عنوان

Cancer :

شابک

038790042X

شابک

354090042X

شابک

9780387900421

شابک

9783540900429

شماره

b554474

عنوان اصلي

Cancer :

نام عام مواد

[Book]

ساير اطلاعات عنواني

experiments and concepts

نام نخستين پديدآور

R. Süss, V. Kinzel, J. D. Scribner.

محل نشرو پخش و غیره

New York

نام ناشر، پخش کننده و غيره

Springer-Verlag New York

تاریخ نشرو بخش و غیره

1973

نام خاص و کميت اثر

XX, 285 p. ; 23 cm

متن يادداشت

contact inhibition.- Inhibitors guarantee "contact inhibition".- Membranes regulate cell growth.- Summary.- The mitochondria and Warburg's cancer theory.- Energy production in the respiratory chain.- Glycolysis.- Warburg's manometric methods for measurement of respiration and glycolysis.- Cancer cells glycolyze.- Carcinogens damage respiration.- Omne granum e grano.- Path to the tumor cell: selection of cells capable of glycolysis.- Glycolytic energy is "inferior".- Oxygen deficiency in tumor tissue.- Tumor development in two phases.- Cancer prevention by support of respiration.- Not all tumors show the Warburg effect.- Glycolysis and growth rate of a tumor are correlated.- Summary.- Tumor immunology: basics of a host-specific tumor defense.- Donor-recipient relationships in transplantations.- Transplantable tumors.- Early hopes for a protective injection against tumors.- Tumor-specific antigens in genetically identical animals.- Immune animals can only handle a few cells.- The defense against tumor cells can be pretransferred to a test tube.- Individual tumors have individual antigens.- Virus-induced tumors also have tumor-specific antigens.- Tumor-specific antigens evoke a true immune reaction.- The rejection of syngenic tumor transplants as a model for defense against primary tumors.- A rat can mobilize defenses against its own primary tumor.- Do tumor-specific antigens necessarily belong to tumor growth?.- Are there really tumor-specific antigens?.- Antilymphocytic serum promotes tumor growth.- Chemical carcinogens are immunosuppressives.- The double effect of chemical carcinogens.- Immune therapy.- Enhancement: The paradoxical increase in tumor growth by immunization.- Summary.- Natural history of some tumor viruses.- Chicken leukemias.- Rous sarcoma virus (RSV).- Shope papilloma virus in rabbits.- Bittner's milk factor.- Polyoma.- Mouse leukemia and mouse sarcoma viruses.- Human medical digression.- Human and monkey viruses: adenoviruses and SV-40.- Classification of animal viruses.- Summary.- DNA tumor viruses in tissue culture.- Counting live viruses in the plaque test.- Transformation in vitro.- Transformation and cell death.- The cell can choose between production and transformation.- Masked viruses.- On the trail of masked tumor viruses-virus-specific antigens.- On the trail of masked DNA tumor viruses: virus-specific ribonucleic acids.- Virus DNA is retained in transformed cells.- Unmasking of the tumor virus: cell fusion forces virus production.- The virus DNA is responsible for transformation.- A DNA tumor virus has only a few genes.- Which genes are suspected of transformation?.- The role of the cell once more.- A side glance at RNA tumor viruses.- Summary.- Genetics and cancer.- Chromosome alterations in tumor cells: the Philadelphia chromosome.- Inheritance factors in tumor induction: animal strains with guaranteed tumor incidence.- Tumor induction by species crossing: tumor-bearing hybrids.- "Artificial" carcinogenesis and heredity.- Mutagenic and carcinogenic activity can be correlated.- Mutation hypothesis as a theoretical necessity.- Objections to the mutation theory.- Concluding words on the mutation theory.- Summary.- DNA and carcinogenesis.- Tumor DNA as a carcinogen.- Infectious tumor virus DNA, a potent "chemical carcinogen".- Carcinogens disturb DNA synthesis.- Carcinogens disturb the formation of adaptive enzymes.- Chemical carcinogens react with the cell DNA.- Covalent bonds between carcinogens and guanine.- Eventual consequences of the reactions with guanine.- Cells can repair defective DNA.- Neoplastic transformations work better with proliferating cells.- Binding without bonds: intercalation.- Summary.- A few models for tumor chemotherapy.- Alkylating agents.- Nitrogen mustard with a fuse.- Direct attack on tumor DNA.- Antimetabolites in tumor therapy.- Immunosuppressive side effects.- Asparaginase starves tumor cells.- Labilization of tumor cells by excessive acid.- Many tumor cells are especially heat-sensitive.- Multistep therapy.- Chain reactions lead to a "natural" cell death.- Virus tumor therapy?.- A new star?.- Summary.- Dogmas of tumor induction.- Not all tumor cells grow faster.- Dogma of transformation.- Dogma of selection.- Dogma of isolation.- Transplantability does not have to be a criterion of a tumor.- Dogma of irreversibility.- Dogma of the reprogramed tumor cell.- Summary.- Tumor theories in dialogue.- Summary: a program for a computer.- Appendix: morphological glossary.- Reference works.

