keratosis/tyrosine

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Inflammation of actinic keratoses subsequent to therapy with sorafenib, a multitargeted tyrosine-kinase inhibitor.

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The Ras-Raf-MEK-ERK signalling pathway is frequently dysregulated in human malignancies, as is angiogenesis and the vascular endothelial growth factor receptor (VEGF/VEGFR) pathway. These kinases are therefore important anticancer targets. The novel, oral treatment sorafenib (BAY 43-9006), has been

Induction of Tyrosine Phosphorylation of UV-Activated EGFR by the Beta-Human Papillomavirus Type 8 E6 Leads to Papillomatosis.

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Epidemiological evidence is accumulating that beta-human papillomaviruses (HPV) synergize with UV-light in the development of precancerous actinic keratosis, and cutaneous squamous cell carcinomas (cSCC), one of the most common cancers in the Caucasian population. We previously demonstrated the

Dysregulation of epidermal growth factor receptor in actinic keratosis and squamous cell carcinoma.

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The epidermal growth factor receptor (EGFR) is a receptor tyrosine kinase. Its correct function is required for normal skin development and homeostasis, while dysregulation of EGFR signalling results in cellular hyper-proliferation and defects in differentiation, leading to impaired wound healing,

Nilontinib induced keratosis pilaris atrophicans.

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Keratosis pilaris (KP) is a disorder of follicular keratinization that is characterized by keratin plugs in the hair follicles with surrounding erythema. A 46-year-old man with chronic myelogenous leukemia (CML) was started on nilotinib, a second generation tyrosine kinase inhibitor (TKI). Two

Intensified inflammatory reaction of actinic keratoses after single application of topical 5-fluorouracil in a patient treated with nilotinib for chronic myeloid leukemia.

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Actinic keratoses frequently occur in sun-exposed areas of the skin and, today, a variety of therapeutic options are available, including topical application of 5-fluorouracil (5-FU). Usually, 5-FU ointment needs to be applied twice daily for 2-4 weeks to achieve a therapeutic skin reaction. Here,

Richner-Hanhart's syndrome: ultrastructural abnormalities of epidermal keratinization indicating a causal relationship to high intracellular tyrosine levels.

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Richner-Hanhart's syndrome (corneal dystrophies, palmoplantar keratoses, and mental retardation) is caused by high levels of L-tyrosine in the blood, probably due to a defect of soluble tyrosine aminotransferase. Biopsies of skin lesions of 3 cases revealed peculiar ultrastructural changes that were

Activating mutations of the tyrosine kinase receptor FGFR3 are associated with benign skin tumors in mice and humans.

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Specific germline activating point mutations in the gene encoding the tyrosine kinase receptor FGFR3 (fibroblast growth factor receptor 3) result in autosomal dominant human skeletal dysplasias. The identification in multiple myeloma and in two epithelial cancers-bladder and cervical carcinomas-of

Erlotinib-responsive actinic keratoses.

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Erlotinib is an inhibitor of the tyrosine-kinase domain of the epidermal growth factor receptor-1 (EGFR). This drug is used to treat some solid cancers, particularly advanced non-small-cell lung carcinoma. Similar to other EGFR inhibitors, erlotinib is responsible for a series of skin adverse

Sustained Akt Activity Is Required to Maintain Cell Viability in Seborrheic Keratosis, a Benign Epithelial Tumor.

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Seborrheic keratoses (SKs) are common benign skin tumors that share many morphological features with their malignant counterpart, squamous cell carcinoma. SKs frequently have acquired oncogenic mutations in the receptor tyrosine kinase/phosphatidylinositol 3-kinase/Akt signaling cascade. We

Tyrosinemia without liver or renal damage with plantar and palmar keratosis and keratitis (hypertyrosinemia type II).

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A boy of 3 2/12 years of age with Richner-Hanhart syndrome (plantar and palmar keratosis and chronic keratitis) was found to have hypertyrosinemia and to excrete the hydroxyacids derived from tyrosine. A diet poor in phenylalanine and tyrosine cured the skin and corneal lesions. Clinical and

Activation of Src-family tyrosine kinases in hyperproliferative epidermal disorders.

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BACKGROUND Src-family tyrosine kinases (SFKs) are important regulators of keratinocyte growth and differentiation. In a broad range of cell types, persistent activation of SFKs correlates with increased cell proliferation. In this study, we determined if SFK activity is increased in cutaneous

Unique Cutaneous Reaction to Second- and Third-Generation Tyrosine Kinase Inhibitors for Chronic Myeloid Leukemia.

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BACKGROUND Recently developed tyrosine kinase inhibitors (TKIs) offer first-line alternatives to patients with chronic myeloid leukemia. While these medications are generally well tolerated, cutaneous reactions occur frequently and can present a management challenge. We describe a newly recognized

A positive FGFR3/FOXN1 feedback loop underlies benign skin keratosis versus squamous cell carcinoma formation in humans.

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Seborrheic keratoses (SKs) are common, benign epithelial tumors of the skin that do not, or very rarely, progress into malignancy, for reasons that are not understood. We investigated this by gene expression profiling of human SKs and cutaneous squamous cell carcinomas (SCCs) and found that several

Keratosis pilaris-like eruption secondary to nilotinib in a child

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Nilotinib is a new multitargeted tyrosine kinase inhibitor, which is used to treat chronic myelogenous leukemia when intolerance or recurrence to imatinib occurs. We report the case of a 14-year-old patient being treated with nilotinib who developed a keratosis pilaris-like eruption. This cutaneous

Nilotinib-Induced Keratosis Pilaris.

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Nilotinib is a second-generation Bcr-Abl tyrosine kinase inhibitor (TKI) that is approved for the treatment of imatinib-resistant chronic myeloid leukaemia expressing the Bcr-Abl mutation. Cutaneous adverse drug reactions occur more frequently in patients using this medication. We present a case of

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