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Hypoxia and miscoupling between reduced energy efficiency and signaling to cell proliferation drive cancer to grow increasingly faster Free
Juan Cui1,†, Xizeng Mao1,†, Victor Olman1, P. J. Hastings2, and Ying Xu1,3,*
1Computational Systems Biology Laboratory, Department of Biochemistry and Molecular Biology and Institute of Bioinformatics, University of Georgia, Athens, GA, USA
2Department of Molecular and Human Genetics, Baylor College of Medicine, Houstan, TX, USA
3College of Computer Science and Technology, Jilin University, China *Correspondence to:Ying Xu, E-mail: xyn@bmb.uga.edu
J Mol Cell Biol, Volume 4, Issue 3, June 2012, 174-176,  https://doi.org/10.1093/jmcb/mjs017

The question we address here is what drives cancer to grow in an accelerated fashion as it evolves. Various proposals have been made regarding the possible drivers of cancer growth such as driver mutations and autonomous growth signaling. While these are clearly relevant, they rely too much on specific types of genomic mutations or molecular abnormalities by chance across different cancer types, which makes the probability for cancer to occur/progress significantly lower than what we have witnessed about the current cancer occurrence rates worldwide, hence making them less probable to be the ultimate drivers of cancer growth (Loeb, 1998).
We present here a model for the (accelerated) growth of a cancer based on the discovered gene-expression patterns derived from genome-scale transcriptomic data of seven solid carcinoma types, namely breast, kidney, liver, lung, ovary, pancreatic, and stomach cancers.