The DOI matches its Crossref record; 41 of the 42 references it cites were found in a registry or an index.
Glucose Deprivation Contributes to the Development of KRAS Pathway Mutations in Tumor Cells
Open accessAbstract
Desperately Seeking Glucose: Mutations in oncogenes and tumor suppressor genes allow cancer cells to outgrow their neighboring healthy cells. What microenvironmental conditions provide a selective growth advantage to these cells? Yun et al. (p. 1555 , published online 6 August) identify low glucose availability as a microenvironmental factor driving the acquisition of KRAS oncogenic mutations that allow cancer cells to survive and grow. In genetically matched colorectal cancer cells that differed only in the mutational status of the KRAS oncogene, mutant cells selectively overexpressed glucose transporter-1 and exhibited enhanced glucose uptake and glycolysis. When cells with wild-type KRAS were placed in a low-glucose environment, very few cells survived but most of the survivors expressed high levels of glucose transporter-1, and a small percentage of the survivors had acquired new KRAS mutations. Thus, glucose deprivation may help to drive the acquisition of cell growth–promoting oncogenic mutations during tumor development.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Gene expression and metabolic flux analyses have shown that it upregulates the expression of the GLUT1 glucose transporter to promote glucose uptake by cells, as well as inducing expression of hexokinase 1 and 2 (HK1 and HK2) rate-limiting enzymes of glycolysis, to increase glycolytic activity27–30 (Fig. 2a).”
From The metabolic landscape of RAS-driven cancers from biology to therapy (2021) · cites this paper as [30]
In the citing paper
“Oncogenic KRAS or BRAF mutations contribute to the Warburg effect, in part by upregulating GLUT1 (REF46).”
From Targeting cancer vulnerabilities with high-dose vitamin C (2019) · cites this paper as [46]
In the citing paper
“Direct data concerning dose-response characteristics of cancers to glucose are sparse, but it is relevant that most cancers have highly effective upregulated, insulin-independent glucose uptake mechanisms (67) and therefore may not derive a further growth advantage from hyperglycemia.”
From Diabetes and Cancer (2010) · cites this paper as [67]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Understanding the Warburg Effect: The Metabolic Requirements of Cell Proliferation
Vander Heiden, M. G., Cantley, L. C., & Thompson, C. B. (2009) · Science · doi:10.1126/science.1160809 · Cited by 16,197
Warburg, O. (1956) · Science · doi:10.1126/science.123.3191.309 · Cited by 13,425
Mutations of the BRAF gene in human cancer
Davies, H., Bignell, G. R., Cox, C., Stephens, P., Edkins, S., Clegg, S., Teague, J., Woffendin, H., Garnett, M. J., Bottomley, W., et al. (2002) · Nature · doi:10.1038/nature00766 · Cited by 10,674
An Integrated Genomic Analysis of Human Glioblastoma Multiforme
Parsons, D. W., Jones, S., Zhang, X., Lin, J. C.-H., Leary, R. J., Angenendt, P., Mankoo, P., Carter, H., Siu, I.-M., Gallia, G. L., et al. (2008) · Science · doi:10.1126/science.1164382 · Cited by 5,857
Self-citationras oncogenes in human cancer: a review.
Bos, J. L. (1989) · PubMed · Cited by 5,061
Why Do Cancers Have High Aerobic Glycolysis?
Gatenby, R. A., & Gillies, R. J. (2004) · Nature reviews. Cancer · doi:10.1038/nrc1478 · Cited by 4,784
Cancer genes and the pathways they control
Vogelstein, B., & Kinzler, K. W. (2004) · Nature Medicine · doi:10.1038/nm1087 · Cited by 4,346
Self-citationTargeting RAS signalling pathways in cancer therapy
Downward, J. (2003) · Nature reviews. Cancer · doi:10.1038/nrc969 · Cited by 3,354
Cancer cell metabolism: warburg and beyond
Hsu, P. P., & Sabatini, D. M. (2008) · Cell · doi:10.1016/j.cell.2008.08.021 · Cited by 2,452
PI3K pathway alterations in cancer: variations on a theme
Yuan, T. L., & Cantley, L. C. (2008) · Oncogene · doi:10.1038/onc.2008.245 · Cited by 1,845
Flagged first, then by citations
1 of the 42 references couldn’t be matched to a known paper.
