Evidence map›Paper›PMID 35046405›Full record

ArticleNPJ systems biology and applications2022

Diffusion kernel-based predictive modeling of KRAS dependency in KRAS wild type cancer cell lines.

Bastian Ulmer, Margarete Odenthal, Reinhard Buettner, Wilfried Roth, Michael Kloth

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

Article in NPJ systems biology and applications, 2022. 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
0.1field-weighted citation impact, top 60% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

5 authors at 2 institutions in 1 country.

Bastian UlmerInstitute of Pathology, Cologne University Hospital, Cologne, Germany. bastian.ulmer@uk-koeln.de.ORCID http://orcid.org/0000-0002-0883-6481
Margarete OdenthalInstitute of Pathology, Cologne University Hospital, Cologne, Germany.
Reinhard BuettnerInstitute of Pathology, Cologne University Hospital, Cologne, Germany.ORCID http://orcid.org/0000-0001-8806-4786
Wilfried RothInstitute of Pathology, Mainz University Hospital, Mainz, Germany.
Michael KlothInstitute of Pathology, Mainz University Hospital, Mainz, Germany.
University Hospital Cologne · DEJohannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent progress in clinical development of KRAS inhibitors has raised interest in predicting the tumor dependency on frequently mutated RAS-pathway oncogenes. However, even without such activating mutations, RAS proteins represent core components in signal integration of several membrane-bound kinases. This raises the question of applications of specific inhibitors independent from the mutational status. Here, we examined CRISPR/RNAi data from over 700 cancer cell lines and identified a subset of cell lines without KRAS gain-of-function mutations (KRAS

Indexed as

NeoplasmsProto-Oncogene Proteins p21(ras)Cell LineHumansMutationras ProteinsKRAS protein, humanProto-Oncogene Proteins p21(ras)ras Proteins

Identifiers

PMID35046405
PMCPMC8770632
OpenAlexW4205245308

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.