Evidence map›Paper›PMID 31754788›Full record

ReviewDer Pathologe2019

[RAS mutations at the molecular tumor conference].

R Schäfer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Der Pathologe, 2019. 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
–field-weighted citation impact, top 85% 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, 0 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

1 author at 1 institution in 1 country.

R SchäferComprehensive Cancer Center, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Deutschland. reinhold.schaefer@charite.de.
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Members of the rat sarcoma (RAS) gene family belong to the most frequently mutated genes that drive pathogenesis and therapy response. As the discovery of their malignant potential dates back more than three decades, cellular mutated RAS genes and their products belong to the best characterized cancer genes. Despite urgent clinical needs, RAS therapies are still elusive and limited to preclinical studies. However, very recently, novel and promising approaches have become a reality in clinical applications and trials. In the near future, interesting therapeutic options will emerge that are capable of targeting "undruggable" RAS. This will be even more important as the detection of RAS mutations has already been an integral part of routine molecular diagnostics for many years.

Indexed as

Molecular Targeted TherapyNeoplasmsHumansMutationras Proteinsras ProteinsColorectal neoplasmsMolecular targeted therapyOncogenesRas genesSignal transduction

Identifiers

PMID31754788
OpenAlexW2989655616

What OpenQuestion holds

Textmetadata
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.