5 edition of Cell transformation and radiation-induced cancer found in the catalog.
|Statement||edited by K.H. Chadwick, C. Seymour, B. Barnhart.|
|Series||Publication no. EUR 12248 of the Scientific and Technical Communication Unit, Commission of the European Communities, Directorate-General Telecommunications, Information Industries and Innovation, Luxembourg, EUR (Series) ;, 12248.|
|Contributions||Chadwick, K. H. 1937-, Seymour, C., Barnhart, Benjamin J., Ireland. Nuclear Energy Board., United States. Dept. of Energy., Commission of the European Communities.|
|LC Classifications||RC268.55 .C45 1989|
|The Physical Object|
|Pagination||xi, 414 p. :|
|Number of Pages||414|
|LC Control Number||89024698|
Radiation impedes cancer cell growth by inducing cytotoxicity, mainly caused by DNA damage. However, radiation can also simultaneously induce multiple pro-survival signaling pathways, such as those mediated by AKT, ERK and ATM/ATR, which can lead to suppression of apoptosis, induction of cell cycle arrest and/or initiation of DNA repair. Purchase Viruses, Cell Transformation, and Cancer, Volume 5 - 1st Edition. Print Book & E-Book. ISBN ,
Radiation-induced release of TGF-α activates the EGF receptor and MAPK pathway in carcinoma cells leading to increased proliferation and protection from radiation-induced cell death. Mol Biol Cell ; – Crossref, Medline, ISI, Google Scholar: Joiner MC, Lambin P, Malaise EP, Robson T, Arrand JE, Skov KA, et al. NCI's Dictionary of Cancer Terms provides easy-to-understand definitions for words and phrases related to cancer and medicine.
spontaneous cancer (Mitchel et al. ) as well as radiation-induced can- cer (Mitchel et al. ), it would appear that, at least within a certain R. E. J. Mitchel. Mechanisms of Cell Survival Following Space Radiation-Induced Mitotic Catastrophe: Implications for Cancer Risk Risk of Radiation Carcinogenesis Cancer Determine the role of radiation quality on carcinogenesis and shared biology with other degenerative diseases.
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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 : P.J.
Smith. ISBN: OCLC Number: Notes: "Proceedings of a workshop jointly organised by the Nuclear Energy Board of Ireland, the United States Department of Energy, and the Commission of the European Communities, held in Dublin, Ireland, on April ".
Cell Transformation and Radiation-induced Cancer The Short ranged, monoenergetic electrons produced by soft x-rays have been found to be more effective than conventional x-rays in a variety of radiobiological studies.
First results on the action of soft x-rays came from experiments with Drosophi. The preceding discussion of potential mechanisms for radiation-induced cancer has indicated an important role for radiation-induced DNA DSBs, damage response pathways, and gene or chromosomal mutations in the initial events leading to cancer development.
Radiation can cause cancer in most parts of the body, in all animals, and at any age, although radiation-induced solid tumors usually take 10–15 years, and can take up to 40 years, to become clinically manifest, and radiation-induced leukemias typically require 2–9 years to appear.
SOD2 activity modulates radiation induced transformation frequency. Initially, we determined whether changes in SOD2 activity affect cellular redox environment and plating efficiency (Figure 1). Exponentially growing asynchronous cultures of MEFs were harvested and total cellular protein extracts were used for measurements of antioxidant enzyme.
CANCER LETTERS ELSEVIER Cancer Letters () Inhibitory action of (-)-epigallocatechin gallate on radiation-induced mouse oncogenic transformation Kenshi Komatsu'1'*, Hiroshi Tauchi'1, Nozomi Yano'1, Satoru Endo'1, Shinya Matsuura'1, Shuneki Shoji1' ''Department o/Radiation Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University.
This book discusses human cell transformation advances in cell models for the study of cancer and aging. Papers come from a conference at Cell transformation and radiation-induced cancer book University in June and cover a range of topics ranging from different types of cancer to tumor microenvironment, homogeneity, and future therapies.
Cancer Res. ;76(5) Demaria S, Formenti SC. Can abscopal e ects of local radiotherapy be predicted by modeling T cell tra cking. J Immunother Cancer. ; doi: 1 0. 11 8 6 / s 4 0 4 2 5 - 0 1 6 - 0 1 3 3 - 1.
