Elimination of metabolic cooperation in Chinese hamster cells by a tumor promoter.

Wild-type Chinese hamster V79 cells (6-thioguanine-sensitive) reduce the recovery of 6-thioguanine-resistant cells when they are cultured together at high densities, through a form of intercellular communication (metabolic cooperation). Cooperation is inhibited by 12-O-tetradecanoyl phorbol-13-acetate, rescuing the 6-thioguanine-resistant cells. These results may be useful in the study of an aspect of the mechanism of tumor promotion and in assaying for promoters.

[1]  M. Lewin,et al.  Co-carcinogenic effects of dietary cholesterol in experimental colon cancer , 1978, Nature.

[2]  J. de Vellis,et al.  Cellular interactions uncouple beta-adrenergic receptors from adenylate cyclase. , 1978, Science.

[3]  G. Rovera,et al.  Tumor promoters: effects on proliferation and differentiation of cells in culture. , 1978, Life sciences.

[4]  E. Newcomb,et al.  Malignant mouse melanoma cells do not form tumors when mixed with cells of a non‐malignant subclone: Relationships between plasminogen activator expression by the tumor cells and the host's immune response , 1978, Journal of cellular physiology.

[5]  E. Stanbridge,et al.  Analysis of malignancy in human cells: malignant and transformed phenotypes are under separate genetic control. , 1978, Proceedings of the National Academy of Sciences of the United States of America.

[6]  B. Migeon,et al.  Comparison of contact-mediated communication in normal and transformed human cells in culture. , 1977, Proceedings of the National Academy of Sciences of the United States of America.

[7]  B. Migeon,et al.  Contact-mediated communication of ouabain resistance in mammalian cells in culture , 1977, Nature.

[8]  J. Bertram Effects of serum concentration on the expression of carcinogen-induced transformation in the C3H/10T1/2 CL8 cell line. , 1977, Cancer research.

[9]  H. Witschi,et al.  Enhancement of urethan tumorigenesis in mouse lung by butylated hydroxytoluene. , 1977, Journal of the National Cancer Institute.

[10]  G. I. Bell Models of carcinogenesis as an escape from mitotic inhibitors. , 1976, Science.

[11]  E. Wynder,et al.  Promoting effect of sodium deoxycholate on colon adenocarcinomas in germfree rats. , 1976, Journal of the National Cancer Institute.

[12]  E. Staffeldt,et al.  Comparative enhancing effects of phenobarbital, amobarbital, diphenylhydantoin, and dichlorodiphenyltrichloroethane on 2-acetylaminofluorene-induced hepatic tumorigenesis in the rat. , 1975, Cancer research.

[13]  F. Marks,et al.  Effect of tumor-promoting phorbol esters and of acetic acid on mechanisms controlling DNA synthesis and mitosis (Chalones) and on the biosynthesis of histidine-rich protein in mouse epidermis. , 1974, Cancer research.

[14]  J. Dancis,et al.  Metabolic cooperation in cell culture: Studies of the mechanisms of cell interaction , 1974, Journal of cellular physiology.

[15]  J. Dancis,et al.  Communication between normal and enzyme deficient cells in tissue culture. , 1972, Experimental cell research.

[16]  D. Gaudin,et al.  DNA repair inhibition: a possible mechanism of action of co-carcinogens. , 1971, Biochemical and biophysical research communications.

[17]  R. Evans,et al.  Cooperation of Immune Lymphoid Cells with Macrophages in Tumour Immunity , 1970, Nature.

[18]  E. Neufeld,et al.  Scheie and Hurler Syndromes: Apparent Identity of the Biochemical Defect , 1970, Science.

[19]  C. W. Hall,et al.  Hurler and Hunter Syndromes: Mutual Correction of the Defect in Cultured Fibroblasts , 1968, Science.

[20]  B. L. Van Duuren,et al.  Phenotypic Expression of Transformation: Induction in Cell Culture by a Phorbol Ester , 1967, Science.

[21]  L. Sachs,et al.  THE DIFFERENCE IN CONTACT INHIBITION OF CELL REPLICATION BETWEEN NORMAL CELLS AND CELLS TRANSFORMED BY DIFFERENT CARCINOGENS* , 1966, Proceedings of the National Academy of Sciences of the United States of America.

[22]  J. Tischfield,et al.  Comparative effects of adenine analogs upon metabolic cooperation between Chinese hamster cells with different levels of adenine phosphoribosyltransferase activity. , 1978, Mutation research.