DEK expression in melanocytic lesions

Summary The diagnosis of malignant melanoma presents a clinical challenge and relies principally on histopathological evaluation. Previous studies have indicated that increased expression of the DEK oncogene, a chromatin-bound factor, could contribute to the development of melanoma and may be a freq...

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Bibliographic Details
Published in:Human pathology 2011-07, Vol.42 (7), p.932-938
Main Authors: Kappes, Ferdinand, PhD, Khodadoust, Michael S., MD, PhD, Yu, Limin, MD, Kim, David S.L., MD, PhD, Fullen, Douglas R., MD, Markovitz, David M., MD, Ma, Linglei, MD, PhD
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Aged, 80 and over
Benign nevi
Biological and medical sciences
Child
Child, Preschool
Chromosomal Proteins, Non-Histone - metabolism
Colleges & universities
DEK
Dermatology
Female
Humans
Immunohistochemistry
Infant
Invasive melanomas
Investigative techniques, diagnostic techniques (general aspects)
Male
Medical sciences
Melanoma - metabolism
Melanoma - pathology
Melanoma progression
Metastatic melanomas
Middle Aged
Nevus - metabolism
Nevus - pathology
Oncogene Proteins - metabolism
Pathology
Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques
Poly-ADP-Ribose Binding Proteins
Skin cancer
Skin Neoplasms - metabolism
Skin Neoplasms - pathology
Statistical analysis
Tumors of the skin and soft tissue. Premalignant lesions
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Summary:Summary The diagnosis of malignant melanoma presents a clinical challenge and relies principally on histopathological evaluation. Previous studies have indicated that increased expression of the DEK oncogene, a chromatin-bound factor, could contribute to the development of melanoma and may be a frequent event in melanoma progression. Here, we investigated DEK expression by immunohistochemistry in a total of 147 melanocytic lesions, including ordinary nevi, dysplastic nevi, Spitz nevi, melanoma in situ, primary invasive melanomas, and metastatic melanomas. Most benign nevi (ordinary, dysplastic, and Spitz nevi) were negative or exhibited weak staining for DEK, with only 4 of 49 cases showing strong staining. Similar to benign nevi, melanoma in situ also demonstrated low levels of DEK expression. In contrast, the expression of DEK in primary invasive melanomas was significantly higher than benign nevi ( P < .0001). Moreover, DEK expression was significantly increased in deep melanomas (Breslow depth >1 mm) and metastatic melanomas as compared with superficial melanomas (Breslow depth ≤1 mm) ( P < .05). Our findings indicate that DEK overexpression may be a frequent event in invasive melanomas, and further augmentation of DEK expression may be associated with the acquisition of ominous features such as deep dermal invasion and metastasis. These data suggest a role of DEK in melanoma progression.
ISSN:0046-8177
1532-8392
DOI:10.1016/j.humpath.2010.10.022