title: Seborrheic Keratoses: The Rodney Dangerfield of Skin lesions, and Why They Should Get Our Respect.
abstract: Neel et al. have demonstrated that seborrheic keratosis, the most common of all skin tumors, is dependent on acutely transforming retrovirus AKT8 in rodent T-cell lymphoma signaling. The authors found that these lesions are hypersensitive to Akt inhibitors which bind to the ATP binding site of Akt. Cutaneous squamous cell carcinoma is resistant to Akt inhibitors. The implications of this study are not limited to seborrheic keratosis. The presence of wild type p53 (seborrheic keratosis) or mutant p53 (cutaneous squamous cell carcinoma) appears to dictate whether a lesion is sensitive to Akt inhibition or not.
authors.affiliation: Department of Dermatology, Emory School of Medicine, and Winship Cancer Institute, Atlanta, Georgia, USA; Dermatology Veterans Affairs Medical Center, Decatur, Georgia, USA. Electronic address: jarbise@emory.edu.
authors.forename: Jack L
authors.initials: JL
authors.lastname: Arbiser
authors.affiliation: Department of Dermatology, Emory School of Medicine, and Winship Cancer Institute, Atlanta, Georgia, USA.
authors.forename: Michael Y
authors.initials: MY
authors.lastname: Bonner
mesh_terms: D002470:Cell Survival / Q000235:genetics*; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D006801:Humans; D017492:Keratosis, Seborrheic / Q000473:pathology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D051498:Receptor, Fibroblast Growth Factor, Type 3 / Q000235:genetics*
chemical_list: D051498:Receptor, Fibroblast Growth Factor, Type 3; D051057:Proto-Oncogene Proteins c-akt