1,720,993 research outputs found
Successful treatment of keratoacanthoma and actinic keratoses with imiquimod 5% cream
No abstract availabl
Usefulness of dermoscopy to monitor clinical efficacy of imiquimod treatment for lentigo maligna
No abstract availabl
Dermoscopic features of actinic keratosis
Actinic keratosis (AK) is a keratinocytic neoplasm that typically develops on sun-damaged skin of elderly individuals. Only a few reports so far have described the dermoscopic diagnostic features of AK, mainly focusing on facial non-pigmented AKs. A typical feature of facial non-pigmented AK is a composite pattern named "strawberry pattern", characterized by a background erythema/red pseudonetwork consisting of unfocused, large vessels located between the hair follicles, associated with prominent follicular openings surrounded by a white halo. Dermoscopic characteristics of pigmented AK on the face include multiple slate-gray to dark-brown dots and globules around the follicular ostia, annular-granular pattern and brown to gray pseudonetwork. Recognizing specific dermoscopic features of AK can be useful in guiding the clinician in the differential diagnosis of AK with melanocytic skin lesions such as LM and non-melanocytic lesions. Histopathologic examination should be performed whenever clinical and/or dermoscopic differential diagnosis is inconclusive
Efficacy of tetracycline treatment to prevent the acneiform eruption secondary to cetuximab therapy
Letter: Changes in dermoscopic features in superficial basal cell carcinomas treated with imiquimod
No abstract availabl
Molecular genetic aspects of cutaneous melanoma
The etiopathogenesis of cutaneous melanoma has been correlated to both genetic and environmental factors. During the last decade, molecular-genetic studies have demonstrated that high-penetrance genes such as cyclin-dependent kinase inhibitor 2A (CDKN2A) and cyclin-dependent kinase (CDK4), and low-penetrance genes such as MC1R play an important role in the pathogenesis of melanoma. CDKN2A and CDK4 genes function as cell cycle regulators, while MC1R gene is an important determinant of cutaneous pigmentation. Several studies have emphasized that CDKN2A gene, a tumor suppressor gene located at 9p21, has a crucial role in the development of familial, multiple and sporadic melanoma. Germline mutations of the CDKN2A gene have been identified in approximately 25-40% of familial melanoma kindreds worldwide and in 8-20% of patients with multiple primary melanoma (MPM). In contrast, somatic mutations of the CDKN2A gene have been frequently identified in sporadic melanoma. Mutations of the CDK4 oncogene have been described at a low frequency in familial and sporadic melanoma, and no alterations have been identified in patients with MPM. Recent studies showed that specific allelic variants of the MC1R gene confer susceptibility to melanoma and modify the risk of developing melanoma in patients who harbor CDKN2A mutations. Finally, based on the low number of studies, it is not yet clear the precise role of some putative oncogene or tumor suppressor genes located on chromosomes 1, 6, 7, 10, 11 and 17, which have been previously shown to be altered in cutaneous melanoma
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