Cancer Metastasis: Molecular and Cellular Biology, Host by E. V. Sugarbaker, D. N. Seckinger, O. O. Frankfurt (auth.),

By E. V. Sugarbaker, D. N. Seckinger, O. O. Frankfurt (auth.), Prof. Dr. Volker Schirrmacher, Dr. Reinhard Schwartz-Albiez (eds.)

These are the court cases of the 2d foreign Metastasis Congress of the Metastasis learn Society which came about within the city corridor (Stadthalle) of Heidelberg, FRG, in September, 1988. this primary Metastasis Congress within the FRG used to be prepared along side the German organization of melanoma learn (SEK) of the German melanoma Society. The congress subject generated large curiosity and attracted approximately four hundred scientists from 22 international locations. such a lot individuals got here from Europe, Israel, and the U.S.. Why did we set up the Metastasis Congress? basically approximately 50% of every body who advance a few kind of melanoma are curable. regardless of more suitable sufferer care and more and more cutting edge and powerful ideas for diagnosing and treating basic cancers, the improvement of secondary melanoma colonies, i. e. , metastasis, can't be avoided and is the main reason behind dying. within the Federal Republic of Germany there are nonetheless as many as one hundred sixty 000 melanoma sufferers according to yr who succumb to their disorder, frequently after sessions of bad pain, and this total determine isn't enhancing. partially as a result of the complexity of the method, easy learn on metastasis has lagged at the back of different disciplines comparable to carcino­ genesis and melanoma genetics. Metastasis formation contains the facility of malig­ nant cells to invade adjoining tissue and to penetrate into lymphatic or blood circulatory platforms, or either, and to unfold to close or far-off websites to shape new tumor colonies. in the meantime, study on metastasis is receiving a lot attention.

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Extra resources for Cancer Metastasis: Molecular and Cellular Biology, Host Immune Responses and Perspective for Treatment

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In collaboration with Dr. Israel Vlodavsky we analyzed the capacity of the invasive hybrids to degrade extracellular matrix (ECM) material formed by bovine aortic endothelial cells (N aparstek et al. 1984). Neither the noninvasive BW5147 cell line nor the invasive hybrids were able to degrade ECM material. In addition no urokinase- or tissue-type plasminogen activator activity could be detected in the conditioned medium of either cell types. So, thus far we have found no differences in properties associated with metastatic capacity between invasive and noninvasive T cell hybrids.

This view also highlights the need to develop comparative staging systems for experimental animals tumors, of which few, if any, presently exist. 26 R. S. Kerbel et al. Acknowledgments. The excellent secretarial assistance of I. Stratton and L. Woodcock is gratefully acknowledged. K. is a Terry Fox Scientist of the National Cancer Institute of Canada. References Fidler II (1986) Cancer and Metastasis Rev 5:29-49 Heppner GH, Miller ME, Miller FR (1983) Biochim Biophys Acta 695:215-226 Her/yn M, Balaban G, Beunicelli J, Guerry D, Halaban R, Her/yn D, Elder DE, et al (1985) INCI 74:283-289 Hill RP, Young SD, Cillo C, Ling V (1986) Cancer Rev 5:118-151 Holzmann B, Brocker EB, Lehmann JM, Ruiter DJ, Sorg C, Riethmtiller G, Johnson JP (1987) Int J Cancer 39:466-471 Kerbel RS, Waghorne C, Man S, Elliott BE, Breitman ML (1987) Proc Natl Acad Sci USA 84:1263-1267 Kerbel RS, Waghorne C, Korczak B, Lagarde A, Breitman M (1988) Cancer Surv, (in press) Korczak B, Robson IB, Lamarche C, Bernstein A, Kerbel RS (1988) Mol Cell Bioi 8:3143-3149 Ling V, Chambers AF, Harvis JF, Hill RP (1985) Cancer Metastasis Rev 4:173-194 Miller FR (1981) Invasion Metastasis 1:220-226 Nowell PC (1976) Science 56:561-569 Poste G, Greig R (1982) Invasion Metastasis 2:137-177 Price J (1987) Development 101:409-419 Talmadge JE, Fidler II (1982) Nature 297:593-594 Talmadge JE, Zbar B (1987) JNCI 178:315-320 Vaage J (1988) Int J Cancer 41:855-858 Waghorne C, Kerbel RS, Breitman ML (1987) Oncogene 1:149-155 Waghorne C, Thomas M, Lagarde A, Kerbel RS, Breitman ML (1988) Cancer Res, 48:6109-6114 Weiss L (1986) Cancer Rev 3:1-24 Oncogenes and Tumor Progression: State of the Art* F.

Subsequent selection for a cotransfected selectable marker and, after that, for the invasive phenotype should result in invasive transfectants with a reduced amount of human chromosome 7-specific DNA sequences. Repeated transfection rounds should allow isolation of the human DNA sequences responsible for the induction of the invasive phenotype. Although thousands of transfectants were screened, clonally as well as in mass selections, up to this point no invasive transfectants could be isolated.

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