tailieunhanh - Regulation of cancer cell metabolism

Survival statistics can be produced by population-based cancer reg- istries that follow up their cases, either actively or passively. Although survival analysis of data from population-based registries cannot evaluate specific treatments (this can be done only in clinical randomized trials), it provides a useful evaluation of cancer care in the area covered by the registry, since all cancer cases will be included regardless of the type of treatment they may have received. The methods used in survival analyses are those discussed in Chapter 12. The first requirement for the application of these methods is a clear and well defined case definition. This should clearly specify the site of the cancer. | REVIEWS Regulation of cancer cell metabolism Rob A. Cairns Isaac S. Harris and Tak W. Mak Abstract Interest in the topic of tumour metabolism has waxed and waned over the past century of cancer research. The early observations of Warburg and his contemporaries established that there are fundamental differences in the central metabolic pathways operating in malignant tissue. However the initial hypotheses that were based on these observations proved inadequate to explain tumorigenesis and the oncogene revolution pushed tumour metabolism to the margins of cancer research. In recent years interest has been renewed as it has become clear that many of the signalling pathways that are affected by genetic mutations and the tumour microenvironment have a profound effect on core metabolism making this topic once again one of the most intense areas of research in cancer biology. Redox status Balance of the reduced state versus the oxidized state of a biochemical system. This balance is influenced by the level of reactive oxygen and nitrogen species ROS and RNS relative to the capacity of antioxidant systems to eliminate ROS and RNS. The Campbell Family Cancer Research Institute 610 University Avenue Toronto ON M56 2M9 Canada. These authors contributed equally to this work. Correspondence to . e-mail trmk@Uuwessrtorrttoc doi nrc2981 Over the past 25 years the oncogene revolution has stimulated research revealing that the crucial phenotypes that are characteristic of tumour cells result from a host of mutational events that combine to alter multiple signalling pathways. Moreover high-throughput sequencing data suggest that the mutations leading to tumorigenesis are even more numerous and heterogeneous than previously thought1 2. It is now clear that there are thousands of point mutations translocations amplifications and deletions that may contribute to cancer development and that the mutational range can differ even among histopathologi-cally identical tumours. .