Research works printed but not linked: 4
- Bos J. L., Cancer Res. 49, 4682 (1989).2547513
- Airley R., et al.., Clin. Cancer Res. 7, 928 (2001).11309343
- Yasuda S., et al.., J. Nucl. Med. 42, 989 (2001).11438616
- Delbeke D., et al.., J. Nucl. Med. 38, 1196 (1997).9255148
Cited by
Sorted by citations
Items 901–910 of 910
Aguiari, G., Bianchi, N., & Franzese, O. (2026) · Cells · doi:10.3390/cells15121074
Kawabe, N. (2026) · Institutional Repositories DataBase (IRDB)
Hexokinase 2 elevation links obesity to increased risk of acute kidney injury
Lv, H., Li, J., Wang, A., Wang, J., Wang, D., Guo, X., Gao, Y., Chen, X., Li, H., Chen, L., et al. (2026) · Cellular Signalling · doi:10.1016/j.cellsig.2026.112758
Chen, B., Gao, S., Chen, X., Shi, Q., Mingli, S., & Han, J. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27167495
Targeting GLUTs in Cancer: Mechanisms, Combination Strategies, and Translational Challenges
Shi, M.-N., Yang, D.-F., Chu, T., Zheng, D.-Y., & Ma, W. (2026) · Current Medical Science · doi:10.1007/s11596-026-00245-1
Cancer-derived lactic acid as a potential upstream contributor to tumor hypoxia
Kang, N., & Wang, Y. Z. (2026) · Communications Biology · doi:10.1038/s42003-026-11151-6
Guerrero‐López, P., & Garcia-Aznar, J. M. (2026) · Annals of Biomedical Engineering · doi:10.1007/s10439-026-04377-2
BindingDB (2026) · UC San Diego · doi:10.7270/q23n2879
Marini, A. (2014) · UnissResearch (Università degli Studi di Sassari)
Metadata
- Authors
- Yun, J., Rago, C., Cheong, I., Pagliarini, R., Angenendt, P., Rajagopalan, H., Schmidt, K., Willson, J. K. V., Markowitz, S., Zhou, S., Diaz, L. A., Velculescu, V. E., Lengauer, C., Kinzler, K. W., Vogelstein, B., & Papadopoulos, N.
- Affiliations
- Howard Hughes Medical Institute (US)
- The Ludwig Center for Cancer Genetics and Therapeutics and The Howard Hughes Medical Institute at the Johns Hopkins Kimmel Cancer Center, Baltimore, MD 21231, USA.
- Harold C. Simmons Comprehensive Cancer Center (US)
- Corresponding author
- Rajagopalan, Harith
- Vogelstein, Bert
- ORCID
- Venue
- Science
- Published
- 2009-09-18
- Volume
- 325
- Issue
- 5947
- Pages
- 1555-1559
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC2820374
- OpenAlex
- W1970766774
- Cited by
- 914
- References
- 42
- Citations by year
- 2026: 21 · 2025: 39 · 2024: 43 · 2023: 47 · 2022: 48 · 2021: 60 · 2020: 70 · 2019: 75 · 2018: 61 · 2017: 60 · 2016: 63 · 2015: 51 · 2014: 87 · 2013: 48 · 2012: 61
- FWCI
- 15.77
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Cancer Institute (CA43460, R37CA043460, P50CA062924, CA 62924)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- glucose deprivation, KRAS mutation, BRAF mutation, GLUT1, glucose transporter 1, colorectal cancer cell lines, tumor progression, glycolysis, glucose uptake, 3-bromopyruvate, transcriptome
- MeSH terms
- Animals, Glucose, Glycolysis, Humans, Mice, Nude, Mutation, Neoplasm Transplantation, Pyruvates, Genes, ras, Transplantation, Heterologous, Colorectal Neoplasms, Gene Expression Regulation, Neoplastic, Gene Targeting, Lactic Acid, Oligonucleotide Array Sequence Analysis, Cell Line, Tumor, Proto-Oncogene Proteins B-raf, Cell Proliferation, Glucose Transporter Type 1, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
