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2 edition of Population kinetics of normal, transforming and neoplastic cell lines. found in the catalog.

Population kinetics of normal, transforming and neoplastic cell lines.

Klas Norrby

Population kinetics of normal, transforming and neoplastic cell lines.

by Klas Norrby

  • 369 Want to read
  • 28 Currently reading

Published by Munksgaard in Copenhagen .
Written in English

    Subjects:
  • Cell proliferation.,
  • Cancer cells -- Proliferation.

  • Edition Notes

    Bibliography: p. 46-49.

    StatementStatistics by Esbjörn Carlström. Translation by Klas Magnus Lindskog.
    SeriesActa pathologica et microbiologica Scandinavica. Supplementum, no. 214
    Classifications
    LC ClassificationsRC269 .N6713
    The Physical Object
    Pagination50 p.
    Number of Pages50
    ID Numbers
    Open LibraryOL4859943M
    LC Control Number75851402

    Initiation and promotion of neoplastic cell transformation have also been demonstrated in vitro in mouse and rat cell culture systems (Table ). Initiation occurs when a tissue is treated with low levels of a complete carcinogen or an initiator, and is an irreversible process (Figure ). Integrating Proteomics and Enzyme Kinetics Reveals Tissue-Specific Types of the Glycolytic and Gluconeogenic PathwaysCited by:

    Suggested Citation:"2 Molecular and Cellular Responses to Ionizing Radiation."National Research Council. Health Risks from Exposure to Low Levels of Ionizing Radiation: BEIR VII Phase gton, DC: The National Academies Press. doi: / Cancer cells seemed to have lost these genes, ostensibly through mutations that resulted in inactivated versions of the genes present in normal cells. When reintroduced into the cancer cells via cell fusion, the normal alleles reimposed control on the cancer cells, restoring their behavior to that of a normal cell.

    contents in brief. 1 overview of the immune system, 1. 11 activation and function of t cells, 2 innate immunity, 12 cytokines, 3 adaptive immunity,   Searches for effective yet nontoxic oncotherapies are searches for exploitable differences between cancer and normal cells. In its core of cell division, cancer resembles normal life, coordinated by the master transcription factor MYC. Outside of this core, apoptosis and differentiation programs, which dominantly antagonize MYC to terminate cell division, necessarily differ between cancer and Cited by: 6.


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Population kinetics of normal, transforming and neoplastic cell lines by Klas Norrby Download PDF EPUB FB2

Get this from a library. Population kinetics of normal, transforming and neoplastic cell lines. [Klas Norrby]. Abstract.

The preceding chapters in this book have largely been concerned with the morphological description of the death of cells, with its mechanisms, and the role of cell death in maintaining tissue homoeostasis; in this chapter, however, we approach the phenomenon as a Cited by: The major problem in the therapy of the cancer patient is presented by disseminated neoplastic lesions, either primary (e.g.

leukemia) or secondary (metastases from primary tumors). BASERGA, R. (ED.): The cell cycle and cancer, vol. In: the biochemistry of disease. Population kinetics of normal, transforming and neoplastic cell lines Author: R.

Baserga. Read this article to learn about cell transformation and general characteristics of transformed cells. The four aspects of Cell Transformation are: (1) Genetic Instability (2) Immortalization (3) Aberrant Growth Control and (4) Tumorigenicity. Cell transformation due to changes in the genetic material, Population kinetics of normal cell cloning involving the production of a population single cell are described here.

Transforming growth factor-β1 cooperates with anti-immunoglobulin for the induction of apoptosis in group I (biopsy-like) Burkitt lymphoma cell lines March Blood 87(3) The normal stem cell reserve contains cells that can replicate, differentiate, or die.

These cells are grouped into two compartments, proliferating (P) and nonproliferating (Q) liferating cells are G 1-phase cells grouped together with quiescent cells are activated and transmitted to the proliferating compartment at a rate (β(Q)) that is reciprocal to the number of.

Function. CD is a cytokine receptor expressed on the surface of hematopoietic stem cells as well as other cell types. Altered forms of this receptor may be associated with some types of cancer.

