ReviewInternational journal of clinical oncology2017
Targeting metabolic reprogramming in KRAS-driven cancers.
Review in International journal of clinical oncology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05132244 (Pancreatic Cancer Glucose Assessment and Regulation Study), which is not on this map. Cited by 72 papers.
What it found
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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.
Pancreatic Cancer Glucose Assessment and Regulation Study
Who cites it
72 citing papers in PubMed, 138 citations in OpenAlex.
- Time-frequency analysis of serum with proton nuclear magnetic resonance for diagnosis of pancreatic cancer.Scientific reports · 2020Trial
- Research Advances on Targets and Mechanisms in Cancers Complicated by Cardiovascular Diseases.OncoTargets and therapy · 2026Review
- Advances in biomarkers of resistance to KRAS mutation-targeted inhibitors.Discover oncology · 2025Review
- Post-translational modifications and the reprogramming of tumor metabolism.Discover oncology · 2025Review
- Poorly controlled type II diabetes mellitus significantly enhances postoperative chemoresistance in patients with stage III colon cancer.World journal of gastroenterology · 2025Article
- Crosstalk between the tumor immune microenvironment and metabolic reprogramming in pancreatic cancer: new frontiers in immunotherapy.Frontiers in immunology · 2025Review
- Autophagy in the lung: guardian of homeostasis or driver of disease.Autophagy reports · 2025Review
- Crosstalk between FTH1 and PYCR1 dysregulates proline metabolism and mediates cell growth in KRAS-mutant pancreatic cancer cells.Experimental & molecular medicine · 2024Article
- Growth characteristics of HCT116 xenografts lacking asparagine synthetase vary according to sex.Human genomics · 2024Article
- Sotorasib inhibits ubiquitination degradation of TXNIP and suppresses glucose metabolism inAmerican journal of cancer research · 2024Article
- Unveiling the genetic and epigenetic landscape of colorectal cancer: new insights into pathogenic pathways.Medical oncology (Northwood, London, England) · 2023Review
- The Warburg effect modulates DHODH role in ferroptosis: a review.Cell communication and signaling : CCS · 2023Review
- Nucleotide metabolism: a pan-cancer metabolic dependency.Nature reviews. Cancer · 2023Review
- Review
- Role and therapeutic targeting of glutamine metabolism in non‑small cell lung cancer (Review).Oncology letters · 2023Review
- Cancer immune evasion through KRAS and PD-L1 and potential therapeutic interventions.Cell communication and signaling : CCS · 2023Review
- Multi-omics analyses of glucose metabolic reprogramming in colorectal cancer.Frontiers in immunology · 2023Article
- Rewiring glucose metabolism improves 5-FU efficacy in p53-deficient/KRASCommunications biology · 2022Article
- Targeting Asparagine Synthetase in Tumorgenicity Using Patient-Derived Tumor-Initiating Cells.Cells · 2022Article
- Tumor growth of neurofibromin-deficient cells is driven by decreased respiration and hampered by NADCell death and differentiation · 2022Article
12 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
Mutations of KRAS are found in a variety of human malignancies, including in pancreatic cancer, colorectal cancer, and non-small cell lung cancer at high frequency. To date, no effective treatments that target mutant variants of KRAS have been introduced into clinical practice. In recent years, a number of studies have shown that the oncogene KRAS plays a critical role in controlling cancer metabolism by orchestrating multiple metabolic changes. One of the metabolic hallmarks of malignant tumor cells is their dependency on aerobic glycolysis, known as the Warburg effect. The role of KRAS signaling in the regulation of aerobic glycolysis has been reported in several types of cancer. KRAS-driven cancers are characterized by altered metabolic pathways involving enhanced nutrients uptake, enhanced glycolysis, enhanced glutaminolysis, and elevated synthesis of fatty acids and nucleotides. However, Just how mutated KRAS can coordinate the metabolic shift to promote tumor growth and whether specific metabolic pathways are essential for the tumorigenesis of KRAS-driven cancers are questions which remain to be answered. In this context, the aim of this review is to summarize current data on KRAS-related metabolic alterations in cancer cells. Given that cancer cells rely on changes in metabolism to support their growth and survival, the targeting of metabolic processes may be a potential strategy for treating KRAS-driven cancers.
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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.