dermatitis/tyrosine

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Radiation recall dermatitis triggered by multi-targeted tyrosine kinase inhibitors: sunitinib and sorafenib.

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Small molecule tyrosine kinase inhibitors are rapidly being integrated into the management of cancer. This is the first report of sorafenib and sunitinib, both small molecule tyrosine kinase inhibitors of vascular endothelial growth factor and platelet-derived growth factor receptors, triggering

Expression of T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain on CD4+ T cells in patients with atopic dermatitis.

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The T-cell immunoglobulin and immunoreceptor tyrosine-based inhibitory motif domain (TIGIT) is a co-inhibitory receptor mainly expressed on T cells. Although TIGIT plays an important role in various autoimmune diseases, its role in atopic dermatitis (AD) remains unclear. In this study, we examined

Protein tyrosine phosphatase conjugated with a novel transdermal delivery peptide, astrotactin 1-derived peptide recombinant protein tyrosine phosphatase (AP-rPTP), alleviates both atopic dermatitis-like and psoriasis-like dermatitis.

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BACKGROUND Atopic dermatitis (AD) and psoriasis are the 2 most common chronic inflammatory skin diseases. There is an unmet medical need to overcome limitations for transcutaneous drug development posed by the skin barrier. OBJECTIVE We aimed to identify a novel transdermal delivery peptide and to

The oral Janus kinase/spleen tyrosine kinase inhibitor ASN002 demonstrates efficacy and improves associated systemic inflammation in patients with moderate-to-severe atopic dermatitis: results from a randomized double-blind placebo-controlled study.

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ASN002 is an oral dual inhibitor of Janus kinase and spleen tyrosine kinase, which are involved in the pathogenesis of atopic dermatitis (AD) through their regulatory role on T helper (Th)1, Th2 and Th17/Th22 pathways.The objectives of this study were to

The Syk Tyrosine Kinase Is Required for Skin Inflammation in an In Vivo Mouse Model of Epidermolysis Bullosa Acquisita.

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The inflammatory form of epidermolysis bullosa acquisita is caused by autoantibodies against type VII collagen (C7), a component of the dermal-epidermal junction. We have previously shown that myeloid Src family kinases mediate skin inflammation triggered by anti-C7 antibodies. Here we identify the

Hyperactivation of JAK1 tyrosine kinase induces stepwise, progressive pruritic dermatitis.

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Skin homeostasis is maintained by the continuous proliferation and differentiation of epidermal cells. The skin forms a strong but flexible barrier against microorganisms as well as physical and chemical insults; however, the physiological mechanisms that maintain this barrier are not fully

IgE hyperproduction through enhanced tyrosine phosphorylation of Janus kinase 3 in NC/Nga mice, a model for human atopic dermatitis.

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IgE hyperproduction frequently observed in patients with atopic dermatitis (AD) may greatly contribute to the pathogenesis of AD, but its mechanisms are still unclear. NC/Nga mice raised in nonsterile circumstances spontaneously suffered from AD-like skin lesions with elevation of plasma IgE levels.

Increased halogenated tyrosine levels are useful markers of human skin ageing, reflecting proteins denatured by past skin inflammation.

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BACKGROUND Photoageing of skin is thought to be caused by protein denaturation, which can be induced by ultraviolet radiation. Previous studies have also reported that inflammation is related to protein denaturation; however, the influence of inflammation on skin ageing has not been explored in

Inhibition of chronic and acute skin inflammation by treatment with a vascular endothelial growth factor receptor tyrosine kinase inhibitor.

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Although vascular remodeling is a hallmark of many chronic inflammatory disorders, antivascular strategies to treat these conditions have received little attention to date. We investigated the effects of a newly identified vascular endothelial growth factor (VEGF) receptor tyrosine-kinase inhibitor,

Photoinduced dermatitis and oral lichenoid reaction in a chronic myeloid leukemia patient treated with imatinib mesylate.

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BACKGROUND Imatinib mesylate (IM) is a phenylaminopyrimidine that represents the first-line treatment for chronic myeloid leukemia (CML), Philadelphia chromosome-positive. It acts as a potent and selective inhibitor of the bcr-abl fusion protein by a competitive inhibition at the adenosine

[Safety of subcutaneous immunotherapy with tyrosine-adsorbed house dust mite extracts in patients with allergic disease].

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In spite of allergen-specific immunotherapy (SIT) multiple benefits, its use is restricted in some countries owing to concerns about severe adverse reactions. To evaluate systemic adverse reactions in patients with atopic dermatitis, allergic asthma, allergic rhinitis and allergic conjunctivitis who

Protein tyrosine phosphatase SHP-1: resurgence as new drug target for human autoimmune disorders.

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Recognition of self-antigen and its destruction by the immune system is the hallmark of autoimmune diseases. During the developmental stages, immune cells are introduced to the self-antigen, for which tolerance develops. The inflammatory insults that break the immune tolerance provoke immune system

Nintedanib ameliorates animal model of dermatitis.

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Nintedanib, a receptor tyrosine kinase (RTK) inhibitor has been developed as therapeutics for idiopathic pulmonary fibrosis and non-small lung cancer. We found that the expression levels of RTK, especially VEGFR1 is increased in skin biopsies of dermatitis patients from multiple independent

Sorafenib induced radiation recall dermatitis after spine radiosurgery.

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Radiation recall dermatitis has been documented to occur in previously irradiated skin (within the radiation port) the administration of some chemotherapeutic agents. Clinically, it can occur weeks or months after radiation therapy, and resembles the appearance of acute radiation skin reaction. The

Radiation recall dermatitis induced by pazopanib.

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BACKGROUND Pazopanib is a multi-targeted tyrosine kinase inhibitor that has recently been approved for treatment of advanced clear cell renal cell carcinoma (RCC). There are no previous reports of pazopanib triggering radiation recall dermatitis (RRD). METHODS A 60-year-old male patient was

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