ArticleThe journal of physical chemistry. B2024
Kinetic Trajectories of Glucose Uptake in Single Cancer Cells Reveal a Drug-Induced Cell-State Change Within Hours of Drug Treatment.
Jungwoo Kim, Rachel H Ng, JingXin Liang, Dazy Johnson, Young Shik Shin, Arion F Chatziioannou, Michael E Phelps, Wei Wei, Raphael D Levine, James R Heath
Abstract read
In one paragraphArticle in The journal of physical chemistry. B, 2024. 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
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1 · What the graph read from itWhat 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
10 authors.
Jungwoo KimInnovation Center for R&D Regulation and Management, Korea Institute of Science & Technology Evaluation and Planning, Eumseong-gun, Chungcheongbuk-do 27740, Korea.
JingXin LiangDepartment of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, California 91125, United States.
Dazy JohnsonDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, United States.
Young Shik ShinDepartment of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, California 91125, United States.ORCID 0000-0002-1097-9035 Arion F ChatziioannouDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, United States.
Michael E PhelpsDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, United States.
Wei WeiDepartment of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, California 91125, United States.ORCID 0000-0002-1018-7708 Raphael D LevineDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, California 90095, United States.ORCID 0000-0001-5423-1582 James R HeathDepartment of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, California 91125, United States.ORCID 0000-0001-5356-4385 Funding
Spatiotemporal Tumor Analytics for Guiding Sequential Targeted-Inhibitor: Immunotherapy Combinations (ST-Analytics)U54CA274509 · NCI · INSTITUTE FOR SYSTEMS BIOLOGY · PI James R. Heath · 2022 to 2026
$15.6MNano and biomolecular engineered technologies for neoantigen-specific T cell capture and characterizationR01CA264090 · NCI · INSTITUTE FOR SYSTEMS BIOLOGY · PI HEATH, JAMES R. · 2021 to 2025
$2.7MNCI NIH HHS R01 CA264090NCI NIH HHS U54 CA274509
6 · The paper itselfAbstract
The development of drug resistance is a nearly universal phenomenon in patients with glioblastoma multiforme (GBM) brain tumors. Upon treatment, GBM cancer cells may initially undergo a drug-induced cell-state change to a drug-tolerant, slow-cycling state. The kinetics of that process are not well understood, in part due to the heterogeneity of GBM tumors and tumor models, which can confound the interpretation of kinetic data. Here, we resolve drug-adaptation kinetics in a patient-derived in vitro GBM tumor model characterized by the epithelial growth factor receptor (EGFR) variant(v)III oncogene treated with an EGFR inhibitor. We use radiolabeled
Indexed as
ErbB ReceptorsGlioblastomaGlucoseAntineoplastic AgentsBrain NeoplasmsFluorodeoxyglucose F18HumansKineticsSingle-Cell AnalysisAntineoplastic AgentsErbB ReceptorsFluorodeoxyglucose F18Glucose
Identifiers
PMID39115241
PMCPMC12327372
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