by U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Cancer Institute, International Cancer Research Data Bank, Supt. of Docs., G.P.O. [distributor in [Bethesda, Md.?], Washington, DC .
Written in English
|Other titles||Selected abstracts on the cell cycle in cancer prognosis.|
|Statement||Arthur B. Pardee, consulting reviewer.|
|Contributions||International Cancer Research Data Bank.|
|The Physical Object|
|Pagination||x, 127,  p.|
|Number of Pages||127|
Cancer comprises many different diseases caused by a common mechanism: uncontrolled cell growth. Despite the redundancy and overlapping levels of cell-cycle control, errors do occur. One of the critical processes monitored by the cell-cycle checkpoint surveillance mechanism is the proper replication of DNA during the S phase. Cancer is the result of unchecked cell division caused by a breakdown of the mechanisms regulating the cell cycle. The loss of control begins with a change in the DNA sequence of a gene that codes for one of the regulatory molecules. Faulty instructions lead to a protein that does not function as it should. Cancer is the result of unchecked cell division caused by a breakdown of the mechanisms that regulate the cell cycle. The loss of control begins with a change in the DNA sequence of a gene that codes for one of the regulatory molecules. The genes that code for the positive cell-cycle regulators are called proto-oncogenes. Proto-oncogenes are normal genes that, when mutated, become oncogenes —genes that cause a cell to become cancerous. Consider what might happen to the cell cycle in a cell with a recently acquired oncogene.
Cancer comprises many different diseases caused by a common mechanism: uncontrolled cell growth. Despite the redundancy and overlapping levels of cell cycle control, errors do occur. One of the critical processes monitored by the cell cycle checkpoint surveillance mechanism is the proper replication of DNA during the S phase. Introduction. The majority of cells in the human body are not cycling and instead reside in ‘out‐of‐cycle’ states. A minority of cells are actively cycling (proliferating) and these are located mainly in the stem‐transit amplifying compartments of self‐renewing tissues, such as epithelia and bone marrow contrast, most functional cells have irreversibly withdrawn from the cell Cited by: As a previously unreported gene, future research is required to validate our findings and illuminate the molecular mechanisms. In conclusion, we systemically analyze the expression, prognostic value, and likely role of TIGD1, the unknown function gene, in cancer. Our finding provides evidence that TIGD1 involve in the cell : Li Yin, Jia Yan, Yuanyuan Wang, Qinghui Sun. Such treatments preferentially kill certain kinds of cancer cells because these mutants have a diminished ability to survive the damage. Normal cells, when treated with radiation, for example, will suffer damage to their DNA, but will then arrest their cell cycle until they have repaired it (Figure ). Tumor cells that have defects in various cell-cycle checkpoints, on the other Author: Bruce Alberts, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, Peter Walter.
The cell cycle, the process by which cells progress and divide, lies at the heart of cancer. In normal cells, the cell cycle is controlled by a complex series of signaling pathways by which a cell grows, replicates its DNA and divides. This process also includes mechanisms to ensure errors are corrected, and if not, the cells commit suicide. The Cell Cycle is an account of the mechanisms that control cell division, beginning with a description of the phases and main events of the cell cycle and the main model organisms in cell-cycle analysis, including Xenopus, Drosophila, and yeasts. Later chapters focus on the molecules and mechanisms of the cell-cycle control system, including the cyclin-dependent . HER2 overexpression enhances cell proliferation through rapid degradation of the cyclin-dependent kinase (CdK) inhibitor p27 and the upregulation of factors that promote cell cycle progression such as CdK6 and cyclins D1 and E. HER2 is used as prognostic, prognosis, and predictive biomarker in breast : Guy Joseph Lemamy. HDAC inhibition has been shown as a potent cell cycle arrestor in liver cancer cell lines. TSA induces cell cycle arrest in both HepG2 and Huh-7 cells . Cell cycle arrest is often associated with increased levels of cells with a differentiated hepatocyte phenotype [47,48,57].