Evidence map›Paper›PMID 32409593›Full record

ArticleCancer prevention research (Philadelphia, Pa.)2020

Inhibition of miR-21 Regulates Mutant KRAS Effector Pathways and Intercepts Pancreatic Ductal Adenocarcinoma Development.

Nina J Chu, Robert A Anders, Elana J Fertig, Minwei Cao, Alexander C Hopkins, Bridget P Keenan, Aleksandra Popovic, Todd D Armstrong, Elizabeth M Jaffee, Jacquelyn W Zimmerman

Abstract read
In one paragraph

Article in Cancer prevention research (Philadelphia, Pa.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
–field-weighted citation impact
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

11 citing papers in PubMed.

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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.

Nina J ChuDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.
Robert A AndersDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.
Elana J FertigDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.
Minwei CaoDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.
Alexander C HopkinsDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.
Bridget P KeenanDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0001-6075-489X
Aleksandra PopovicDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0002-5510-155X
Todd D ArmstrongDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.
Elizabeth M JaffeeDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland.ORCID 0000-0003-3841-6549
Jacquelyn W ZimmermanDepartment of Oncology, Skip Viragh Center for Pancreas Cancer, Bloomberg Kimmel Institute for Cancer Immunotherapy, and the Sidney Kimmel Cancer Center at Johns Hopkins University School of Medicine, Baltimore, Maryland. jzimme27@jhmi.edu.

Funding

Tumor Antigens for Individual Signatures and TherapyP50CA062924 · NCI · JOHNS HOPKINS UNIVERSITY · PI JAFFEE, ELIZABETH M. · 1993 to 2022
$54.6M
ONCOLOGY: CHEMOTHERAPY, IMMUNOLOGY, BIOLOGYT32CA009071 · NCI · JOHNS HOPKINS UNIVERSITY · PI Mary Y Armanios, Nilofer S. Azad · 1985 to 2026
$12.8M
Training Program in Cellular and Molecular MedicineT32GM008752 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI RAO, RAJINI · 2000 to 2019
$11.7M
MOLECULAR AND CELLULAR IMMUNOLOGYT32AI007334 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 1988 to 2023
$11.0M
Targeting the Immunosuppressive Tumor Microenvironment of Pancreatic Cancer with a Neoadjuvant Platform Clinical TrialR01CA197296 · NCI · JOHNS HOPKINS UNIVERSITY · PI William Reece Burns, Eric Christenson · 2015 to 2026
$5.7M
(PQB-3) Driver gene-induced inflammation in pancreatic cancer developmentR01CA184926 · NCI · JOHNS HOPKINS UNIVERSITY · PI JAFFEE, ELIZABETH M. · 2014 to 2017
$3.1M
NCI NIH HHS P50 CA062924NCI NIH HHS R01 CA184926NCI NIH HHS R01 CA197296NCI NIH HHS T32 CA009071NIAID NIH HHS T32 AI007334NIGMS NIH HHS T32 GM008752
6 · The paper itself

Abstract

Almost all pancreatic ductal adenocarcinomas (PDA) develop following KRAS activation, which triggers epithelial transformation and recruitment of desmoplastic stroma through additional transcriptional and epigenetic regulation, but only a few of these regulatory mechanisms have been described. We profiled dysregulated miRNAs starting with the earliest premalignant pancreatic intraepithelial neoplasias (PanIN) in genetically engineered mutated KRAS and P53 (KPC) mice programmed to recapitulate human PDA tumorigenesis. We identified miR-21 and miR-224 as cell-specific and compartment-specific regulators in PanINs and PDA. miR-21 is overexpressed in tumor epithelial cells of premalignant ducts, while miR-224 is overexpressed in cancer-associated fibroblasts in PDA stroma. Inhibition of miR-21 reverted protumorigenic functionalities to baseline levels. Overexpression of miR-224 induced activated phenotypes in normal fibroblasts.

Indexed as

Gene Expression Regulation, NeoplasticMutationAnimalsApoptosisBiomarkers, TumorCarcinoma, Pancreatic DuctalCell ProliferationHumansMiceMice, Inbred C57BLMicroRNAsPancreatic NeoplasmsPrognosisProto-Oncogene Proteins p21(ras)Tumor Cells, CulturedBiomarkers, TumorHras protein, mouseMicroRNAsMIRN21 microRNA, mouseProto-Oncogene Proteins p21(ras)

Identifiers

PMID32409593
PMCPMC7372516

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.