Colon Cancer Prevention: Dietary Modulation of Cellular and Molecular Mechanisms (Advances in Experimental Medicine and Biology) (Advances in Experimental Medicine and Biology, 470, Band 470) - Softcover
Buch 126 von 544: Advances in Experimental Medicine and Biology
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This volume covers recent research on all aspects of colon cancer prevention, including normal and abnormal colonic development, chemoprevention of colon cancer, the role of dietary factors in prevention, experimental approaches and mechanisms in prevention, as well as whether cell proliferation and apoptosis is the link between relative risk and prevention. Topics include: transcriptional regulation in intestinal development; colonic cell proliferation, differentiation and apoptosis; defects in the regulation of beta-catenin in colorectal cancer; dietary lipids, inflammation, and colon cancer; sulindac sulfone-induced regression of rectal polyps in patients with familial adenomatous polyposis; prevention of colon cancer and modulation of aberrant crypt foci; cell proliferation and apoptosis by retinoids and NSAIDs; mechanisms by which energy restriction inhibits carcinogenesis; dietary intervention studies of colorectal cancer; the genetics of hereditary non-polyposis colorectal cancer and non-polypotic colon cancer; familial association; colonic cell proliferation and apoptosis in rodent species; and nonsteroidal anti-inflammatory drugs (NSAIDs), cyclooxygenase and the cell cycle and their interactions in cancer.
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Colon Cancer Prevention: Dietary Modulation of Cellular and Molecular Mechanisms (Advances in Experimental Medicine and Biology, 470)
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Taschenbuch. Zustand: Neu. This item is printed on demand - it takes 3-4 days longer - Neuware -The Eighth Annual Research Conference of the American Institute for Cancer Research, held in Washington, D.C., September 3-4, 1998, was on the subject 'Colon Cancer Prevention: Dietary Modulation of Cellular and Molecular Mechanisms,' with participants representing various disciplines interested in this area. One of the speak ers provided an appropriate quote from 17th century physician Thomas Adams: 'Pre vention is better than healing because it saves the labor of being sick,' which aptly describes the need for the prevention of cancer. An overview of normal and abnormal colonic development emphasized that although the typical human colon undergoes 1013 cell divisions by age 60, with the asso ciated possibilities for error, relatively few colon tumors develop. Since dietary modu lation leads to extremely small changes in colonic cells over a long period, animal models are useful to time, observe, and delineate the events associated with colon cancer. In the development colon cancer, the inactivation of the adenomatous polyposis coli (Apc) gene is one of the earliest known events. Normally Apc downregulates the cellular protein beta-catenin, but this is lost during cancer development. Beta-catenin may itself be an oncogene; it has a short half-life, but it is stabilized by binding to is more prevalent in the cell nucleus, the gene shuttles caherin. Although the Apc between the nucleus and the cytoplasm. 176 pp. Englisch. Bestandsnummer des Verkäufers 9781461368618
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Taschenbuch. Zustand: Neu. This item is printed on demand - Print on Demand Titel. Neuware -The Eighth Annual Research Conference of the American Institute for Cancer Research, held in Washington, D.C., September 3-4, 1998, was on the subject 'Colon Cancer Prevention: Dietary Modulation of Cellular and Molecular Mechanisms,' with participants representing various disciplines interested in this area. One of the speak ers provided an appropriate quote from 17th century physician Thomas Adams: 'Pre vention is better than healing because it saves the labor of being sick,' which aptly describes the need for the prevention of cancer. An overview of normal and abnormal colonic development emphasized that although the typical human colon undergoes 1013 cell divisions by age 60, with the asso ciated possibilities for error, relatively few colon tumors develop. Since dietary modu lation leads to extremely small changes in colonic cells over a long period, animal models are useful to time, observe, and delineate the events associated with colon cancer. In the development colon cancer, the inactivation of the adenomatous polyposis coli (Apc) gene is one of the earliest known events. Normally Apc downregulates the cellular protein beta-catenin, but this is lost during cancer development. Beta-catenin may itself be an oncogene; it has a short half-life, but it is stabilized by binding to is more prevalent in the cell nucleus, the gene shuttles caherin. Although the Apc between the nucleus and the cytoplasm.Springer-Verlag KG, Sachsenplatz 4-6, 1201 Wien 176 pp. Englisch. Bestandsnummer des Verkäufers 9781461368618
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Taschenbuch. Zustand: Neu. Druck auf Anfrage Neuware - Printed after ordering - The Eighth Annual Research Conference of the American Institute for Cancer Research, held in Washington, D.C., September 3-4, 1998, was on the subject 'Colon Cancer Prevention: Dietary Modulation of Cellular and Molecular Mechanisms,' with participants representing various disciplines interested in this area. One of the speak ers provided an appropriate quote from 17th century physician Thomas Adams: 'Pre vention is better than healing because it saves the labor of being sick,' which aptly describes the need for the prevention of cancer. An overview of normal and abnormal colonic development emphasized that although the typical human colon undergoes 1013 cell divisions by age 60, with the asso ciated possibilities for error, relatively few colon tumors develop. Since dietary modu lation leads to extremely small changes in colonic cells over a long period, animal models are useful to time, observe, and delineate the events associated with colon cancer. In the development colon cancer, the inactivation of the adenomatous polyposis coli (Apc) gene is one of the earliest known events. Normally Apc downregulates the cellular protein beta-catenin, but this is lost during cancer development. Beta-catenin may itself be an oncogene; it has a short half-life, but it is stabilized by binding to is more prevalent in the cell nucleus, the gene shuttles caherin. Although the Apc between the nucleus and the cytoplasm. Bestandsnummer des Verkäufers 9781461368618
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