Evidence map›Paper›PMID 35149086›Full record

ArticleExperimental cell research2022

Resistance to mutant KRAS

Nao Muraki, Mizuki Yamada, Hinako Doki, Riho Nakai, Kazuki Komeda, Daiki Goto, Nozomi Kawabe, Kohei Matsuoka, Miyoko Matsushima, Tsutomu Kawabe and 5 more

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

Article in Experimental cell research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

15 authors at 3 institutions in 2 countries.

Nao MurakiDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan.
Mizuki YamadaDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan.
Hinako DokiDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan.
Riho NakaiDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan.
Kazuki KomedaDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan; Dept. of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Daiki GotoDept. of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Nozomi KawabeDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan.
Kohei MatsuokaDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan.
Miyoko MatsushimaDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan.
Tsutomu KawabeDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan.
Ichidai TanakaDept. of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Masahiro MoriseDept. of Respiratory Medicine, Nagoya University Graduate School of Medicine, Japan.
Jerry W ShayDept. of Cell Biology and the Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.
John D MinnaHamon Center for Therapeutic Oncology Research and the Simmons Comprehensive Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Mitsuo SatoDivision of Host Defense Sciences, Dept. of Integrated Health Sciences, Nagoya University Graduate School of Medicine, Japan. Electronic address: msato@met.nagoya-u.ac.jp.
Nagoya University · JPSouthwestern Medical Center · USThe University of Texas Southwestern Medical Center · US

Funding

UNIVERSITY OF TEXAS--SPORE IN LUNG CANCERP50CA070907 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI HEYMACH, JOHN V., MINNA, JOHN D. · 1996 to 2024
$57.4M
NCI NIH HHS P50 CA070907
6 · The paper itself

Abstract

Mutant KRAS, the most frequently occurring (∼30%) driver oncogene in lung adenocarcinoma, induces normal epithelial cells to undergo senescence. This phenomenon, called "oncogene-induced senescence (OIS)", prevents mutant KRAS-induced malignant transformation. We have previously reported that mutant KRAS

Indexed as

TelomeraseBronchiCarrier ProteinsCell LineCell Transformation, NeoplasticCellular SenescenceCyclin-Dependent Kinase 4Epithelial CellsGuanine Nucleotide Exchange FactorsHumansProto-Oncogene Proteins p21(ras)Carrier ProteinsCDK4 protein, humanCyclin-Dependent Kinase 4Guanine Nucleotide Exchange FactorsKRAS protein, humanProto-Oncogene Proteins p21(ras)RIN2 protein, humanTelomeraseKRAS, oncogene, telomerase, senescence

Identifiers

PMID35149086
PMCPMC10228173
OpenAlexW4210834090

What OpenQuestion holds

Textmetadata
LicenceTDM
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.