ReviewCancer reports (Hoboken, N.J.)2018
How do cancer cells replenish their fuel supply?
Review in Cancer reports (Hoboken, N.J.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Cardiolipin Dysregulation in Glioblastoma-Effects on Mitochondrial Function Tumor Cell Death and Sensitivity to Mitochondria-Targeting Drugs.Journal of cellular physiology · 2025Review
- Redox Status Response of Physical Exercise Training in Women with Breast Cancer during Trastuzumab Therapy.Healthcare (Basel, Switzerland) · 2022Article
- Distinct glycolytic pathway regulation in liver, tumour and skeletal muscle of mice with cancer cachexia.Cell biochemistry and function · 2021Article
- APE1/Ref-1 - One Target with Multiple Indications: Emerging Aspects and New Directions.Journal of cellular signaling · 2021Article
- How do cancer cells replenish their fuel supply?Cancer reports (Hoboken, N.J.) · 2018Review
- An Introduction to the Mathematical Modeling in the Study of Cancer Systems Biology.Cancer informatics · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMultiple genetic changes, availability of cellular nutrients and metabolic alterations play a pivotal role in oncogenesis
aimsWe focus on cancer cell's metabolic properties, and we outline the cross talks between cellular oncogenic growth pathways in cancer metabolism. The review also provides a synopsis of the relevant cancer drugs targeting metabolic activities that are at various stages of clinical development.
methodsWe review literature published within the last decade to include select articles that have highlighted energy metabolism crucial to the development of cancer phenotypes.
resultsCancer cells maintain their potent metabolism and keep a balanced redox status by enhancing glycolysis and autophagy and rerouting Krebs cycle intermediates and products of β-oxydation.
conclusionsThe processes underlying cancer pathogenesis are extremely complex and remain elusive. The new field of systems biology provides a mathematical framework in which these homeostatic dysregulation principles may be examined for better understanding of cancer phenotypes. Knowledge of key players in cancer-related metabolic reprograming may pave the way for new therapeutic metabolism-targeted drugs and ultimately improve patient care.
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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.