Journal Article10.1038/NM1087
Cancer genes and the pathways they control.
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TL;DR: The purposes of this review are to highlight examples of progress in many areas of cancer research, indicate where knowledge is scarce and point out fertile grounds for future investigation.
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Abstract: The revolution in cancer research can be summed up in a single sentence: cancer is, in essence, a genetic disease. In the last decade, many important genes responsible for the genesis of various cancers have been discovered, their mutations precisely identified, and the pathways through which they act characterized. The purposes of this review are to highlight examples of progress in these areas, indicate where knowledge is scarce and point out fertile grounds for future investigation.
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TL;DR: It is found that pancreatic cancers contain an average of 63 genetic alterations, the majority of which are point mutations, which defined a core set of 12 cellular signaling pathways and processes that were each genetically altered in 67 to 100% of the tumors.
Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits
TL;DR: Owing to the importance of these tumour-associated phenotypes in metastasis and cancer-related mortality, targeting the products of such cellular plasticity is an attractive but challenging approach that is likely to lead to improved clinical management of cancer patients.
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Consensus coding sequences of human breast and colorectal cancers
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TL;DR: In this paper, the authors analyzed 13,023 genes in 11 breast and 11 colorectal cancers and found that individual tumors accumulate an average of 90 mutant genes but only a subset of these contribute to the neoplastic process.
References
•Journal Article
Disorders in cell circuitry associated with multistage carcinogenesis: exploitable targets for cancer prevention and therapy.
I. B. Weinstein,Martin Begemann,P Zhou,E. K.-H. Han,Alessandro Sgambato,Y. Doki,N Arber,Marco Ciaparrone,Hirofumi Yamamoto +8 more
TL;DR: It is hypothesized that, because of their disordered circuitry, cancer cells suffer from "gene addiction" and "gree hypersensitivity," disorders that might be exploited in both cancer prevention and therapy.
Cyclin D-dependent kinases, INK4 inhibitors and cancer.
TL;DR: A series of mouse models have been developed to study the in vivo function of individual components of this pathway in both normal homeostasis and tumor development, and several novel molecules, such as Cdk inhibitors, are under development as potential anti-cancer drugs.
Host genetics and tumour metastasis
TL;DR: The observations could be reconciled by combining the theories, with genetic background influencing both metastatic efficiency and predictive gene expression profiles, upon which, subsequently, metastasis-promoting mutational and epigenetic events occur.
Chronic Myelogenous Leukemia
TL;DR: Through rational drug development, STI571, a bcr-abl tyrosine kinase inhibitor, has emerged as targeted therapy that offers new hope for expanded treatment options for patients with CML.
Haploinsufficiency for tumour suppressor genes: when you don't need to go all the way.
Manuela Santarosa,Alan Ashworth +1 more
TL;DR: The genes that undergo this phenomenon are described and possible mechanisms that allow haploinsufficiency to display a phenotype and facilitate the pathogenesis of cancer are discussed.