Evidence map›Paper›PMID 35402225›Full record

ArticleFrontiers in oncology2022

RelA Is an Essential Target for Enhancing Cellular Responses to the DNA Repair/Ref-1 Redox Signaling Protein and Restoring Perturbated Cellular Redox Homeostasis in Mouse PDAC Cells.

Mahmut Mijit, Randall Wireman, Lee Armstrong, Silpa Gampala, Zonera Hassan, Christian Schneeweis, Guenter Schneider, Chi Zhang, Melissa L Fishel, Mark R Kelley

Open access · goldAbstract read
In one paragraph

Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.1field-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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. The inhibitor of the redox activity of APE1/REF-1, APX2009, reduces the malignant phenotype of breast cancer cells.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2024
    Article
  7. International journal of molecular sciences · 2023
    Article
  8. Article
  9. Article
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

10 authors at 4 institutions in 2 countries.

Mahmut MijitDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, United States.
Randall WiremanDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, United States.
Lee ArmstrongDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, United States.
Silpa GampalaDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, United States.
Zonera HassanDepartment of Clinic and Polyclinic for Internal Medicine II, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Christian SchneeweisDepartment of Clinic and Polyclinic for Internal Medicine II, Klinikum rechts der Isar, Technical University of Munich, Munich, Germany.
Guenter SchneiderDepartment of General, Visceral and Pediatric Surgery, University Medical Center Göttingen, Göttingen, Germany.
Chi ZhangDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, United States.
Melissa L FishelDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, United States.
Mark R KelleyDepartment of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, United States.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · USTechnical University of Munich · DEUniversitätsmedizin Göttingen · DE

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI David W Clapp · 1999 to 2026
$59.3M
Novel Role of Ref-1 in Pancreatic Cancer Etiology and ProgressionR01CA167291 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI FISHEL, MELISSA L., KELLEY, MARK R. · 2013 to 2022
$5.2M
Targeting the Plasminogen Activation System to Limit Pancreatic Cancer Progression and Associated ThrombosisU01HL143403 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FISHEL, MELISSA L., FLICK, MATTHEW J. · 2018 to 2022
$4.2M
(PQ9)Mechanistic Role of APE1 and BER in chemotherapy-induced peripheral neuropathyR01CA205166 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI FEHRENBACHER, JILL C, KELLEY, MARK R. · 2017 to 2021
$2.7M
Hyperglycemia mediated myeloproliferative diseaseR01HL140961 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2019 to 2022
$2.3M
(PQ12) Enhancement of DNA repair in neurons via a targeted APE1 small molecule modifier to decrease and reverse chemotherapy-induced peripheral neuropathy (CIPN)R01CA231267 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI FEHRENBACHER, JILL C, KELLEY, MARK R. · 2018 to 2022
$2.3M
Thrombin-dependent mechanisms of pancreatic ductal adenocarcinoma diseaseR01CA211098 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FLICK, MATTHEW J. · 2017 to 2022
$2.2M
Investigation of novel signaling protein in 3D and in vivo PDAC models using second generation Ref-1 inhibitorsR01CA254110 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI FISHEL, MELISSA L., HAN, BUMSOO · 2021 to 2025
$2.1M
Targeting the Ref-1 signaling node for treating ocular neovascularizationR01EY031939 · NEI · INDIANA UNIVERSITY INDIANAPOLIS · PI CORSON, TIMOTHY W, KELLEY, MARK R. · 2020 to 2023
$1.7M
NCI NIH HHS R01 CA167291NCI NIH HHS R01 CA205166NCI NIH HHS R01 CA211098NCI NIH HHS R01 CA231267NCI NIH HHS R01 CA254110NEI NIH HHS R01 EY031939NHLBI NIH HHS R01 HL140961NHLBI NIH HHS U01 HL143403
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is one of the deadliest cancers with a poor response to current treatment regimens. The multifunctional DNA repair-redox signaling protein Ref-1 has a redox signaling function that activates several transcriptional factors (TFs) including NF-κB (RelA), STAT3, AP-1. These have been implicated in signaling in PDAC and associated with cancer progression and therapy resistance. Numerous studies have shown a role for RelA in PDAC inflammatory responses and therapy resistance, little is known as to how these inflammatory responses are modulated through Ref-1 redox signaling pathways during pancreatic pathogenesis. RelA and STAT3 are two major targets of Ref-1 and are important in PDAC pathogenesis. To decipher the mechanistic role of RelA in response to Ref-1 inhibition, we used PDAC cells (KC3590) from a genetically engineered

Indexed as

Ape1DNA repairpancreatic ductal adenocarcinoma (PDAC)PRDX1redox signalingrelASTAT3transcriptional factors

Identifiers

PMID35402225
PMCPMC8988139
OpenAlexW4220915396

What OpenQuestion holds

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Registered trials

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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.