In one paragraphArticle in Science signaling, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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.
2 · The registryThe 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.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
12 authors.
Hyun LeeDepartment of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.ORCID 0009-0007-8230-8963 Jacob M HughesDepartment of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.ORCID 0009-0007-6686-5014 Joseph P LaMorteDepartment of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.ORCID 0009-0004-3160-0938 Bridget A FinniffDepartment of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Picabo BinetteDepartment of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.
Sarasi K GunasekaraDepartment of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.ORCID 0009-0007-6616-3282 Ariana CovasDepartment of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.ORCID 0009-0001-2611-559X Vanessa E WallProtein Expression Laboratory, NCI RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.ORCID 0000-0002-6972-239X Dominic EspositoProtein Expression Laboratory, NCI RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc., Frederick, MD 21702, USA.ORCID 0000-0002-9987-1687 Matthew D WilkersonDepartment of Anatomy, Physiology, and Genetics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.ORCID 0000-0003-2727-0230 Marielle E YoheLaboratory of Cell and Developmental Signaling, Center for Cancer Research, National Cancer Institute, NIH, Frederick, MD 21701, USA.ORCID 0000-0001-5356-9426 Robert L KortumDepartment of Pharmacology and Molecular Therapeutics, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA.ORCID 0000-0002-1634-4882 Funding
Isoform-specific signaling as a determinant of RAS-driven oncogenesisR01CA255232 · NCI · HENRY M. JACKSON FDN FOR THE ADV MIL/MED · PI Robert Kortum · 2022 to 2026
$1.7MNCI NIH HHS R01 CA255232
6 · The paper itselfAbstract
Wild-type RAS family members determine the signaling and therapeutic response in cancers driven by mutant HRAS and KRAS because they activate alternate RAS effector pathways. Here, we found that the requirement for wild-type RAS to support mutant NRAS-driven transformation correlated with codon-specific differences in GTP hydrolysis. NRAS with mutations at either Gly
Indexed as
Cell Transformation, NeoplasticCodonGTP PhosphohydrolasesMembrane ProteinsMutationProto-Oncogene Proteins p21(ras)AllelesAnimalsGuanosine TriphosphateHumansMicePhosphatidylinositol 3-KinasesSignal TransductionCodonGTP PhosphohydrolasesGuanosine TriphosphateHRAS protein, humanMembrane ProteinsNRAS protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins p21(ras)
Identifiers
PMID42709866
PMCPMC13670066
What OpenQuestion holds
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