Titlebook: IGF and Nutrition in Health and Disease; M. Sue Houston,Jeffrey M. P. Holly,Eva L. Feldman Book 2004 Springer Science+Business Media New Y

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Nutrition and Healthhttp://image.papertrans.cn/i/image/460270.jpg

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enetic understanding of the disease. However, our review is by no means exhaustive, and the interested reader should explore these topics from the references provided at the end of the chapter. We start with explaining cancer as a neoplastic disease and some reasons for its occurrence. Next, we disc

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gnant lesions to invasive carcinoma.. Our basic understanding of human carcinogenesis indicates that the process proceeds through multiple discernible stages of molecular and cellular alterations that provide the basis and scientific rationale for clinical cancer chemoprevention. There are, however,

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Martin L. Adamo,Lai Wang,Lisa Heron,Dalit Ben-Yosef,Hong Zhao,Derek Le Roithated, confer a significantly increased risk of cancer. Additional genes that confer a more modest risk of cancer are also being discovered. Together with improved understandings of environmental risk factors, increasingly accurate predictions of individual cancer risk will become available. Further,

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hibitor .. By some estimates, . carries gain-of-function mutations in 32% of colorectal cancers, 36% of hepatocellular carcinomas, 36% of endometrial carcinomas, 25% of breast carcinomas, 15% of anaplastic oligodendrogliomas, and 5% of medulloblastomas and anaplastic astrocytomas (recently reviewed

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Jean-Paul Thissen,Véronique Beauloye,Jean-Marie Ketelslegers,Louis E. Underwoodour relatively cell-autonomous processes. Consequently, in the late 1980s–mid-1990s, neoplastic growth was described largely as a net imbalance between cell accumulation and loss, brought about through mutations in cancer genes (Evan and Littlewood, 1998). In the last 10 years, a more holistic under

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M. Sue Houstonour relatively cell-autonomous processes. Consequently, in the late 1980s–mid-1990s, neoplastic growth was described largely as a net imbalance between cell accumulation and loss, brought about through mutations in cancer genes (Evan and Littlewood, 1998). In the last 10 years, a more holistic under

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hibitor .. By some estimates, . carries gain-of-function mutations in 32% of colorectal cancers, 36% of hepatocellular carcinomas, 36% of endometrial carcinomas, 25% of breast carcinomas, 15% of anaplastic oligodendrogliomas, and 5% of medulloblastomas and anaplastic astrocytomas (recently reviewed

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