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MTOR, Metabolism, and Cancer

Andrew Yoon Choo

出版	Harvard University, 2009
URL	http://books.google.com.hk/books?id=VZt2YgEACAAJ&hl=&source=gbs_api

註釋

In order to maintain hometostasis, cells interpret and coordinate responses to diverse environmental cues such as growth factors, energy status, and the availability of glucose and other nutrient sources. Mutations in the pathways that coordinate these responses can contribute to metabolic or inflammatory disorders and often promote tumorigenesis. One such pathway is the m ammalian T arget o f R apamycin complex 1 (mTORC1) pathway, whose activity is tightly controlled by numerous oncogenes and tumor suppressors and is deregulated in many cancers. Therefore, rapamycin, which allosterically inhibits mTORC1, is currently being evaluated as an anti-cancer agent. However, early clinical data suggest that many tumors are refractory to rapamycin's cytostatic effects, mandating the identification of potential resistance mechanisms as well as other novel methods to target mTORC1-activated cancers. My thesis attempts to tackle both of these issues by studying the effects of long-term rapamycin treatment and the biological requirements and consequences of mTORC1 hyperactivation by using biochemical, genetic, and cell biological approaches.