Evidence map›Paper›PMID 32807225›Full record

ReviewJournal of hematology & oncology2020

The MAPK and AMPK signalings: interplay and implication in targeted cancer therapy.

Jimin Yuan, Xiaoduo Dong, Jiajun Yap, Jiancheng Hu

Open access · goldAbstract readReview
In one paragraph

Review in Journal of hematology & oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 296 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
296citing papers in PubMed, 2 pooled it
20.8field-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

296 citing papers in PubMed, 2 syntheses or guidelines pooled it, 488 citations in OpenAlex.

  1. Pooled it
  2. Liposomal delivery of gene therapy for ovarian cancer: a systematic review.Reproductive biology and endocrinology : RB&E · 2023
    Pooled it
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Macrophage Extracellular Traps in Immunity and Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Review

236 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

4 authors at 3 institutions in 2 countries.

Jimin YuanDepartment of Urology, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, 518020, Guangdong, China. yuan.jimin@szhospital.com.
Xiaoduo DongShenzhen People's Hospital, 1017 Dongmen North Road, Shenzhen, 518020, China.
Jiajun YapCancer and Stem Cell Program, Duke-NUS Medical School, 8 College Road, Singapore, 169857, Singapore.
Jiancheng HuCancer and Stem Cell Program, Duke-NUS Medical School, 8 College Road, Singapore, 169857, Singapore. hu.jiancheng@nccs.com.sg.ORCID 0000-0003-1615-0030
Duke-NUS Medical School · SGJinan University · CNShenZhen People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer is characterized as a complex disease caused by coordinated alterations of multiple signaling pathways. The Ras/RAF/MEK/ERK (MAPK) signaling is one of the best-defined pathways in cancer biology, and its hyperactivation is responsible for over 40% human cancer cases. To drive carcinogenesis, this signaling promotes cellular overgrowth by turning on proliferative genes, and simultaneously enables cells to overcome metabolic stress by inhibiting AMPK signaling, a key singular node of cellular metabolism. Recent studies have shown that AMPK signaling can also reversibly regulate hyperactive MAPK signaling in cancer cells by phosphorylating its key components, RAF/KSR family kinases, which affects not only carcinogenesis but also the outcomes of targeted cancer therapies against the MAPK signaling. In this review, we will summarize the current proceedings of how MAPK-AMPK signalings interplay with each other in cancer biology, as well as its implications in clinic cancer treatment with MAPK inhibition and AMPK modulators, and discuss the exploitation of combinatory therapies targeting both MAPK and AMPK as a novel therapeutic intervention.

Indexed as

Molecular Targeted TherapyAdenylate KinaseAmino AcidsAntineoplastic AgentsAutophagyCell DifferentiationCell DivisionClinical Trials as TopicDrug SynergismEnergy MetabolismEnzyme ActivationHomeostasisHumansMAP Kinase Signaling SystemNeoplasm ProteinsNeoplasmsAdenylate KinaseAmino AcidsAntineoplastic AgentsNeoplasm ProteinsProtein Kinase InhibitorsProto-Oncogene Proteins p21(ras)raf KinasesTumor Suppressor ProteinsAMPK activatorsAMPK inhibitorsAMPK signalingAutophagyCellular metabolismInterplayRAF/MEK/ERK inhibitorsRas/RAF/MEK/ERK signalingTargeted therapyTumorigenesis

Identifiers

PMID32807225
PMCPMC7433213
OpenAlexW3049642946

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.