Evidence map›Paper›PMID 38882927›Full record

ArticleAnnual review of cancer biology2024

RAS and SHOC2 Roles in RAF Activation and Therapeutic Considerations.

Daniel A Bonsor, Dhirendra K Simanshu

Abstract read
In one paragraph

Article in Annual review of cancer biology, 2024. 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

2 authors.

Daniel A BonsorNCI RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.ORCID 0000-0001-5746-6002
Dhirendra K SimanshuNCI RAS Initiative, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD, USA.ORCID 0000-0002-9717-4618

Funding

WORK ORDER 126643 B539 EXPAND IC SUITE75N91019D00024 · NIAID · LEIDOS BIOMEDICAL RESEARCH, INC. · PI PENDLETON, RICHARD · 2019 to 2025
$3932.6M
CCR NIH HHS HHSN261200800001CNCI NIH HHS 75N91019D00024NCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

Mutations in RAS proteins play a pivotal role in the development of human cancers, driving persistent RAF activation and deregulating the Mitogen-Activated Protein Kinase (MAPK) signaling pathway. While progress has been made in targeting specific oncogenic RAS proteins, effective drug-based therapies for the majority of RAS mutations remain limited. Recent investigations on RAS-RAF complexes and the SHOC2-MRAS-PP1C holoenzyme complex have provided crucial insights into the structural and functional aspects of RAF activation within the MAPK signaling pathway. Moreover, these studies have also unveiled new blueprints for developing inhibitors allowing us to think beyond the current RAS and MEK inhibitors. In this review, we explore the roles of RAS and SHOC2 in activating RAF and discuss potential therapeutic strategies to target these proteins. A comprehensive understanding of the molecular interactions involved in RAF activation and their therapeutic implications holds the potential to drive innovative approaches in combating RAS/RAF-driven cancers.

Indexed as

14-3-3MRASPP1CRAFRASSHOC2

Identifiers

PMID38882927
PMCPMC11178279

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.