Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Consumption of the epidermis (COE), defined as thinning of the epidermis with attenuation of basal and suprabasal layers and loss of rete ridges adjacent to collections of melanocytes, is a recently coined term encompassing changes of the epidermal architecture associated with melanoma. To evaluate this feature as an additional diagnostic criterion for melanoma, we examined COE in 453 melanocytic lesions, including 213 invasive melanomas from a population-based series and 240 suspicious pigmented lesions from a clinic-based series, excluding halo and Spitz nevi. In the population-based series, COE was identified in 92/213 (43%) invasive melanomas and became progressively more frequent with increasing Breslow depth (P < 0.0001) and Clark level (P = 0.0002). COE was more frequent when mitotic figures (P < 0.0001), ulceration (P = 0.005), or vertical growth phase (P = 0.009) were present, but it was not significantly associated with age, gender, site, regression, or tumor-infiltrating lymphocytes. In the clinic-based series of pigmented lesions, COE was present in 2/25 (8%) in situ melanomas, 1/29 (3%) lesions classified as melanoma in situ/high-grade dysplastic nevi, and 1/40 (2.5%) high-grade dysplastic nevi. COE was not identified in 146 low-grade dysplastic, congenital, or common nevi. In the combined datasets, 94/96 (98%) lesions exhibiting COE were classified as melanoma. This study demonstrates that COE is frequently present in invasive melanomas, is associated with more aggressive histopathologic features (including increased Breslow depth and ulceration) and may be a useful supplementary diagnostic criterion for melanoma. Furthermore, the process leading to COE may be the first step in a progression to ulceration.
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PMID:Consumption of the epidermis: a criterion in the differential diagnosis of melanoma and dysplastic nevi that is associated with increasing breslow depth and ulceration. 1803 46

Phosphorylase kinase (PhK) is a unique enzyme in which the spatial arrangements of the specificity determinants can be manipulated to allow the enzyme to recognize substrates of different specificities. In this way, PhK is capable of transferring high energy phosphate bonds from ATP to serine/threonine and tyrosine moieties in serine/threonine kinases and tyrosine kinases, thus playing a key role in the activation of multiple signaling pathways. Phosphorylase kinase is released within five minutes following injury and is responsible for activating inflammatory pathways in injury-activated scarring following burns. In photo-damaged skin, PhK plays an important role in promoting photocarcinogenesis through activation of NF-kB-dependent signaling pathways with inhibition of apoptosis of photo-damaged cells, thus promoting the survival of precancerous cells and allowing for subsequent tumor transformation. Curcumin, the active ingredient in the spice, turmeric, is a selective and non-competitive PhK inhibitor. By inhibition of PhK, curcumin targets multiple PhK-dependent pathways, with salutary effects on a number of skin diseases induced by injury. In this paper, we show that curcumin gel produces rapid healing of burns, with little or no residual scarring. Curcumin gel is also beneficial in the repair of photo-damaged skin, including pigmentary changes, solar elastosis, thinning of the skin with telangiectasia (actinic poikiloderma), and premalignant lesions such as actinic keratoses, dysplastic nevi, and advanced solar lentigines, but the repair process takes many months.
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PMID:Signaling pathways targeted by curcumin in acute and chronic injury: burns and photo-damaged skin. 2323 6