Titlebook: Genomic Instability and Immortality in Cancer; Enrico Mihich,Leland Hartwell Book 1997 Springer Science+Business Media New York 1997 DNA.M

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https://doi.org/10.1007/978-3-642-67529-4ntion of end to end fusion and prot7ection from exonucleolytic degradation [3]. A ribonucleoprotein complex called telomerase, which was first isolated in . and shown to be a specialised reverse transcriptase, facilitates . synthesis of terminal repeats to compensate for sequence loss caused by inco

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The FDA and the Drug Development Processant mixture of surgery and radio- and chemo-therapy, all of which can carry severe side effects and are of limited efficacy. Cancer is therefore both a very common disease and a frequent cause of death. Tumours are, however, clonal in origin: they arise from single mutant cells that progressively ev

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https://doi.org/10.1057/978-1-137-57889-1clones of cells with accumulated genetic errors (Nowell, 1976). Some clones gain selective proliferative advantages, and eventually a subclone evolves that has acquired the capacity for invasion, becoming an early carcinoma. There is now substantial evidence that human cancers develop in association

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https://doi.org/10.1007/978-1-4939-1607-8s form heterodimers and transactivate genes, some of which are required for cell cycle progression or DNA synthesis.. The product of the retinoblastoma tumor suppressor gene,. pRb, binds to some members of the E2F family, including E2F-1, and transforms them into transcriptional repressors.. In this

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