Evidence map›Paper›PMID 38105263›Full record

ReviewSignal transduction and targeted therapy2023

Targeting the RAS/RAF/MAPK pathway for cancer therapy: from mechanism to clinical studies.

Md Entaz Bahar, Hyun Joon Kim, Deok Ryong Kim

Open access · goldAbstract readReview
In one paragraph

Review in Signal transduction and targeted therapy, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 572 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
572citing papers in PubMed, 1 pooled it
105.6field-weighted citation impact, top 1% 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

572 citing papers in PubMed, 1 synthesis or guideline pooled it, 688 citations in OpenAlex.

  1. Pooled it
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  11. The evolving landscape of drug targets.Nature reviews. Drug discovery · 2026
    Review
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  18. Aporphine AlkaloidPharmaceuticals (Basel, Switzerland) · 2026
    Article
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512 more citing papers are in PubMed but not listed here.

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

3 authors at 1 institution in 1 country.

Md Entaz BaharDepartment of Biochemistry and Convergence Medical Sciences and Institute of Medical Science, Gyeongsang National University, College of Medicine, Jinju, South Korea.ORCID 0000-0002-5369-3889
Hyun Joon KimDepartment of Anatomy and Convergence Medical Sciences and Institute of Medical Science, Gyeongsang National University, College of Medicine, Jinju, South Korea.
Deok Ryong KimDepartment of Biochemistry and Convergence Medical Sciences and Institute of Medical Science, Gyeongsang National University, College of Medicine, Jinju, South Korea. drkim@gnu.ac.kr.
Gyeongsang National University · KR

Funding

National Research Foundation of Korea (NRF) RS-2023-00219399National Research Foundation of Korea (NRF) RS-2023-00238051
6 · The paper itself

Abstract

Metastatic dissemination of solid tumors, a leading cause of cancer-related mortality, underscores the urgent need for enhanced insights into the molecular and cellular mechanisms underlying metastasis, chemoresistance, and the mechanistic backgrounds of individuals whose cancers are prone to migration. The most prevalent signaling cascade governed by multi-kinase inhibitors is the mitogen-activated protein kinase (MAPK) pathway, encompassing the RAS-RAF-MAPK kinase (MEK)-extracellular signal-related kinase (ERK) pathway. RAF kinase is a primary mediator of the MAPK pathway, responsible for the sequential activation of downstream targets, such as MEK and the transcription factor ERK, which control numerous cellular and physiological processes, including organism development, cell cycle control, cell proliferation and differentiation, cell survival, and death. Defects in this signaling cascade are associated with diseases such as cancer. RAF inhibitors (RAFi) combined with MEK blockers represent an FDA-approved therapeutic strategy for numerous RAF-mutant cancers, including melanoma, non-small cell lung carcinoma, and thyroid cancer. However, the development of therapy resistance by cancer cells remains an important barrier. Autophagy, an intracellular lysosome-dependent catabolic recycling process, plays a critical role in the development of RAFi resistance in cancer. Thus, targeting RAF and autophagy could be novel treatment strategies for RAF-mutant cancers. In this review, we delve deeper into the mechanistic insights surrounding RAF kinase signaling in tumorigenesis and RAFi-resistance. Furthermore, we explore and discuss the ongoing development of next-generation RAF inhibitors with enhanced therapeutic profiles. Additionally, this review sheds light on the functional interplay between RAF-targeted therapies and autophagy in cancer.

Indexed as

Lung NeoplasmsMelanomaExtracellular Signal-Regulated MAP KinasesHumansMitogen-Activated Protein Kinase Kinasesraf KinasesExtracellular Signal-Regulated MAP KinasesMitogen-Activated Protein Kinase Kinasesraf Kinases

Identifiers

PMID38105263
PMCPMC10725898
OpenAlexW4389861133

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.