mycosis fungoides/protease

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In situ localization of HuHF serine protease mRNA and cytotoxic cell-associated antigens in human dermatoses. A novel method for the detection of cytotoxic cells in human tissues.

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Ingia / Ingia

Human Hanukah Factor (HuHF) is a trypsinlike serine protease associated with cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells. Employing a radiolabeled RNA probe for the HuHF gene, cells containing HuHF mRNA in situ were detected in skin lesions from patients with a variety of reactive

The serine protease granzyme M is preferentially expressed in NK-cell, gamma delta T-cell, and intestinal T-cell lymphomas: evidence of origin from lymphocytes involved in innate immunity.

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Ingia / Ingia

Granzyme M (GM) is a novel serine protease whose expression is highly restricted to natural killer (NK) cells, CD3(+)CD56(+) T cells, and gamma delta T cells. Using a GM-specific monoclonal antibody, we analyzed the expression of GM in 214 mature T-cell and NK-cell lymphomas. GM was preferentially

Most CD8+ cells in skin lesions of CD3+ CD4+ mycosis fungoides are CD3+ T cells that lack CD11b, CD16, CD56, CD57, and human Hanukah factor mRNA.

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Ingia / Ingia

To define further the characteristics of CD8+ cells in skin lesions of CD3+ CD4+ mycosis fungoides (MF), the authors used single- and double-label immunohistologic techniques and in situ hybridization to detect antigens and transcripts associated with certain types of cytotoxic or suppressor

Mechanisms of itching in mycosis fungoides: grade of itching correlates with eosinophil infiltration and kallikrein 5 expression.

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Ingia / Ingia

Mycosis fungoides (MF) is the most common variant of cutaneous T-cell lymphomas (CTCL). Itching can be a major symptom for patients with CTCL, however, itching associated with MF is not relieved by conventional therapy using anti-histamines, suggesting that histamine is not the main

Ubiquitin-specific protease 2 decreases p53-dependent apoptosis in cutaneous T-cell lymphoma.

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Ingia / Ingia

Treatment of advanced cutaneous T-cell lymphomas (CTCL) is challenging because they are resistant to conventional chemotherapy. USP2 has been shown to promote resistance to chemotherapeutic agents in several cancer models.We show here USP2 is expressed in quiescent and activated T-cells and its

Brentuximab vedotin therapy for CD30-positive cutaneous T-cell lymphoma: a targeted approach to management.

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Ingia / Ingia

CD30-positive primary cutaneous T-cell lymphoma (CTCL) includes mycosis fungoides, anaplastic large-cell lymphoma and lymphomatoid papulosis type A. Brentuximab vedotin (BV) consists of an antibody targeting CD30 with a protease-cleavable linker to vedotin. CD30 binding allows internalization of BV

[Angiogenesis and anti-angiogenesis in human neoplasms. Recent developments and the therapeutic prospects].

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Ingia / Ingia

Angiogenesis entails new vessel formation from preexisting vessels. It follows vasculogenesis during embryo development. In post-natal life, it occurs both in physiological conditions (wound repair and cyclically in the female genital system) and pathological conditions such as tumors. Several

Brentuximab vedotin for treatment of non-Hodgkin lymphomas: A systematic review.

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Ingia / Ingia

BACKGROUND Brentuximab vedotin (BV) is an antibody-drug conjucate (ADC) comprising a CD30-directed antibody, conjugated to the microtubule-disrupting agent MMAE via a protease cleavable linker. BV is FDA approved for use in relapsed classical Hodgkin lymphoma (HL) and relapsed systemic anaplastic

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