Lung cancer molecular markers. The search for a cancer biomarker or targetable genetic aberration requires years of preclinical studies in vitro and in tly there are approximately a dozen biomarkers that have demonstrated clinical benefit and another dozen are currently under investigation ().Of these, several are considered lung cancer driver genes by the NCI’s lung cancer.
This thoroughly revised 3rd Edition explores the scientific basis for our current understanding of malignant transformation and the pathogenesis and treatment of cancer. A team of leading experts thoroughly explain the molecular biologic principles that underlie the diagnostic tests and therapeutic interventions now being used in clinical.
Sensitization of cancer cells to the cytotoxic effect of radiation by adjuvant therapy targeting oncogenic signaling circuitries may represent a promising approach toward improving radiation outcome (Begg et al., ).In this regard, activation of the mTOR pathway has been recently recognized as a frequent event driving neoplastic transformation, including HNSCC (Molinolo et al., ), the.
Figure 4. Resisting cell death. The p53 tumor suppressor protein is encoded by the TP53 gene in humans. In normal cells, p53 suppresses abnormal growth in part through interactions with the proapoptotic protein Bax, whereas in tumor cells, mutations in the TP53 gene lead to loss of tumor suppression, loss of interaction with Bax, and inhibition of apoptosis.
Download PDF: Sorry, we are unable to provide the full text but you may find it at the following location(s): g (external link). The idea that cell killing is caused by radiation effects on cell membranes is not new. InAlper 30 proposed that in addition to DNA, cell membranes were also a target for radiation damage, especially in well-oxygenated cells.
This idea was lent support by studies, mainly in the s, showing that lipid-soluble vitamins and anaesthetics modify radiation response. 31 The idea of. Malignant transformation of an established simple cyst is exceptionally rare and may never happen but it is possible for a renal cell carcinoma to present as an apparently simple cyst initially.
12 Reports of these rare malignant, simple cysts usually show that the cyst is large and symptomatic in its own right at presentation. Likewise, in endemic areas of the world, hydatid disease may very.
DiPaolo JA. Quantitative in vitro transformation of Syrian golden hamster embryo cells with the use of frozen stored cells. J Natl Cancer Inst. Jun; 64 (6)– Donaldson K, Li XY, Dogra S, Miller BG, Brown GM.
Asbestos-stimulated tumour necrosis factor release from alveolar macrophages depends on fibre length and opsonization. Radiation induced senescence in securin-deficient breast cancer cells through the ATM and p38 pathways.
Western blot analysis was first used to confirm the securin protein levels in MCF-7 (low securin expression; p53 wild-type), MDA-MB (high securin expression; pmutant) and securin-knockdown MDA-MBA (pmutant) human breast cancer cells (Fig.
1A, lower). When indicated, BEPCs were irradiated by exposing them to Cs γ-rays at a dose rate of 5 Gy/minute using an IBL C source.
The doses used in the experiments to assess radiation-induced transformation of breast cells in the present study were 0, 1, and 2 Gy. Clonogenic survival assays usually require cell transformation, which can interfere with the inherent radiosensitivity of cells [41,42,43], and variations in radiation-induced cell survival between different cell types from the same individual complicate assessments [44,45].
It has been observed by many investigators that radiation- induced transformation in vitro can be modified in the same way as radiation- induced cancer in animals, with the yields of malignant cells varying similarly in response to different characteristics of the radiation (such as total dose, dose rate, fractionation pattern, linear energy.
To understand how cancer develops and progresses, researchers first need to investigate the biological differences between normal cells and cancer cells.
This work focuses on the mechanisms that underlie fundamental processes such as cell growth, the transformation of normal cells to cancer cells, and the spread, or metastasis, of cancer cells.CANCER RESEARCH January I.
Advances in Brief Radiation-induced Neoplastic Transformation of Human Prostate Epithelial Cells' Michael R. Kuettel,2 Peter J. Thraves, Mira Jung, Susan P. Varghese, Sarada C. Prasad, Johng S. Rhim, and.