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hyperpigmentation/tyrosine

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Persistent cutaneous hyperpigmentation after tyrosine kinase inhibition with imatinib for GIST.

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Imatinib mesylate, a tyrosine kinase inhibitor targeting the Bcr-Abl protein, c-kit (KIT) and the platelet-derived growth factor receptors (PDGFR), is an important part of the therapeutic armamentarium used in chronic myelogenous leukemia and gastrointestinal stromal tumors. A multitude of

The Dark Side of Gefitinib: Reflectance Confocal Microscopy Applied to Hair Hyperpigmentation.

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Gefitinib is a multi-target tyrosine kinase inhibitor used for the treatment of non-small cell lung cancer. Papulo-pustular and/or paronychia, abnormalities in hair growth, itching, and dryness due to epidermal growth factor inhibitors - i.e., PRIDE Complex - are a common effect of tyrosine kinase

Hyperpigmentation during interferon-alpha therapy for chronic hepatitis C virus infection.

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Many types of skin disorders concomitantly occur with hepatitis C virus infection. These skin lesions may be induced or worsened during antiviral therapy with interferon-alpha (IFN). To our knowledge, hyperpigmentation of the skin--and especially of the tongue--has not been reported so far. We
In moderately colored guinea-pig skin, UVB, PUVA, and allergic contact dermatitis were shown to induce hyperpigmentation that resembled the pigmentary changes observed in mongoloid human skin. Using this model, we examined the effects of chemical agents, including tyrosinase inhibitors and sunscreen

Novel c-KIT germline mutation in a family with gastrointestinal stromal tumors and cutaneous hyperpigmentation.

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Mutations in the c-KIT gene have been identified in many sporadic and familial cases of gastrointestinal stromal tumor (GIST). We report a familial case of GIST with cutaneous hyperpigmentation associated with a novel germline mutation in the c-KIT gene. Screening for mutations in exon 11 of the

Imatinib-induced Extensive Hyperpigmentation in a Case of Chronic Myeloid Leukemia.

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Imatinib, a tyrosine kinase inhibitor, is well known to cause hypopigmentation because of its inhibitory effect on melanocytes. Herewith we report a case of chronic myeloid leukemia who developed extensive hyperpigmentation following imatinib therapy.

Diffuse hypopigmentation followed by hyperpigmentation in an african american woman with hemangiopericytoma treated with dasatinib.

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Dasatinib is a second-generation multi-target tyrosine kinase inhibitor (TKI) that has activity against many imatinib-resistant BCR-ABL mutant forms, Src, and c-Kit tyrosine kinases. While skin hypopigmentation is a well recognized adverse effect of first generation TKIs; it has rarely been reported
Hyperpigmentation disorders negatively influence an individual's quality of life and may cause emotional distress. Over the years, various melanogenesis inhibitors (mainly tyrosinase inhibitors) have been developed, most of which with low efficacy or high toxicity. Although metabolic engineering by

Hyperpigmentation of the hard palate mucosa in a patient with chronic myeloid leukaemia taking imatinib.

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UNASSIGNED Imatinib mesylate is an inhibitor of the tyrosine kinase Bcr-Abl and a first-line treatment for Philadelphia chromosome-positive chronic myeloid leukaemia (CML). Dermatological side effects include superficial oedema, pustular eruption, lichenoid reactions, erythroderma, and skin rash.
BACKGROUND Imatinib mesylate is a tyrosine-kinase inhibitor used as the first-line treatment in chronic myeloid leukemia patients, but it is also indicated for other hematological diseases and solid tumors. Imatinib treatment is often associated with hypopigmentation, but only a few cases of

Sesamol Inhibited Ultraviolet Radiation-Induced Hyperpigmentation and Damage in C57BL/6 Mouse Skin.

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Melanin is synthesized through a series of oxidative reactions initiated with tyrosine and catalyzed by melanogenesis-related proteins such as tyrosinase, tyrosinase-related protein-1 (TRP-1), dopachrome tautomerase (TRP-2), and microphthalmia-associated transcription factor (MITF). Our previous
Dermatologic manifestations from therapy with imatinib are well known and frequently include hypopigmentation, and less commonly, hyperpigmentation. There have been few reports of oral hyperpigmentation. We present a case of palatal melanosis related to imatinib therapy for chronic myelogenous

Disruption of hmgA by DNA Duplication is Responsible for Hyperpigmentation in a Vibrio anguillarum Strain.

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Vibrio anguillarum 531A, isolated from a diseased fish in the Atlantic Ocean, is a mixture composed of about 95 and 5% of highly pigmented cells (strain 531Ad) and cells with normal levels of pigmentation (strain 531Ac), respectively. Analysis of the V. anguillarum 531Ad DNA region encompassing

Short-sequence oligopeptides with inhibitory activity against mushroom and human tyrosinase.

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Cutaneous hyperpigmentation is a common disorder due to excess melanin production by the enzyme tyrosinase. The gold standard for treatment is hydroquinone (HQ), which reduces pigmentation through its toxicity to melanocytes rather than via tyrosinase inhibition. We screened an internal library for

Serendipitous discovery of short peptides from natural products as tyrosinase inhibitors.

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Tyrosinase, which is the crucial copper-containing enzyme involved in melanin synthesis, is strongly associated with hyperpigmentation disorders, cancer, and neurodegenerative disease; thus, it has attracted considerable interest in the fields of medicine and cosmetics. The known tyrosinase
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