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Appetite for destruction: the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors

Overview of attention for article published in BMC Biology, October 2011
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Title
Appetite for destruction: the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors
Published in
BMC Biology, October 2011
DOI 10.1186/1741-7007-9-69
Pubmed ID
Authors

Alfredo Csibi, John Blenis

Abstract

The elevated metabolic requirements of cancer cells reflect their rapid growth and proliferation and are met through mutations in oncogenes and tumor suppressor genes that reprogram cellular processes. For example, in tuberous sclerosis complex (TSC)-related tumors, the loss of TSC1/2 function causes constitutive mTORC1 activity, which stimulates glycolysis, resulting in glucose addiction in vitro. In research published in Cell and Bioscience, Jiang and colleagues show that pharmacological restriction of glucose metabolism decreases tumor progression in a TSC xenograft model.

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The data shown below were collected from the profiles of 6 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 37 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Korea, Republic of 1 3%
United Kingdom 1 3%
United States 1 3%
Brazil 1 3%
Unknown 33 89%

Demographic breakdown

Readers by professional status Count As %
Researcher 9 24%
Student > Ph. D. Student 8 22%
Other 4 11%
Professor 3 8%
Student > Doctoral Student 3 8%
Other 8 22%
Unknown 2 5%
Readers by discipline Count As %
Agricultural and Biological Sciences 14 38%
Medicine and Dentistry 7 19%
Biochemistry, Genetics and Molecular Biology 4 11%
Chemistry 2 5%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Other 4 11%
Unknown 5 14%