Recurrent post-herpetic erythema multiforme mimicking polymorphic light and juvenile spring eruption: report of two cases in young boys.
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Betamethasone↗
Biomedical subjects
R Fink-Puches
Publications and source records attributed to R Fink-Puches.
Inhibition of K1735-M2 melanoma cell invasion in vitro by retinoic acid.
Melanoma cell invasion in vitro was tested by means of confrontation cultures of melanoma multicellular spheroids with rounded fragments of embryonic chick heart tissue. Quantitative determination of invasion was performed using a computerized image analysis program, facilitating the evaluation of the efficacy of potentially anti-invasive compounds. Retinoic acid (RA; 1 microM) [corrected] considerably impaired K1735-M2 melanoma cell invasion, as demonstrated by various measuring parameters. Parameter TUMAREA, expressing the amount of tumor tissue, indicates a growth inhibitory effect and the invasion parameter STRCSTR shows that after treatment with RA the stromal component was better preserved than in untreated controls. Besides the inhibitory effect of RA on melanoma cell invasion in confrontation cultures, RA increased the dynamics of adhesion of melanoma cells to the extracellular matrix components type I collagen and laminin, and slightly impaired melanoma cell directional migration. Fluorescence microscopy using rhodamine-labeled phalloidin showed that RA also modulated the organization of the actin cytoskeleton by inducing the formation of actin-containing stress fibers. Our data show that 1 microM RA exhibited a pronounced anti-invasive effect on highly metastatic melanoma cells in vitro. Impairment of host tissue degradation, altered adhesion abilities, changes in the actin cytoskeleton, as well as the antiproliferative effect may all account for inhibition of melanoma cell invasion.
Actin Cytoskeleton↗
Cytoskeleton and motility: an immunohistological and computer simulation analysis of melanocytic skin tumors.
Tumor cell motility and tumor cell proliferation are supposed to be essential for tumor invasion. The cytoskeleton, which consists of different components, is considered to be important for maintaining cell shape and facilitating cell movement. Numerous data are available about tumor cell motility in vitro, but the behavior of tumor cells in vivo is as yet poorly understood. In the present study, estimates of tumor cell motility and proliferation were statistically derived from morphological tumor patterns in human melanocytic skin tumors, and their relationship to expression of certain cytoskeletal components was evaluated. Overexpression of vimentin within tumor cells correlated with low actual tumor cell motility and proliferation, indicating a structurally stabilizing function of these filaments. An overexpression of actin was found within tumor cells of high motility and proliferation, suggesting the contribution of cytocontractile elements to active tumor cell locomotion in situ. Concerning the cytoskeleton of the stromal cells, expression of actin, myosin and tubulin correlated with a high number of motile tumor cells and high mitotic counts. Thus increased tumor cell motility seems to be associated with cytoskeletal changes not only of the tumor cells themselves but also of the surrounding stromal cells.
Cell Division↗
Inhibition of melanoma cell directional migration in vitro via different cellular targets.
In malignant melanoma active movement of cancer cells is considered to be essential for tissue invasion. Various mechanisms, such as the Ca(2+)-calmodulin-proteinkinase C cascade or G-protein-dependent processes are considered to play a role in tumor cell functions. The assay of directional migration, combined with computer-assisted image analysis, was used to evaluate the antimigratory efficacy of drugs interfering with different steps of signal transduction pathways. Treatment with different compounds showed a more or less concentration-dependent reduction of migration rates: The Ca(2+)-channel blockers verapamil and devapamil showed a slight reduction of motility. The effect was more pronounced when the calmodulin antagonist flunarizine was used or the proteinkinase C inhibitors dequalinium, tamoxifen and H-7 were applied. A marked inhibition of motility was found with the G-protein antagonist L 651582. Thus, our results indicate that different signal transduction pathways are involved in the regulation of directional migration of K1735-M2 melanoma cells.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Effect of dequalinium on K1735-M2 melanoma cell growth, directional migration and invasion in vitro.
Cationic lipophilic compounds have an antiproliferative effect on certain tumour systems in vitro and in vivo. We have investigated whether the cationic lipophilic compound dequalinium affects not only proliferation but also motility and invasion of the highly metastatic and highly invasive melanoma cell line K1735-M2. Proliferation was assessed in monolayer cultures and in multicellular spheroids, motility was estimated in the assay of directional migration, and invasiveness was tested through confrontation cultures of tumour multicellular spheroids with embryonic chick heart tissue evaluated by computerized image analysis. 2 mumol/l dequalinium impaired melanoma cell proliferation, reduced directional migration and significantly blocked invasion in vitro. On the ultrastructural level, dequalinium caused obvious changes in mitochondria of both melanoma and embryonic chick heart cells. The mechanisms of the antiproliferative, antimigrating and antiinvasive effects remain to be determined. Inhibition of protein kinase C, calmodulin antagonism, DNA intercalation and/or direct effects on mitochondrial functions may be considered.
Animals↗
No evidence for c-erbB-2 overexpression in cutaneous melanoma.
BACKGROUND: Recent studies have demonstrated the expression of the c-erbB-2 (HER-2/neu) oncoprotein in several malignant tumors and have related its overexpression with poor prognosis. Because cutaneous melanoma is a malignant tumor associated with poor prognosis, we investigated the expression of c-erbB-2 protein in cutaneous melanoma and in melanoma metastatic to the skin. MATERIALS AND METHODS: The expression of c-erbB-2 protein in 20 primary cutaneous melanomas and in 10 melanomas metastatic to the skin was investigated using a semi-quantitative immunohistochemical assay. RESULTS: No specific staining with c-erbB-2 antibody was observed in any of the 20 cases of primary malignant melanoma or 10 cases of melanoma metastatic to the skin. CONCLUSION: c-erbB-2 overexpression does not appear to play a role in the development of primary cutaneous melanoma or in the development of metastatic melanoma, indicating that mechanisms other than c-erbB-2 overexpression are involved in the pathogenesis of cutaneous melanoma.
Humans↗
Langerhans cells in epithelial skin tumors. A quantitative immunohistological and morphometric investigation.
In the present study we investigated whether there is a correlation between Langerhans cell density, peritumoral infiltrate or intraepithelial T-lymphocyte density within 17 epithelial skin tumors using immunohistologic and morphometric methods. We found a significant difference between seborrheic keratosis, basal cell carcinoma, and squamous cell carcinoma. No correlation was found between the Langerhans cell density and the number of intraepithelial T lymphocytes or between Langerhans cell density and the peritumoral infiltrate. A significant (inverse) correlation was found between mean nuclear area of the epithelial tissue and the number of Langerhans cells. These data might indicate that the number of Langerhans cells does not influence the extent of the anti-tumoral immune response, but that there is an association between the differentiation state of the epithelium and Langerhans cell density.
Cell Count↗