CD is a receptor tyrosine kinase type III, which binds to stem cell factor (a substance that causes certain types of cells to grow), also known as "steel factor" or "c-kit ligand".Aliases: KIT, C-Kit, CD, PBT, SCFR, KIT proto.

applications of cell lines as bioreactors and in vitro models Article (PDF Available) in International Journal of Applied Biology and Pharmaceutical Technology 2(4) October with. The long-term survival of a tissue, either normal or neoplastic, is dependent on its capacity to self-renew, whereas its overall size is determined by the balance between the rates of cell proliferation and cell death (or removal) across its various components.

38 In normal tissues, stem cell numbers are under tight genetic regulation Author: Piero Dalerba, Michael F. Clarke, Irving L. Weissman, Maximilian Diehn. As applied to stem cell fractionation, Visser et al were the first to use flow sorting based on wheat germ agglutinin binding as a means to enrich (6-fold) CFU-S compared with unfractionated bone marrow cells.

66 Later it was possible to sort on the basis of cell cycle status using Hoechst dyes, and in this way CFU-S were distinguished from the Cited by: Mitosis, or cell division, is the basic biologic process that results in an increase in somatic cell numbers over time. The term growth applies to the increasing volume of a cellular population and is measured in units of volume (eg, cubic centimeters) or weight (eg, milligrams).

Growth is largely the consequence of increasing numbers of cells but also can be influenced by the increasing size. Cancer stem cells (CSCs) are similar to normal stem cells in their ability to self‐renew and to generate large populations of more differentiated descendants.

In contrast to theCited by:   Self-replication is the engine that drives all biologic evolution, including neoplastic evolution. A key oncotherapy challenge is to target this, the heart of malignancy, while sparing the normal self-replication mandatory for health and life.

Self-replication can be demystified: it is activation of replication, the most ancient of cell programs, uncoupled from activation of lineage Cited by: 5.

Cambridge Core - Oncology - The Biological Basis of Cancer - by Robert G. McKinnellCited by: The cell population from the center of the tumor has normal intercellular connections, with the presence of desmosomes and junctional complexes, while these are absent or reduced at the periphery. In areas with a high invasive rhythm, cells are completely detached from the tumor mass, and interconnections disspear altogether [ 74 ].Cited by: 8.

Pancreatic cancer (PC) is the third leading cause of adult cancer mortality in the United States. The poor prognosis for patients with PC is mainly due to its aggressive course, the limited efficacy of active systemic treatments, and a metastatic behavior, demonstrated throughout the evolution of the disease.

On average, 80% of patients with PC are diagnosed with metastatic disease, and the Cited by:   The mammary gland epithelial components are thought to arise from stem cells that undergo both self-renewal and differentiation.

Self-renewal has been shown to be regulated by the Hedgehog, Notch, and Wnt pathways and the transcription factor B lymphoma Mo-MLV insertion region 1 (Bmi-1). We review data about the existence of stem cells in the mammary gland and the pathways Cited by: Due to the rigorous aseptic techniques, this is one of the most famous cell lines (described in many articles, e.g., cell line birthday was celebrated annually in the New York World Telegram); it was maintained until when the cell line culture was finally terminated, 2 years after Carrel's death.

Carrel's cell line was a phenomenon for Cited by: 6. Daniel ("Dan") Walter Nebert is an American physician-scientist, molecular biologist, and geneticist.

He has authored/coauthored publications in fields of biochemistry, molecular biology, pediatrics, developmental biology, pharmacology, drug metabolism, toxicology, mouse genetics, human genetics, evolutionary genomics, gene nomenclature, and cancer.

Alma mater: Wesleyan University, Connecticut. You can write a book review and share your experiences. Other readers will always be interested in your opinion of the books you've read.

Whether you've loved the book or not, if you give your honest and detailed thoughts then people will find new books that are right for them., Free ebooks since.

Unfortunately, this book can't be printed from the OpenBook. If you need to print pages from this book, we recommend downloading it as a PDF. Visit to get more information about this book, to buy it in print, or to download it as a free PDF. The hepatitis B virus X gene (HBX 1) transcript was expressed at a much higher level than that observed in vivo (Hohne et al.

). In subsequent studies, it was concluded that overexpression of the HBX was required for malignant transformation of the cell line (Seifer et al. ).Cited by: In this study, we demonstrated that the TNC + cell population has a 43% overlap with the CD + cell population in the HSR-GBM1 cell line and overlaps with part of the CD – cell population.

Previous investigations have indicated that CD – cells also have the capability to generate GBM tumors in immunodeficient nude mice or by: