{"title":"Abnormalities of cell structures in tumors: apoptosis in tumors.","authors":"Herman H Cheung, Vinay Arora, Robert G Korneluk","doi":"10.1007/3-7643-7378-4_9","DOIUrl":null,"url":null,"abstract":"<p><p>A conceptual shift has occurred in recent years from considering cancer as simply a disease of deregulated cell proliferation to a view that incorporates the aberrant control of apoptosis into the equation. Apoptosis is an organized, genetically programmed cell death process by which multicellular organisms specifically destroy, dismantle and dispose of cells. In cancer cells, this tightly controlled process is suppressed by genetic lesions, allowing cancer cells to survive beyond their normal life span even in hostile environments that are prone to hypoxia and lack many trophic factor supports. In the last two decades, cancer researchers have made great strides in our understanding of the underlying molecular mechanism of apoptosis in chemoresistance generation and tumorigenesis. This tremendous increase in our knowledge of apoptosis in tumors has greatly impacted our perspective on carcinogenesis. Key regulators of apoptosis such as members of the Inhibitors of Apoptosis family and Bcl-2 family have been shown to play a pivotal role in allowing most cancer cells to escape apoptosis. The identification of specific targets involved in the suppression of apoptosis in cancer cells has facilitated the design and development of therapeutic strategies based on rational molecular approaches that aim to modulate apoptotic pathways. Many promising apoptosis-dependent strategies have been translated into clinical trials in the continued assessment of regimens that can effectively eradicate cancers.</p>","PeriodicalId":77125,"journal":{"name":"EXS","volume":" 96","pages":"201-21"},"PeriodicalIF":0.0000,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/3-7643-7378-4_9","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"EXS","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1007/3-7643-7378-4_9","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5
Abstract
A conceptual shift has occurred in recent years from considering cancer as simply a disease of deregulated cell proliferation to a view that incorporates the aberrant control of apoptosis into the equation. Apoptosis is an organized, genetically programmed cell death process by which multicellular organisms specifically destroy, dismantle and dispose of cells. In cancer cells, this tightly controlled process is suppressed by genetic lesions, allowing cancer cells to survive beyond their normal life span even in hostile environments that are prone to hypoxia and lack many trophic factor supports. In the last two decades, cancer researchers have made great strides in our understanding of the underlying molecular mechanism of apoptosis in chemoresistance generation and tumorigenesis. This tremendous increase in our knowledge of apoptosis in tumors has greatly impacted our perspective on carcinogenesis. Key regulators of apoptosis such as members of the Inhibitors of Apoptosis family and Bcl-2 family have been shown to play a pivotal role in allowing most cancer cells to escape apoptosis. The identification of specific targets involved in the suppression of apoptosis in cancer cells has facilitated the design and development of therapeutic strategies based on rational molecular approaches that aim to modulate apoptotic pathways. Many promising apoptosis-dependent strategies have been translated into clinical trials in the continued assessment of regimens that can effectively eradicate cancers.