TOSHIO KUROKI and MANFRED F. RAJEWSKY
The focus of this Workshop was on genes, proteins and molecular mechanisms involved in different pathways of repair of various forms of DNA damage, on the relevance of DNA repair for carcinogenesis and cancer therapy, and on some aspects of the molecular epidemiology of DNA damage and mutational spectra. A keynote lecture on "DNA repair: its origins and its importance in carcinogenesis, cancer therapy and environmental risk assessment" was presented by Dr. R.B. Setlow.
Dr. T. Kuroki (Tokyo) discussed the regulation of proliferation and differentiation in epithelial cells from which about 90% of human cancers arise. A 3-dimensional organotypic culture system was established for normal human keratinocytes and the expression of differentiation-associated genes in vitro was demonstrated. It was found that nPKCq, a Ca2+-independent isoform of protein kinase C (PKC), is predominantly expressed in epithelial cells, in close association with epithelial differentiation. Two other PKC isoforms. cPKCa and nPKCS, are also expressed in epithelial tissue, but no cPKCy was detected. Different isoforms of PKC may thus be involved in the control of epithelial proliferation and differentiation. Lastly, epidermal keratinocytes-the target cells in UV-induced carcinogenesis-were shown to be defective in UV-induced unscheduled DNA synthesis (UDS) in Xeroderma pigmentosum (XP) patients, as measured in keratinocytes grown in culture from small skin-biopsy specimens. Dependent on complementation groups, the extent of UDS reduction is similar in the dermal counterpart cells, with the exception of XP variant keratinocytes which, unlike fibroblasts, exhibit the UDS defect to some degree. Dr. F. Hunaoku 'This Workshop (September 2-4,1993) continued the series of biennial Japanese-German Workshops on "Molecular and Cellular Aspects of Carcinogenesis" organized traditionally at the