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2 edition of Growth kinetics and biochemical regulation of normal and malignant cells found in the catalog.

Growth kinetics and biochemical regulation of normal and malignant cells

Symposium on Fundamental Cancer Research Anderson Hospital and Tumor Institute 1976.

Growth kinetics and biochemical regulation of normal and malignant cells

a collection of papers presented at the twenty-ninth annual Symposium on Fundamental Cancer Research, 1976

by Symposium on Fundamental Cancer Research Anderson Hospital and Tumor Institute 1976.

  • 336 Want to read
  • 4 Currently reading

Published by Published for the University of Texas System Cancer Center, M. D. Anderson Hospital and Tumor Institute [by] Williams & Wilkins Co. in Baltimore .
Written in English

    Subjects:
  • Cell proliferation -- Congresses.,
  • Cellular control mechanisms -- Congresses.,
  • Cancer cells -- Growth -- Regulation -- Congresses.

  • Edition Notes

    Includes bibliographies and indexes.

    StatementBenjamin Drewinko and Ronald M. Humphrey, editors.
    ContributionsDrewinko, Benjamin., Humphrey, Ronald M.
    Classifications
    LC ClassificationsQH587 .S95 1976
    The Physical Object
    Paginationxv, 900 p. :
    Number of Pages900
    ID Numbers
    Open LibraryOL4898538M
    LC Control Number76041425

      Also, cell-to-cell contacts initiate prolonged nuclear localization of p21 that leads to growth arrest and apoptosis and this effect may have been accentuated due to exogenous p21 up-regulation. Normal alveolar epithelial cells or A cells, exposed to sub-lethal doses of cigarette smoke, over-express p21 and undergo cellular senescence both. Fig. 3. HCS of Ca 2+ kinetics with automated fluorescence microscopy. Screen shot from the Pathway Bioimager showing Ca 2+ changes over time (seconds) in Fura‐2‐labeled C6 cells exposed to ATPs (50 μM) first and then to the Ca 2+ ionophore, ionomycin (1 μM).The upper graph shows color‐coded, single‐cell Ca 2+ responses (one trace = one cell; cells being imaged) and the lower.

    The daily percentage of cells proliferating and dying were determined for normal, premalignant, and cancerous prostatic cells within the prostate as well as for prostatic cancer cells in lymph. SUMMARY Growth kinetics, i.e., the relationship between specific growth rate and the concentration of a substrate, is one of the basic tools in microbiology. However, despite more than half a century of research, many fundamental questions about the validity and application of growth kinetics as observed in the laboratory to environmental growth conditions are still unanswered.

    The relationship of signaling to cellular growth and death, transcriptional regulation, mitosis, cellular differentiation and organogenesis, cell adhesion, motility and chemotaxis are more complex topics under investigation. Alterations in signaling leading to oncogenesis, unregulated growth and . Besides its canonical role in stabilizing telomeres, telomerase reverse transcriptase (TERT) may promote tumor growth/progression through extra-telomeric functions. Our previous in vitro studies demonstrated that short-term TERT inhibition by BIBR (BIBR), an inhibitor of TERT catalytic activity, negatively impacts cell proliferation and viability via telomeres’ length-independent.


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Growth kinetics and biochemical regulation of normal and malignant cells by Symposium on Fundamental Cancer Research Anderson Hospital and Tumor Institute 1976. Download PDF EPUB FB2

Growth kinetics and biochemical regulation of normal and malignant cells. Baltimore: Published for the University of Texas System Cancer Center, M.D. Anderson Hospital and Tumor Institute [by] Williams & Wilkins Co., (OCoLC) Full text Full text is available as a scanned copy of the original print version.

Get a printable copy (PDF file) of the complete article (K), or click on a page image below to browse page by by: We’d like to understand how you use our websites in order to improve them. Growth Kinetics and Biochemical Regulation of Normal and Malignant Cells. (PMCID:PMC) Full Text Citations; Related Articles; Data; BioEntities; External Links; Br J Cancer.

May; 37(5): – PMCID: PMC Growth Kinetics and Biochemical Regulation of Normal and Malignant Cells. Growth Kinetics and Biochemical Regulation of Normal and Malignant Cells By B. Lord Topics: Book ReviewAuthor: B. Lord. Drewinko B, Humphrey RM: Growth kinetics and biochemical regulation of normal and malignant cells.

