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Growth factors and tumor promotion implications for risk assessment : proceedings of the Seventh International Conference on Carcinogenesis and Risk Assessment, held in Austin, Texas, on December 1-4, 1993 by International Conference on Carcinogenesis and Risk Assessment (7th 1993 Austin, Tex.)

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Published by Wiley-Liss in New York .
Written in English

Subjects:

  • Carcinogenesis -- Congresses.,
  • Cocarcinogens -- Congresses.,
  • Growth factors -- Congresses.,
  • Carcinogens -- Testing -- Congresses.,
  • Neoplasms -- etiology -- congresses.,
  • Neoplasms -- physiopathology -- congresses.,
  • Carcinogens -- pharmacology -- congresses.,
  • Growth Substances -- metabolism -- congresses.,
  • Risk Assessment -- congresses.

Book details:

Edition Notes

Includes bibliographical references and index.

Statementeditors, R. Michael McClain ... [et al.].
SeriesProgress in clinical and biological research ;, v. 391
ContributionsMcClain, R. Michael.
Classifications
LC ClassificationsRC268.5 .I54 1993
The Physical Object
Paginationxix, 470 p. :
Number of Pages470
ID Numbers
Open LibraryOL1274284M
ISBN 100471121452
LC Control Number95005805

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Diamond L, O’Brien TG, Baird WM () Tumor promoters and the mechanism of tumor promotion. Adv Cancer Res 1–74 PubMed CrossRef Google Scholar Fujiki H, Suganuma M, Tahira T, Yoshioka A, Nakayasu M, Endo Y, Shudo K, Takayama S, Moore RE, Sugimura T () New classes of tumor promoters: Teleoeidin, aplysiatoxin and by: 8.   Growth factors, defined as polypeptides that stimulate cell proliferation, are major growth-regulatory molecules for cells in culture and probably also for cells in vivo. Nontransformed cells show an absolute requirement for growth factors for proliferation in culture and generally more than one growth factor is required. Under usual culture conditions, growth factors are more rapidly Cited by: The loss of or decreased requirement for specific growth factors is a common occurrence in neoplastically transformed cells and may lead to a growth advantage, a cardinal feature of cancer cells. Dear Sir: Fontana et al have shown a strong effect of a low-protein, low-calorie diet and endurance running on circulating concentrations of several growth-promoting hormones and other clinical study was well done, and the dietary associations with the clinical biomarkers are internally consistent. Of particular interest is the finding of a substantial depressing effect of a.

growth factor receptors and downstream signaling proteins, proteins involved in cell cycle checkpoints. 2. Mutational inactivation of apoptotic (cell death) pathways (e.g. growth inhibitory receptors, proteins involved in apoptosis, tumor suppressors). 3. Mutational inactivation of DNA repair mechanisms (e.g. BER, NER, etc). 4. Tumor growth (tumor promotion) is the sum total of a malignant cell proliferation versus cell death. Both processes are strongly affected by inflammation and inflammatory cytokines produced by immune cells, which infiltrate the tumor, such as IL-6 and TNF-α, as they can be used as mitogens and survival factors for premalignant cells (Horng. The epidermal growth factor (EGF) proteins promote cell proliferation and differentiation by binding to the EGF receptor (EGFR), a tyrosine kinase receptor present on the cell surface. This can be blocked by the EGFR inhibitor monoclonal antibody cetuximab, or small molecules that block the tyrosine kinase enzymes (TKIs) such as gefitinib and. tumor regrowth or doubling, tripling, or quadrupling times. Two oth ers (15, 16) analyzed animal survival times but not tumor volumes. Of the articles where ANOVA was used, three () used the Duncan multiple-range test (17) to account for multiple comparisons. One article (14) fit a Gompertz curve to tumor growth in an untreated.

Erika L. Abel, John DiGiovanni, in The Molecular Basis of Cancer (Fourth Edition), Promotion. During the tumor promotion phase of carcinogenesis, growth stimuli and other factors promote clonal expansion of initiated cells. This stage is characterized by altered gene expression and proliferation of initiated cells, some of which maintain stemlike characteristics.   Tumor cells play a critical role in shaping the TME by secreting various cytokines and growth factors, thus continuously modulating its resistance to therapy and immune response. Proinflammatory cytokines and growth factors such as IL-6 and IL-8 have been established as important NO-induced biomarkers that are up-regulated in breast cancer. Growth Factors, Cytokines and Cancer. Growth factors regulate the fundamental cellular process of proliferation and differentiation. Overproduction of growth factors is a common feature of tumor cells, stimulating inappropriate and unregulated proliferation of themselves in an autocrine fashion, and of adjacent cells in a paracrine fashion. Carcinogenesis, also called oncogenesis or tumorigenesis, is the formation of a cancer, whereby normal cells are transformed into cancer process is characterized by changes at the cellular, genetic, and epigenetic levels and abnormal cell division is a physiological process that occurs in almost all tissues and under a variety of circumstances.