ReviewCells2020
Cancer Metabolism: Phenotype, Signaling and Therapeutic Targets.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 309 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
309 citing papers in PubMed, 553 citations in OpenAlex.
- Rabdosin B suppresses proliferation of nonsmall cell lung cancer by regulating the SRC/PI3K/AKT signaling pathway.Pharmaceutical biology · 2026Article
- AI-integrated multi-omics platform to revolutionize anti-metastatic therapy development through circulating tumor cell profiling: SCRUM-MONSTAR-CTC.International journal of clinical oncology · 2026Review
- Blood metabolomic signatures linking air pollution to lung cancer in the Cancer Prevention Studies.Nature communications · 2026Article
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- Article
- Targeting lung cancer with tanshinones: Current mechanistic evidence and emerging opportunities (Review).Oncology reports · 2026Review
- IGF-1 axis: The signalling bond in cancer-associated thrombosis and cachexia?Journal of thrombosis and thrombolysis · 2026Review
- HMGB1 promotes radiotherapy resistance in human cervical cancer HeLa cells through regulating the AMPK/mTOR signaling.World journal of surgical oncology · 2026Article
- Integrated transcriptomic and metabolomic analyses reveal targeting hexokinase 2 disrupts glycolysis and nucleotide metabolism to inhibit NSCLC growth.World journal of surgical oncology · 2026Article
- mTOR inhibition promotes ATRA-induced cancer cell differentiation by overcoming a metabolic hyperactive state.Journal of translational medicine · 2026Article
- Development of a metabolic subtype classifier for low-grade glioma to guide precision therapy.Discover oncology · 2026Article
- AGAP1 and noncanonical GDP binding regulate triple-negative breast cancer development.Cellular and molecular life sciences : CMLS · 2026Article
- Ferroptosis-induced immune modulation: a new frontier in glioblastoma therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Co-assembled structures of FeTranslational cancer research · 2026Article
- ROS-Fueled Allies: STAT3, PKM2, and HIF-1α Influencing Energy Metabolism in Hormone-Independent Cancers.International journal of molecular sciences · 2026Article
- Nutrient Availability Dictates Cancer Metabolism-Based Therapeutic Responses to Nononcology Drugs.Cancer research · 2026Article
- The Roles of SQSTM1/p62 in Selective Autophagy and Oncogenic Signaling.International journal of molecular sciences · 2026Review
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- mTOR-driven autophagy suppression defines metabolic vulnerability in CDK4/6 inhibitor-resistant HRCell death & disease · 2026Article
- ¹H-NMR serum metabolomic profiling from clinical routine identifies signatures of progressive melanoma metastasis.Scientific reports · 2026Article
249 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aberrant metabolism is a major hallmark of cancer. Abnormal cancer metabolism, such as aerobic glycolysis and increased anabolic pathways, has important roles in tumorigenesis, metastasis, drug resistance, and cancer stem cells. Well-known oncogenic signaling pathways, such as phosphoinositide 3-kinase (PI3K)/AKT, Myc, and Hippo pathway, mediate metabolic gene expression and increase metabolic enzyme activities. Vice versa, deregulated metabolic pathways contribute to defects in cellular signal transduction pathways, which in turn provide energy, building blocks, and redox potentials for unrestrained cancer cell proliferation. Studies and clinical trials are being performed that focus on the inhibition of metabolic enzymes by small molecules or dietary interventions (e.g., fasting, calorie restriction, and intermittent fasting). Similar to genetic heterogeneity, the metabolic phenotypes of cancers are highly heterogeneous. This heterogeneity results from diverse cues in the tumor microenvironment and genetic mutations. Hence, overcoming metabolic plasticity is an important goal of modern cancer therapeutics. This review highlights recent findings on the metabolic phenotypes of cancer and elucidates the interactions between signal transduction pathways and metabolic pathways. We also provide novel rationales for designing the next-generation cancer metabolism drugs.
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.