29th annual symposium on fundamental cancer research, MD Anderson Hospital and Tumor Institute. Baltimore: The Williams and Wilkins Co., Google Scholar. Growth kinetics and biochemical regulation of normal and malignant cells: a collection of papers presented at the twenty-ninth Annual Symposium on Fundamental Cancer Research, Baltimore: Williams & Wilkins, Country of Publication: United States Publisher: Baltimore: Williams & Wilkins, Description: p.

KINETICS OF TUMOR GROWTH DEATH DlFFERENTIATlON t INHIBITOR FACTOR ui iynthesir DNA Slish 10 to h) Fig. cycle. Schematic description. For each phase of the cell cycle, the mean duration and the limits of the 95% confi- dence interval are given (for human tumors).

Growth Kinetics and Biochemical Regulations of Normal and Malignant Cells () Williams and Wilkins Baltimore Denekamp, M.M. Ball, Survival of mouse skin epithelial cells following single and divided doses of x-rays Radiat Res () 4.

Schiffer LM, Braunschweiger PG, Poulakos L () Studies on the cell kinetics of human solid tumors. In: Drewinko B, Humphrey RM (eds) Growth kinetics and biochemical regulation of normal and malignant cells.

Williams and Wilkins, Baltimore, pp – Google Scholar Livingston RB, Sulkes A, Thirlwell MP, Murphy WK, Hart JS: Cell kinetic parameters: correlations with clinical response. In: Drewinko B, Humphrey RM (eds) Growth kinetics and biochemical regulation of normal and malignant cells. Baltimore, Williams & Wilkins,pp – Google Scholar.

Abstract. Until recently it was accepted that a hallmark of malignant cells was their lack of responsiveness to normal growth regulation. In fact, malignant cell populations were generally characterized as being rapidly growing and out of control.

Malignant gliomas are highly aggressive tumors of the central nervous system that rely on production of growth factors for tumor progression. Vascular endothelial growth factor (VEGF), interleukin-8 (IL-8), and tumor necrosis factor-α, for example, are up-regulated in these tumors to promote angiogenesis and proliferation.

RNA stability, mediated through adenine and uridine-rich elements (ARE. Watson, The cell proliferation kinetics of the EMT6/M/AC mouse tumour at four volumes during unperturbed growth in vivo, Cell Tissue Kinet.

9, – (). Google Scholar We use Monod cell kinetics to describe the rates of cell proliferation (growth) and death-an empirical relation based on Michaelis-Menten enzymatic kinetics, which has a theoretical basis, and has. Papers on the mechanisms of growth control in normal and malignant breast epithelium; the biochemical and structural analysis of the nerve growth factor receptor; and the isolation, molecular cloning, and mechanism of action of parathyroid hormone-related protein are also considered.

Kinetics of growth refers to the rate at which the number of individual cells (or, more general, of active biomass) changes in a defined system. Analogous to normal tissues (see Chapter II), benign and malignant tumors have two basic components: (1) proliferating neoplastic cells that constitute their parenchyma; and (2) supportive stroma made up of connective tissue and blood vessels.

The parenchyma of neoplasms is characteristic of the specific cells of origin. Tumor growth and evolution are critically dependent on the non. This book is composed of five parts encompassing 21 chapters that specifically describe the initiation and progression of colon cancer cells.

After briefly dealing with the major issues in colorectal carcinoma, this book goes on presenting the in vitro and in vivo models of colon carcinogenesis.

normal melanocytes with the SV40 large T antigen altered specific growth patterns and cell-cyclc kinetics. Our findings indicate that thc SV40 large T-antigen augments progression of melanocytes through the cell cycle and reduces their requirement for basic fibroblast growth factor (bFGF) an essential melanocyte mitogcn.

Metabolic transformations of malignant cells are essential to the development and progression of all cancers. The understanding of the pathogenesis and progression of cancer requires the establishment of the altered genetic/metabolic factors that are essential to the development, growth, and proliferation of the malignant cells.

Recognition of this important relationship has resulted in a.Through our expertise, Cyclacel is developing cell cycle-based, mechanism-targeted cancer therapies that emulate the body's natural process in order to stop the growth of cancer cells. This approach can limit the damage to normal cells and the accompanying side effects caused by conventional chemotherapeutic agents.Microbial Growth Kinetics opens with a critical review of the history of microbial kinetics from the 19th century to the present day.

The results of original investigations into the growth of soil microbes in both laboratory and natural environments are summarised. The book emphasises the analysis of complex dynamic behaviour of microorganism populations.5/5(1).