In one paragraphArticle in Molecular cancer therapeutics, 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
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
25 authors.
Elspeth M BeauchampRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0009-0007-3180-2742 Matt ClutterHigh-Throughput Analysis Laboratory, Chemistry of Life Processes Institute, Northwestern University, Evanston, Illinois.ORCID 0000-0001-6147-892X Dominik NahotkoRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0001-5349-1139 Emely Lopez FajardoRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0009-0005-1481-0535 Sara F DunneHigh-Throughput Analysis Laboratory, Chemistry of Life Processes Institute, Northwestern University, Evanston, Illinois.ORCID 0000-0002-0273-680X Mariafausta FischiettiRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0002-5691-689X Chidera V OkuRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0002-5846-1921 Gavin T BlythRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0009-0002-7141-0202 Rama K MishraDepartment of Biochemistry and Molecular Genetics, Northwestern University Feinberg School of Medicine, Chicago, Illinois.ORCID 0000-0003-3608-2602 Elena KarrasRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0009-0001-2541-8927 Sara G RadeckiRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0001-7585-8333 Connor LantzRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0003-3317-6486 Sidharth AddepalliRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0009-0001-4281-8551 Byoung-Kyu ChoRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0003-3370-6985 Young Ah GooRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0002-8278-3621 Jenna RossoffDivision of Hematology, Oncology and Stem Cell Transplantation, Ann & Robert H. Lurie Children's Hospital of Chicago, Chicago, Illinois.ORCID 0000-0003-0471-9883 Eleanor N FishToronto General Hospital Research Institute, University Health Network, Toronto, Canada.ORCID 0000-0002-1292-4644 Diana SaleiroRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0002-6756-3620 Gary E SchiltzRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0003-4180-5051 Leonidas C PlataniasRobert H. Lurie Comprehensive Cancer Center, Northwestern University, Chicago, Illinois.ORCID 0000-0002-9740-7573 Funding
Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LEONIDAS C. PLATANIAS · 1993 to 2026
$153.9MTR&D 7: Cell Specific ProteomicsP41GM108569 · NIGMS · NORTHWESTERN UNIVERSITY · PI KELLEHER, NEIL L · 2015 to 2024
$13.6MSignal Transduction of Type I Interferons in Malignant CellsR01CA077816 · NCI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 1998 to 2024
$6.6MTargeting Novel Protein Complexes for the Treatment of Acute Myeloid LeukemiaR01CA121192 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PLATANIAS, LEONIDAS C. · 2006 to 2023
$4.1MAcquisition of a Thermo Fisher Scientific Q Exactive UHMR mass spectrometerS10OD025194 · OD · NORTHWESTERN UNIVERSITY · PI COMPTON, PHILIP DANIEL · 2018 to 2018
$795kCSRD VA I01 CX000916National Cancer Institute (NCI) R01-CA121192National Cancer Institute (NCI) R01-CA77816NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA077816NCI NIH HHS R01 CA121192NIGMS NIH HHS P41 GM108569NIH HHS S10 OD025194U.S. Department of Veterans Affairs (VA) I01CX000916
6 · The paper itselfAbstract
The essential role of mTOR in promoting tumorigenesis of many cancers makes it an attractive therapeutic target. However, catalytic mTOR inhibitors, which block both mTORC1 and mTORC2, result in activation of negative feedback loops as a resistance mechanism. Selective mTORC2 inhibitors are expected to have the desired antitumor effects without engaging resistance mechanisms; however, to date, no such mTORC2 inhibitors have been developed. Using in silico screening and medicinal chemistry optimization, we identified several small molecules that bind to the unique mTORC2 component, stress-activated protein kinase-interacting protein 1 (SIN1). We demonstrate that this SIN1 inhibitor alters posttranslational modification, protein-protein interactions, and blocks mTORC2- and rapamycin-sensitive mTORC1-mediated signaling. The SIN1 inhibitor also inhibits wild-type RAS activation and downstream MAPK signaling, as well as cell proliferation of multiple cancer cell line types. SIN1 inhibition can enhance the efficacy of FDA-approved antineoplastic agents in vitro and may provide a novel approach for the treatment of different types of malignancies.
Indexed as
Adaptor Proteins, Signal TransducingAntineoplastic AgentsNeoplasmsProtein Kinase InhibitorsAnimalsCell Line, TumorCell ProliferationHumansSignal TransductionAdaptor Proteins, Signal TransducingAntineoplastic AgentsMAPKAP1 protein, humanProtein Kinase Inhibitors
Identifiers
PMID41423418
PMCPMC12904549
What OpenQuestion holds
Textmetadata
LicenceTDM
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