ReviewOncogene2011
Sugar-free approaches to cancer cell killing.
Review in Oncogene, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
105 citing papers in PubMed, 198 citations in OpenAlex.
- The Mechanism and Regulation of Disulfidptosis and Its Role in Disease.Biomedicines · 2026Review
- Exploiting metabolic cell death for cancer therapy.Nature reviews. Cancer · 2026Review
- Targeting lactic acidosis in the tumor microenvironment: Enhancing TACE efficacy in hepatocellular carcinoma.Liver research (Beijing, China) · 2025Review
- TCF25 serves as a nutrient sensor to orchestrate metabolic adaptation and cell death by enhancing lysosomal acidification under glucose starvation.Cell reports · 2025Article
- Ferroptosis: iron release mechanisms in the bioenergetic process.Cancer metastasis reviews · 2025Review
- Role of disulfide death in cancer (Review).Oncology letters · 2025Review
- FAM3A plays a key role in protecting against tubular cell pyroptosis and acute kidney injury.Redox biology · 2024Article
- Gedatolisib shows superior potency and efficacy versus single-node PI3K/AKT/mTOR inhibitors in breast cancer models.NPJ breast cancer · 2024Article
- Metabolic Adaptation and Cellular Stress Response As Targets for Cancer Therapy.The world journal of men's health · 2024Review
- Molecular landmarks of tumor disulfidptosis across cancer types to promote disulfidptosis-target therapy.Redox biology · 2023Article
- A Disulfidptosis-Related Gene Signature Associated with Prognosis and Immune Cell Infiltration in Osteosarcoma.Bioengineering (Basel, Switzerland) · 2023Article
- Targeted inhibition of protein synthesis renders cancer cells vulnerable to apoptosis by unfolded protein response.Cell death & disease · 2023Article
- Comparing mechanism-based and machine learning models for predicting the effects of glucose accessibility on tumor cell proliferation.Scientific reports · 2023Article
- Article
- Actin cytoskeleton vulnerability to disulfide stress mediates disulfidptosis.Nature cell biology · 2023Article
- Evaluation of changes in Salivary Lactate Dehydrogenase Level for detection of Head and Neck Squamous Cell Carcinoma: A Systematic Review and Meta-Analysis Study.International journal of preventive medicine · 2023Review
- Coordination of the AMPK, Akt, mTOR, and p53 Pathways under Glucose Starvation.International journal of molecular sciences · 2022Article
- Advances in measuring cancer cell metabolism with subcellular resolution.Nature methods · 2022Review
- Article
- Review
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Tumors show an increased rate of glucose uptake and utilization. For this reason, glucose analogs are used to visualize tumors by the positron emission tomography technique, and inhibitors of glycolytic metabolism are being tested in clinical trials. Upregulation of glycolysis confers several advantages to tumor cells: it promotes tumor growth and has also been shown to interfere with cell death at multiple levels. Enforcement of glycolysis inhibits apoptosis induced by cytokine deprivation. Conversely, antiglycolytic agents enhance cell death induced by radio- and chemotherapy. Synergistic effects are likely due to regulation of the apoptotic machinery, as glucose regulates activation and levels of proapoptotic BH3-only proteins such as Bim, Bad, Puma and Noxa, as well as the antiapoptotic Bcl-2 family of proteins. Moreover, inhibition of glucose metabolism sensitizes cells to death ligands. Glucose deprivation and antiglycolytic drugs induce tumor cell death, which can proceed through necrosis or through mitochondrial or caspase-8-mediated apoptosis. We will discuss how oncogenic pathways involved in metabolic stress signaling, such as p53, AMPK (adenosine monophosphate-activated protein kinase) and Akt/mTOR (mammalian target of rapamycin), influence sensitivity to inhibition of glucose metabolism. Finally, we will analyze the rationale for the use of antiglycolytic inhibitors in the clinic, either as single agents or as a part of combination therapies.
Indexed as
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.