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Actinic Keratosis Clinical Course Correlates with Underlying Molecular Mechanisms.

08:00 EDT 12th July 2019 | BioPortfolio

Summary of "Actinic Keratosis Clinical Course Correlates with Underlying Molecular Mechanisms."

Actinic keratoses (AKs) are common premalignant skin lesions triggered by excessive UV exposure. The majority of AKs regress or persist, but some progress to squamous cell carcinomas. The biomarkers associated with their persistence, progression and regression have not been characterized.

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This article was published in the following journal.

Name: The British journal of dermatology
ISSN: 1365-2133
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Medical and Biotech [MESH] Definitions

A compound produced from succinyl-CoA and GLYCINE as an intermediate in heme synthesis. It is used as a PHOTOCHEMOTHERAPY for actinic KERATOSIS.

White or pink lesions on the arms, hands, face, or scalp that arise from sun-induced DNA DAMAGE to KERATINOCYTES in exposed areas. They are considered precursor lesions to superficial SQUAMOUS CELL CARCINOMA.

A family of predominantly nuclear proteins that regulate gene transcription and protein degradation. The expansion of CAG trinucleotide repeats in genes that encode Ataxins is associated with SPINOCEREBELLAR ATAXIAS (SCA). In SCA patients, the number of CAG repeats correlates with the severity of disease and inversely correlates with the age of disease onset.

A heritable disorder of faulty keratinization characterized by the proliferation of abnormal clones of KERATINOCYTES and lesions showing varying atrophic patches surrounded by an elevated, keratotic border. These keratotic lesions can progress to overt cutaneous neoplasm. Several clinical variants are recognized, including porokeratosis of Mibelli, linear porokeratosis, disseminated superficial actinic porokeratosis, palmoplantar porokeratosis, and punctate porokeratosis.

Any horny growth such as a wart or callus.

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