By R. M. MacKie (auth.), Dirk J. Ruiter MD, Kees Welvaart MD, Soldano Ferrone MD (eds.)
In fresh years a lot development has been made in wisdom and figuring out of the biology of cutaneous cancer. during this recognize etiological elements, prognostic components, antigen expression of cancer cells, immune reaction and mechanisms of metastasis formation must be pointed out. it's the goal of this publication to offer a evaluation on basic facets, prognosis and analysis, and therapy of cutaneous cancer and precursor lesions. additionally, formerly unpublished new information are awarded. A post-graduate Boerhaave direction "Cutaneous cancer and Precursor Lesions" was once held at Leiden collage on 12 and thirteen April,. 1984. The court cases are contained during this quantity. The editors want to thank all audio system and chairpersons at the direction, the Boerhaave Committee for its contribution to the supplier of the direction, Upjohn Nederland for its monetary aid and Mrs. I.A. Kruyff for her secretarial information. Dirk Ruiter, Kees Welvaart and Soldano Ferrone, Leiden and Valhalla (NY), June, 1984. VII CONTENTS Preface v Contents VII checklist of First Authors with Co-Authors XI half I: primary elements. The epidemiology of cancer R.M. MACKIE The molecular biology of carcinogenesis nine A.W.M. VAN DER KAMP AND N.G.J. JASPERS 19 Human cancer linked antigens pointed out with monoclonal antibodies: characterization and strength medical program P.G. NATALI, R. CAVLIERE, M. MATSUI, G. BURAGGI, L. CALLEGARO, and S. FERRONE mobile and molecular parameters of tumor development in 38 human malignant cancer J. BRUEGGEN, E.B. BROECKER, L. SUTER, ok. REDMANN, and C.
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Extra info for Cutaneous Melanoma and Precursor Lesions
In this procedure microtiter plates are coated with monoclonal antibodies to a MAA. information has been derived from the application the Then serum is added to the plates. The MAA bound of by the first antibody is measured by adding and quantitating a radiolabelled monoclonal spatially antibody directed to a determinant which is distant from that identified by the first antibody, distinct and but located 27 on the same molecule. DDIAs in microtiter plates are sensitive, reproducible and suitable to screen large numbers of samples.
T. t. J ...... j>. N 25 the panel. Table II summarizes the most frequent phenotypes found in benign and malignant lesions of melanocyte origin. Table 2 Most frequent phenotypes found in benign and malignant lesions of melanocyte origin Cases Junctionalcompound nevi 9/18° Intradermal nevi 15/30 HMW-MAA + 100K MAA + + + + + Class I I HLA + Blue nevi 9/22 Lentigo maligna (LM) 3/4 + + LM melanoma 3/5 + + Superficial 7/16 spreading melanoma + + + Nodular melanoma 6/17 + + + 10/56 + + + Metastatic melanoma Class HLA 115K MAA + + + + + + o n° lesions expressing the indicated combination of antigens/n° lesions tested.
We further determined the production of a tumor angiogenic activity which is important for the neovascularization of tumors (19). As a third parameter we studied the growth of melanoma cells in the nude mouse which distinguishes malignant from normal tissue (20). The plasminogen activator (PA) production of seven melanoma lines ranged from high (A-375) to no detectable (SK Mel-25) activity (for details see 13). The cell lines differed to a great extent in their capacity to grow in the nude mouse: 6 melanoma lines were positive whereas SK Mel-25 was negative.