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.
journal_name
BMC Bioljournal_title
BMC biologyauthors
Csibi A,Blenis Jdoi
10.1186/1741-7007-9-69subject
Has Abstractpub_date
2011-10-21 00:00:00pages
69issn
1741-7007pii
1741-7007-9-69journal_volume
9pub_type
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