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Cutaneous T-cell lymphoma is not a single molecule or receptor, but rather a rare group of non-Hodgkin lymphomas that originate from malignant transformation of skin-homing T lymphocytes. The most common subtypes are mycosis fungoides and Sézary syndrome. These diseases present primarily with skin symptoms such as patches, plaques, tumors or erythroderma and may progress to involve blood and lymph nodes. Treatments include topical therapies for early stages and systemic agents for advanced disease. The underlying pathogenesis involves dysregulated immune signaling pathways in malignant CD4+ helper T cells.[1][2][3][4] Note: "Cutaneous T cells" is not the name of a therapeutic target but refers broadly to normal or malignant populations of skin-associated immune cells. The correct therapeutic targets would be specific molecules expressed by these cancerous cells—such as CD30 or CCR4—or the abnormal signaling pathways within them. Summary: The entry "Cutaneous T cells" is incorrect as a molecular target because it describes either normal immune cell populations in the skin or groups of cancers derived from them—not an individual protein/receptor/enzyme suitable for structured drug-target data extraction.[1][2]
Histone deacetylase inhibition (vorinostat, romidepsin) Retinoid X receptor activation (bexarotene) Antimetabolite inhibition of DNA synthesis (methotrexate)
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