Evidence map›Paper›PMID 35477123›Full record

ArticleAging2022

Wild type and gain of function mutant TP53 can regulate the sensitivity of pancreatic cancer cells to chemotherapeutic drugs, EGFR/Ras/Raf/MEK, and PI3K/mTORC1/GSK-3 pathway inhibitors, nutraceuticals and alter metabolic properties.

James A McCubrey, Akshaya K Meher, Shaw M Akula, Stephen L Abrams, Linda S Steelman, Michelle M LaHair, Richard A Franklin, Alberto M Martelli, Stefano Ratti, Lucio Cocco and 3 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 24% of its field
1 · What the graph read from it

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 registry

The 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 literature

Who cites it

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Exploring Volatiles and Biological Effects ofMolecules (Basel, Switzerland) · 2025
    Article
  2. Review
  3. Article
  4. Gain of Function (GOF) Mutant p53 in Cancer-Current Therapeutic Approaches.International journal of molecular sciences · 2022
    Review
  5. Article
  6. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 3 countries.

James A McCubreyDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
Akshaya K MeherDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
Shaw M AkulaDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
Stephen L AbramsDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
Linda S SteelmanDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
Michelle M LaHairDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
Richard A FranklinDepartment of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, NC 27858, USA.
Alberto M MartelliDepartment of Biomedical and Neuromotor Sciences, Università di Bologna, Bologna, Italy.
Stefano RattiDepartment of Biomedical and Neuromotor Sciences, Università di Bologna, Bologna, Italy.
Lucio CoccoDepartment of Biomedical and Neuromotor Sciences, Università di Bologna, Bologna, Italy.
Fulvio BarbaroDepartment of Medicine and Surgery, Re.Mo.Bio.S. Laboratory, Anatomy Section, University of Parma, Parma, Italy.
Przemysław DudaDepartment of Molecular Physiology and Neurobiology, University of Wroclaw, Wroclaw, Poland.
Agnieszka GizakDepartment of Molecular Physiology and Neurobiology, University of Wroclaw, Wroclaw, Poland.
East Carolina University · USUniversity of Bologna · ITUniversity of Wrocław · PLUniversity of Parma · IT

Funding

BAFF 60mer as a novel therapeutic target for vascular diseasesR01HL146685 · NHLBI · UNIVERSITY OF VIRGINIA · PI MEHER, AKSHAYA KUMAR · 2019 to 2022
$1.5M
NHLBI NIH HHS R01 HL146685
6 · The paper itself

Abstract

TP53 is a master regulator of many signaling and apoptotic pathways involved in: aging, cell cycle progression, gene regulation, growth, apoptosis, cellular senescence, DNA repair, drug resistance, malignant transformation, metastasis, and metabolism. Most pancreatic cancers are classified as pancreatic ductal adenocarcinomas (PDAC). The tumor suppressor gene

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsCell Line, TumorCell ProliferationDietary SupplementsErbB ReceptorsGain of Function MutationGlycogen Synthase Kinase 3HumansMechanistic Target of Rapamycin Complex 1Mitogen-Activated Protein Kinase KinasesMutationPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins p21(ras)Tumor Suppressor Protein p53EGFR protein, humanErbB ReceptorsGlycogen Synthase Kinase 3Mechanistic Target of Rapamycin Complex 1Mitogen-Activated Protein Kinase KinasesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins p21(ras)TP53 protein, humanTumor Suppressor Protein p53chemotherapeutic drugsmetabolic propertiesPDACtargeted therapyTP53

Identifiers

PMID35477123
PMCPMC9085237
OpenAlexW4225092354

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.