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Titlebook: Checkpoint Responses in Cancer Therapy; Wei Dai Book 2008 Humana Press 2008 DNA.apoptosis.biotechnology.cancer.cancer research.cancer ther

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Cancer Drug Discovery and Developmenthttp://image.papertrans.cn/c/image/224213.jpg
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https://doi.org/10.1007/978-1-4302-1834-0 end, RB function is commonly abrogated in tumorigenesis, thereby contributing to the uncontrolled proliferation of cancer cells. However, it is becoming increasingly clear that RB is not only involved in the etiology and progression of cancer, but also modifies the response to specific therapeutic
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https://doi.org/10.1007/978-1-4302-1834-0structure of DNA in the cell, regulate under- and overwinding of the double helix, and remove knots and tangles from the genetic material. In order to perform their critical cellular functions, topoisomerases generate DNA strand breaks as requisite intermediates in their catalytic cycles. Consequent
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https://doi.org/10.1007/978-1-4302-1834-0sm of the G2 checkpoint s cascade. In addition, screening procedures to identify candidate compounds, currently available compounds, and compounds in clinical trials with G2 checkpoint-abrogating potential are discussed.
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Advanced and Alternate MapReduce Techniques,indle checkpoint is a cell-cycle surveillance mechanism that prevents premature sister-chromatid separation and ensures the fidelity of chromosome segregation. A defective spindle checkpoint results in aneuploidy and contributes to tumorigenesis. On the other hand, many tumor cells still exhibit a p
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