Dermatomyositis: a clinicopathological study of 40 patients.

The histopathology of cutaneous lesions of dermatomyositis (DM) may be indistinguishable from acute cutaneous lesions of systemic lupus erythematosus (SLE). Misreported or incomplete clinical information may result in a clinicopathologic discrepancy and a delay in making a correct diagnosis of DM. The aim of this study was to systematically characterize the histopathologic findings of cutaneous lesions of DM and to determine if skin biopsy specimens of DM and SLE could be distinguished by light microscopic examination.

BRAF kinase in melanoma development and progression.

Cutaneous melanoma is increasing in incidence at one of the highest rates for any form of cancer in the USA, with a current lifetime incidence of 1 in 68. Although early-stage disease is often curable, the survival rate for advanced disease is low, with an average life expectancy of 6-10 months. Knowledge of the molecular alterations associated with melanoma development and progression is expected to lead to improved therapies and outcomes.

Comprehensive expression profiling of tumor cell lines identifies molecular signatures of melanoma progression.

Background: Gene expression profiling has revolutionized our ability to molecularly classify primary human tumors and significantly enhanced the development of novel tumor markers and therapies; however, progress in the diagnosis and treatment of melanoma over the past 3 decades has been limited, and there is currently no approved therapy that significantly extends lifespan in patients with advanced disease. Profiling studies of melanoma to date have been inconsistent due to the heterogeneous nature of this malignancy and the limited availability of informative tissue specimens from early stages of disease.

Methodology/principle Findings: In order to gain an improved understanding of the molecular basis of melanoma progression, we have compared gene expression profiles from a series of melanoma cell lines representing discrete stages of malignant progression that recapitulate critical characteristics of the primary lesions from which they were derived.

Id1 expression is transcriptionally regulated in radial growth phase melanomas.

Id genes have been demonstrated to be upregulated in a wide variety of human malignancies and their expression has been correlated with disease prognosis; however, little is known about the mechanisms of Id gene activation in tumors. We have previously shown that the helix-loop-helix transcription factor, Id1, is highly expressed in primary human melanomas during the radial growth phase and that Id1 is a transcriptional repressor of the familial melanoma gene CDKN2A. Here we use a series of melanoma cell lines that recapitulate the phenotypic characteristics of melanomas at varying stages of malignant progression to evaluate the expression levels of Id1 in this model system and determine the mechanism of Id1 dysregulation in these tumor cells.