p53 and MDM2 protein expression in actinic cheilitis
نویسندگان
چکیده
منابع مشابه
p53 AND MDM2 PROTEIN EXPRESSION IN ACTINIC CHEILITIS
Actinic cheilitis is a potentially malignant lip lesion caused by excessive and prolonged exposure to ultraviolet radiation, which can lead to histomorphological alterations indicative of abnormal cell differentiation. In this pathology, varying degrees of epithelial dysplasia may be found. There are few published studies regarding the p53 and MDM2 proteins in actinic cheilitis. Fifty-eight cas...
متن کامل[Photodynamic therapy for actinic cheilitis].
Actinic cheilitis is a subtype of actinic keratosis that mainly affects the lower lip and has a higher risk of malignant transformation. Its location on the labial mucosa influences the therapeutic approach. Vermilionectomy requires local or general anesthetic and is associated with a risk of an unsightly scar, and the treatment with 5-fluorouracil or imiquimod lasts for several weeks and the i...
متن کاملCelecoxib Treatment Alters p53 and MDM2 Expression via COX-2 Crosstalk in A549 Cells
Cyclooxygenase-2 (COX-2) has a pivotal role in the pathogenesis of the lung cancer. It is known that COX-2 negatively regulates the activity of a number of tumor suppressors, including p53. Consequently, inhibition of COX-2 signaling is anticipated to be a promising approach to stabilize p53 functionality. In this regard, we investigated the effect of COX-2 signaling blockade on p53 and COX-2 e...
متن کاملCelecoxib Treatment Alters p53 and MDM2 Expression via COX-2 Crosstalk in A549 Cells
Cyclooxygenase-2 (COX-2) has a pivotal role in the pathogenesis of the lung cancer. It is known that COX-2 negatively regulates the activity of a number of tumor suppressors, including p53. Consequently, inhibition of COX-2 signaling is anticipated to be a promising approach to stabilize p53 functionality. In this regard, we investigated the effect of COX-2 signaling blockade on p53 and COX-2 e...
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ژورنال
عنوان ژورنال: Journal of Applied Oral Science
سال: 2008
ISSN: 1678-7757
DOI: 10.1590/s1678-77572008000600011