ReviewBMC biology2011
Appetite for destruction: the inhibition of glycolysis as a therapy for tuberous sclerosis complex-related tumors.
Review in BMC biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Size-selective microfluidics delineate the effects of combinatorial immunotherapy on T-cell response dynamics at the single-cell level.Microsystems & nanoengineering · 2024Article
- Mechanisms of neural infiltration-mediated tumor metabolic reprogramming impacting immunotherapy efficacy in non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Midkine expression by stem-like tumor cells drives persistence to mTOR inhibition and an immune-suppressive microenvironment.Nature communications · 2022Article
- Interleukin (IL)-7 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021Article
- Article
- Low-dose 2-deoxyglucose and metformin synergically inhibit proliferation of human polycystic kidney cells by modulating glucose metabolism.Cell death discovery · 2019Article
- Renal disease in tuberous sclerosis complex: pathogenesis and therapy.Nature reviews. Nephrology · 2018Review
- Metabolomic studies identify changes in transmethylation and polyamine metabolism in a brain-specific mouse model of tuberous sclerosis complex.Human molecular genetics · 2018Article
- Review
- Application of metabolomics in drug resistant breast cancer research.Metabolites · 2015Review
- Tumor glycolysis as a target for cancer therapy: progress and prospects.Molecular cancer · 2013Review
- Defective glucose metabolism in polycystic kidney disease identifies a new therapeutic strategy.Nature medicine · 2013Article
- Inhibition of mechanistic target of rapamycin promotes dendritic cell activation and enhances therapeutic autologous vaccination in mice.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
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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Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.