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Pathogenesis of Mycosis fungoides

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TLDR
In recent years genetic analyses have uncovered various chromosomal aberrations in the tumour cells of mycosis fungoides that relevance to the pathogenesis and clinical appearance are discussed.
Abstract
Summary Mycosis fungoides is the most common type of primary cutaneous lymphomas. The phenotype of the tumor cell corresponds to an effector/memorytype of helper T cell which, given its repertoire of homing receptors, is specialized for recirculation through the skin. In recent years genetic analyses have uncovered various chromosomal aberrations in the tumour cells of mycosis fungoides. Their relevance to the pathogenesis and clinical appearance are discussed in the following.

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Citations
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Journal ArticleDOI

Whole genome sequencing reveals oncogenic mutations in mycosis fungoides

TL;DR: Genetic alterations in specific pathways in MF were identified that may be viable, effective new targets for treatment and identified 2 other potential contributing factors to MF, ultraviolet light, and a polymorphism in the tumor suppressor p53.
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Oncogenomic analysis of mycosis fungoides reveals major differences with Sézary syndrome

TL;DR: Genetic differences between MF and Sz suggest that the molecular pathogenesis and therefore therapeutic requirements of these cutaneous T-cell lymphomas may be distinct, and novel insight into genetic alterations underlying MF is provided.
Journal ArticleDOI

TH2 Cytokines from Malignant Cells Suppress TH1 Responses and Enforce a Global TH2 Bias in Leukemic Cutaneous T-cell Lymphoma

TL;DR: The results suggest that therapies that inhibit TH2 cytokine activity, by virtue of their ability to improve TH1 responses, may have the potential to enhance both anticancer and antipathogen responses.
Journal ArticleDOI

Evolving Insights in the Pathogenesis and Therapy of Cutaneous T-cell lymphoma (Mycosis Fungoides and Sezary Syndrome)

TL;DR: A better understanding of the cell biology, immunology and genetics underlying the development and progression of CTCL will allow the design of more rational treatment strategies for these malignancies.
Journal ArticleDOI

Vorinostat interferes with the signaling transduction pathway of T-cell receptor and synergizes with phosphoinositide-3 kinase inhibitors in cutaneous T-cell lymphoma

TL;DR: The functional analysis suggests that vorinostat modifies signaling of T-cell receptor, MAPK, and JAK-STAT pathways and shows that combination therapies involving histone deacetylase inhibitors and inhibitors of PI3K are potentially efficacious for the treatment of cutaneous T- cell lymphoma.
References
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Journal ArticleDOI

Immunosuppressive Strategies that are Mediated by Tumor Cells

TL;DR: Different strategies employed by tumors to thwart immune responses, including tumor-induced impairment of antigen presentation, the activation of negative costimulatory signals, and the elaboration of immunosuppressive factors are discussed.
Journal ArticleDOI

Homeostasis of naive and memory T cells.

TL;DR: This review highlights recent advances in how naive and memory T cell homeostasis is regulated.
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Disruption of the ARF–Mdm2–p53 tumor suppressor pathway in Myc-induced lymphomagenesis

TL;DR: It is reported that p53 and ARF also potentiate Myc-induced apoptosis in primary pre-B-cell cultures, and that spontaneous inactivation of the ARF-Mdm2-p53 pathway occurs frequently in tumors arising in Emu-myc transgenic mice.
Journal ArticleDOI

Sézary syndrome and mycosis fungoides arise from distinct T-cell subsets: a biologic rationale for their distinct clinical behaviors

TL;DR: The phenotype of T cells from L-CTCL and MF is studied to suggest that SS is a malignancy of central memory T cells and MF are a malIGNancy of skin resident effector memory T Cells.
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