In one paragraphArticle in Oncogene, 2025. 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
13 authors.
Lepakshe S V MadduriDepartment of Radiation Oncology, University of Nebraska Medical Center, Omaha, NE, USA.
Kelly A O'ConnellEppley Institute for Research in Cancer, University of Nebraska Medical Center, Omaha, NE, USA.
Ashley L HeinDepartment of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE, USA.
Lynette M SmithDepartment of Biostatistics, University of Nebraska Medical Center, Omaha, NE, USA.
Charles A EnkeDepartment of Radiation Oncology, University of Nebraska Medical Center, Omaha, NE, USA.
Keith R JohnsonDepartment of Genetics, Cell Biology, and Anatomy, University of Nebraska Medical Center, Omaha, NE, USA.
Michel M OuelletteDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, USA.
Funding
Tracking and Evaluation CoreU54GM115458 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI GUDA, CHITTIBABU · 2016 to 2025
$42.8MPancreatic Cancer Detection ConsortiumU01CA210240 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI Michael A. Hollingsworth · 2017 to 2026
$12.9MRac1 GTPase in tumorigenesis and progression of pancreatic cancerR01CA206444 · NCI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI BATRA, SURINDER K., OUELLETTE, MICHEL M · 2016 to 2020
$1.9MPR55-alpha controlled PP2A in the regulation of the Hippo/YAP pathwayR01GM143329 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI YAN, YING · 2021 to 2024
$1.3MNCI NIH HHS U01 CA210240Nebraska Department of Health and Human Services (Nebraska DHHS) 2022-59NIGMS NIH HHS R01 GM143329NIGMS NIH HHS U54 GM115458United States Department of Defense | United States Army | Army Medical Command | Congressionally Directed Medical Research Programs (CDMRP) W81XWH-21-1-0700U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA206444U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) 5U54GM115458U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R01GM143329
6 · The paper itselfAbstract
PP2A holoenzymes account nearly 50% of Ser/Thr phosphatase activities in human cells, yet their roles in oncogenesis remain largely unexplored. A PP2A holoenzyme consists of a catalytic subunit, a scaffold subunit, and a regulatory subunit. We previously reported that PR55α, a PP2A regulatory subunit, supports the tumorigenic and metastatic potential of pancreatic cancer cells, and this is associated with its role in promoting YAP activation, which is essential for tumorigenesis and progression in most solid tumors, including pancreatic cancer. However, the direct role of PR55α in tumorigenesis has not yet been assessed. Using telomerase-immortalized human pancreatic ductal cells (HPNE), this research reveals a mechanism in which PR55α/PP2A cooperates with oncogenic KRAS
Indexed as
Adaptor Proteins, Signal TransducingCarcinogenesisCell Transformation, NeoplasticPancreatic NeoplasmsPhosphoproteinsProtein Phosphatase 2Proto-Oncogene Proteins p21(ras)Transcription FactorsAnimalsCell Line, TumorCell MovementCell ProliferationHumansMiceYAP-Signaling ProteinsAdaptor Proteins, Signal TransducingKRAS protein, humanPhosphoproteinsPPP2R2A protein, humanProtein Phosphatase 2Proto-Oncogene Proteins p21(ras)Transcription FactorsYAP1 protein, humanYAP-Signaling Proteins
Identifiers
PMID40571777
PMCPMC12934529
What OpenQuestion holds
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