Titlebook: Cell Cycle Deregulation in Cancer; Greg H. Enders Book 2010 Springer Science+Business Media, LLC 2010 DNA.biology.cancer.cancer therapy.ce

COMMA

Escape from Cellular Quiescencerm refers to a state of dormancy as opposed to a proliferative state. However, quiescent cells are in any other regard metabolically active. In many tissues with relative fast cell renewal rates the primary function of a small group of undifferentiated cells is limited to self-renewal (stem cells).

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Interplay Between Cyclin-Dependent Kinases and E2F-Dependent Transcriptionferation is a fundamental feature of all types of cancer. One of the key regulators of cell proliferation is the E2F transcription factor. E2F controls the expression of many genes that are required for cells to divide and elevated E2F activity is found in most tumor cells. The activation and inacti

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calorie

Mitotic Checkpoint and Chromosome Instability in Cancerly change gene expression patterns on a global scale and provides a mechanism that promotes genetic and biochemical diversity that is used by cells to achieve a transformed state or to survive suboptimal growth conditions. The mitotic checkpoint is a fail-safe mechanism that monitors the fidelity of

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nepotism

p53, ARF, and the Control of Autophagyapoptosis. Recently, both of these proteins were found to be intimately tied to metabolic pathways and to play surprising roles in autophagy. Autophagy (“self-eating”) is a critical response of eukaryotic cells to stress. During this process, portions of the cytosol, including cytoplasmic organelles

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Regulation of Self-Renewing Divisions in Normal and Leukaemia Stem Cells the biological organization of tumours. These cells, named tumour-initiating cells (TICs), or cancer stem cells (CSCs), share phenotypic and functional characteristics with normal stem cells, most notably their ability to self-renew. Here we discuss regulation of self-renewal in normal haematopoiet

伪造者

Maintenance of Telomeres in Cancera cancer cell of origin. Fortunately, this event is made infrequent by the evolution of mechanisms able to preserve genomic stability and to limit the proliferation potential of somatic cells. A crucial role in both of these processes is played by the nucleoproteins that localize to the tips of our

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意外的成功

Cell Cycle Deregulation in Pre-neoplasia: Case Study of Barrett’s Oesophagusrogression to fully fledged cancer would allow for chemoprevention or therapeutic interventions; however in most cases, IEN remains undetected and the exact mechanisms for progression remain unknown. Barrett’s oesophagus, the premalignant stage of oesophageal adenocarcinoma, is the perfect model to