متن يادداشت

The impetus for experimental cancer research.- Melancholia carcinogenica.- Cigarette smoking and lung cancer.- Our daily carcinogens.- The Turkey disaster and the anatoxin story.- Pesticides or humanicides.- Asbestos lung cancer.- "Morality" and genital cancer.- Nuns have an increased risk of breast cancer.- Stomach cancer in the poor.- The cancer staircase again.- Summary and prognosis.- A first step: elucidation of tar cancer.- Experimental tumor research before Yamagiwa.- Yamagiwa and Ichikawa induce the first experimental tumors.- A few grams of 3,4-benzpyrene from two tons of tar.- Polycyclic hydrocarbons can induce other than skin tumors.- Theories on the chemical mechanism of hydrocarbon carcinogenesis.- Polycyclic hydrocarbons are bound to protein.- Proteins could be growth regulators.- Polycyclic hydrocarbons also react with DNA.- Summary.- Aromatic amines: activation through metabolism.- Aniline cancer: aniline itself is not to blame.- Butter yellow and the carcinogenic azo dyes.- Acetylaminofluorene, an aborted insecticide.- Not all aminoazo dyes are carcinogenic.- Aromatic amines must be converted to carcinogens via metabolism.- Ortho ring-hydroxylation: increase in carcinogenicity.- N-Hydroxylation, a necessary but not always sufficient step for activation of aromatic amines.- Aminoazo dyes also form N-hydroxy derivatives.- Azo dyes react with methionine.- N-Hydroxy esters as final steps in the activation to the actual carcinogen ("ultimate carcinogens").- Which esters are the "ultimate carcinogens"?.- The N-Hydroxylation hypothesis has its difficulties.- Carcinogenic aromatic amines are bound to protein.- The stronger the carcinogen, the better the binding to protein.- Carcinogenic aromatic amines are bound preferentially to h2-proteins.- H2-Proteins are greatly reduced in hepatomas.- H2-Proteins inhibit the growth of cell cultures (in vitro).- Summary.- A closer look at chemical carcinogenesis: quantitative aspects.- The Iball index.- Dose-response curves.- Carcinogenic effects are irreversible.- Carcinogenesis as an accelerated process.- There are no subthreshold carcinogenic doses.- Carcinogens differ in their acceleration behavior.- Biological significance of acceleration.- Latent periods and tumor yields are not necessarily coupled.- Summary.- Multiple step hypothesis of chemical carcinogenesis.- The Berenblum-Mottram experiment: two steps lead to papillomas.- Not only croton oil can promote.- Irritation and carcinogenesis.- Rous discovers the two-step process in the rabbit's ear.- Croton oil is not a "chemical cork borer".- Two steps are an insufficient description.- Promotion is reversible.- Initiation is irreversible.- The general validity of the two-step hypothesis is questionable.- Syncarcinogenesis: carcinogens can substitute for each other.- Syncarcinogenesis and cocarcinogenesis: more than a question of semantics.- Summary.- Host factors in tumor induction.- The path to the inner sanctum.- Activation of carcinogens as a limiting step in chemical carcinogenesis.- Danger for carcinogens: detoxication reactions.- Reactivation of glucuronides in the urine: bladder cancer.- Phase rule of carcinogenesis.- Tumor cells can be dormant.- Paradoxical influences of nutrition.- Hormone-dependent tumor growth.- Tumor cells must slip past the immune response.- The pattern of metastases is also determined by the host.- Summary: Host factors, or the "game plan" of tumor development.- Tissue-specific growth regulation ("chalones").- Cybernetic model of tissue-specific growth regulation.- Regulation of liver regeneration by humoral inhibitoi.- Skin as a regenerating system ("wound healing").- Stress hormones suppress mitoses.- Epidermal chalone in an in vitro experiment.- Tentative characterization of the epidermal chalone.- Chalones can block mitosis directly.- Alternatives to the chalone theory: wound hormones.- Chalones as repressors.- Tumor cells as dialone mutants.- Substitution therapy of chalone-deficient tumors.- Chalones, a general principle?.- "Visible" regulation fields.- Summary.- Carcinogenesis and cell organelles.- The inner architecture of a cell.- Isolation of cell organelles in the ultracentrifuge.- The cell as a chemical factory.- The nucleus and carcinogenesis.- Lysosomes.- Carcinogenic hydrocarbons are taken up by lysosomes.- Lysosomal DNases as carcinogens.- Cell membranes, cell sociology, and carcinogenesis.- Cell sociology in tissue culture.- Membrane changes in tumor cells.- Neuraminic acid and phospholipids "negativize" cell membranes.- Binding forces betwen cells.- Cell contacts are specific.- Normal cells can regulate tumor cells.- Carcinogenesis from the membrane perspective.- A small natural philosophy of cell membranes.- Is there really a "contact inhibition"? Growth factors vs.

شماره رده

نشانه اثر

مستند نام اشخاص تاييد نشده

R. Süss, V. Kinzel, J. D. Scribner.

مستند نام اشخاص تاييد نشده

John D Scribner

مستند نام اشخاص تاييد نشده

Rudolf Süss

مستند نام اشخاص تاييد نشده

Volker Kinzel

نام الکترونيکي

نوع ماده

[Book]

تكميل شده

Y