Evidence map›Paper›PMID 34946644›Full record

ReviewMolecules (Basel, Switzerland)2021

Recent Developments in Targeting RAS Downstream Effectors for RAS-Driven Cancer Therapy.

Ozge Tatli, Gizem Dinler Doganay

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2021. 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
0.2field-weighted citation impact, top 46% 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, 10 citations in OpenAlex.

  1. Trial
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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

2 authors at 1 institution in 1 country.

Ozge TatliDepartment of Molecular Biology, Genetics-Biotechnology, Graduate School, Istanbul Technical University, Istanbul 34469, Turkey.
Gizem Dinler DoganayDepartment of Molecular Biology, Genetics-Biotechnology, Graduate School, Istanbul Technical University, Istanbul 34469, Turkey.
Istanbul Technical University · TR

Funding

Scientific and Technological Research Council of Turkey 117Z848
6 · The paper itself

Abstract

Aberrant activity of oncogenic rat sarcoma virus (RAS) protein promotes tumor growth and progression. RAS-driven cancers comprise more than 30% of all human cancers and are refractory to frontline treatment strategies. Since direct targeting of RAS has proven challenging, efforts have been centered on the exploration of inhibitors for RAS downstream effector kinases. Two major RAS downstream signaling pathways, including the Raf/MEK/Erk cascade and the phosphatidylinositol-3-kinase (PI3K) pathway, have become compelling targets for RAS-driven cancer therapy. However, the main drawback in the blockade of a single RAS effector is the multiple levels of crosstalk and compensatory mechanisms between these two pathways that contribute to drug resistance against monotherapies. A growing body of evidence reveals that the sequential or synergistic inhibition of multiple RAS effectors is a more convenient route for the efficacy of cancer therapy. Herein, we revisit the recent developments and discuss the most promising modalities targeting canonical RAS downstream effectors for the treatment of RAS-driven cancers.

Indexed as

Drug Resistance, NeoplasmMAP Kinase Signaling SystemNeoplasmsOncogene Protein p21(ras)Humansraf KinasesOncogene Protein p21(ras)raf KinasesPI3K-mTORRaf/MEK/ErkRAS-driven cancersRAS effectors

Identifiers

PMID34946644
PMCPMC8703923
OpenAlexW4200490180

What Socratic 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 Socratic graph.