome with continuous infusions of methotrexate followed by fluorouracil and leucovorin rescue.

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METHODS The treatment of advanced mycosis fungoides is a therapeutic challenge. A variety of treatment approaches have been used. In our experience, chemotherapy has been most useful. The purpose of this study was to evaluate the effectiveness of the synergy previously demonstrated between

Efficacy of 8-methoxypsoralen vs. 5-methoxypsoralen plus ultraviolet A therapy in patients with mycosis fungoides.

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BACKGROUND Psoralen plus ultraviolet (UV) A (PUVA) is the standard treatment for early stage mycosis fungoides (MF). When 8-methoxypsoralen (8-MOP) is used in PUVA therapy, it often produces intolerance reactions such as nausea, vomiting and headache. OBJECTIVE To investigate whether

Antitumor activity of DAB389IL-2 fusion toxin in mycosis fungoides.

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BACKGROUND DAB389IL-2 is a novel fusion toxin that retargets the cytotoxic A-chain of diphtheria toxin to interleukin-2 (IL-2) receptor-expressing tumors. OBJECTIVE The purpose of this phase I trial was to study the toxicity, maximum tolerated dose, and clinical efficacy of DAB389IL-2 in IL-2

Treatment of pruritus in early-stage hypopigmented mycosis fungoides with aprepitant.

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Pruritus is a symptom that significantly affects the patient's quality of life in cutaneous T cell lymphoma (CTCL). The most effective treatments are those that address the condition itself; however, it is often not possible to control this symptom. Lymphoma-related pruritus normally becomes more

Interventions for mycosis fungoides

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Background: Mycosis fungoides (MF) is the most common type of cutaneous T-cell lymphoma, a malignant, chronic disease initially affecting the skin. Several therapies are available, which may induce clinical remission for a time. This is

Phase II multicentre trial of oral quisinostat, a histone deacetylase inhibitor, in patients with previously treated stage IB-IVA mycosis fungoides/Sézary syndrome.

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BACKGROUND Quisinostat is a hydroxamate, second-generation, orally available pan-histone deacetylase inhibitor. OBJECTIVE To evaluate the efficacy and safety of oral quisinostat in patients with previously treated cutaneous T-cell lymphoma (CTCL). METHODS Patients received quisinostat 8 mg or 12 mg

Final results of a multicenter phase II study of the purine nucleoside phosphorylase (PNP) inhibitor forodesine in patients with advanced cutaneous T-cell lymphomas (CTCL) (Mycosis fungoides and Sézary syndrome).

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BACKGROUND Forodesine is a potent inhibitor of purine nucleoside phosphorylase (PNP) that leads to intracellular accumulation of deoxyguanosine triphosphate (dGTP) in T and B cells, resulting in apoptosis. Forodesine has demonstrated impressive antitumor activity in early phase clinical trials in

Final results of a multicenter phase II study of the purine nucleoside phosphorylase (PNP) inhibitor forodesine in patients with advanced cutaneous t-cell lymphomas (CTCL) (Mycosis fungoides and Sézary syndrome).

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Forodesine is a potent inhibitor of purine nucleoside phosphorylase (PNP) that leads to intracellular accumulation of deoxyguanosine triphosphate (dGTP) in T and B cells, resulting in apoptosis. Forodesine has demonstrated impressive antitumor activity in early phase clinical trials in

Gemcitabine treatment in pretreated cutaneous T-cell lymphoma: experience in 44 patients.

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OBJECTIVE To evaluate the efficacy and toxicity of gemcitabine, a novel pyrimidine antimetabolite with a low-toxicity profile and activity in several solid tumors, in patients with relapsed or refractory cutaneous T-cell lymphomas. METHODS Between May 1997 and February 1999, 44 previously treated

Evaluation of the long-term tolerability and clinical benefit of vorinostat in patients with advanced cutaneous T-cell lymphoma.

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BACKGROUND Vorinostat, an orally active histone deacetylase inhibitor, was approved in October 2006 by the US Food and Drug Administration for the treatment of cutaneous manifestations of cutaneous T-cell lymphoma (CTCL) in patients with progressive, persistent, or recurrent disease during or after

Vorinostat for refractory or relapsing epidermotropic T-cell lymphoma: a retrospective cohort study of 15 patients.

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Since the approval of vorinostat for the treatment of refractory cutaneous epidermotropic T-cell lymphoma (CTCL) in 2006, very little data about this treatment have been published. The aim of this retrospective study was to assess the efficacy and safety of vorinostat in patients with CTCL treated

Gemcitabine as frontline treatment for cutaneous T-cell lymphoma: phase II study of 32 patients.

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BACKGROUND Based on the activity of gemcitabine in heavily pretreated patients with cutaneous T-cell lymphoma (CTCL), the objective of the current study was to determine the role of gemcitabine in the treatment of patients with advanced, untreated CTCL. METHODS Between June 2002 and February 2004,

[A new purine analog in the treatment of hematologic malignancy. I. Fludarabine].

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New purine analogues, fludarabine, 2-chlorodeoxyadenosine and 2-deoxycoformycin are remarkably active in generally incurable malignant lymphoproliferative disorders. The first part of the review summarises pharmacological properties, the mechanism of action, toxicity and clinical use of fludarabine.

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