Evidence map›Paper›PMID 37671815›Full record

ReviewMolecular carcinogenesis2023

The action and resistance mechanisms of Lenvatinib in liver cancer.

Anna Buttell, Wei Qiu

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in Molecular carcinogenesis, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07493668 (A Phase 2, Multicenter, Randomized, Open-label Study Comparing Fostrox + Lenvatinib vs. Lenvatinib in Patients With Locally Advanced or Unresectable Advanced Hepatocellular Carcinoma), which is not on this map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
7.1field-weighted citation impact, top 2% 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.

NCT07493668 phase2recruitingnot on this mapstarted 2026, after this paper: background citation

A Phase 2, Multicenter, Randomized, Open-label Study Comparing Fostrox + Lenvatinib vs. Lenvatinib in Patients With Locally Advanced or Unresectable Advanced Hepatocellular Carcinoma (HCC) Who Have Received First-line Combination Immunotherapy

TypeinterventionalSponsorCHA UniversityRan2026 to 2029Enrolled80ConditionsHepatocellular Carcinoma (HCC)ArmsFostrox, Lenvatinib
3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Hepatocellular carcinoma drug resistance models.Cancer cell international · 2025
    Review
  13. Article
  14. Article
  15. Roles of PDGF/PDGFR signaling in various organs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
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.

Anna ButtellDepartments of Surgery, Loyola University Chicago Stritch School of Medicine, Maywood, Illinois, USA.
Wei QiuDepartments of Surgery, Loyola University Chicago Stritch School of Medicine, Maywood, Illinois, USA.ORCID 0000-0001-8093-3094
Loyola University Chicago · US

Funding

Molecular mechanisms of focal adhesion kinase in promoting hepatocarcinogenesisR01CA197128 · NCI · LOYOLA UNIVERSITY CHICAGO · PI QIU, WEI · 2015 to 2025
$3.6M
NCI NIH HHS R01 CA197128
6 · The paper itself

Abstract

Lenvatinib is a tyrosine kinase inhibitor that prevents the formation of new blood vessels namely by inhibiting tyrosine kinase enzymes as the name suggests. Specifically, Lenvatinib acts on vascular endothelial growth factor receptors 1-3 (VEGFR1-3), fibroblast growth factor receptors 1-4 (FGFR1-4), platelet-derived growth factor receptor-alpha (PDGFRα), tyrosine-kinase receptor (KIT), and rearranged during transfection receptor (RET). Inhibition of these receptors works to inhibit tumor proliferation. It is through these inhibition mechanisms that Lenvatinib was tested to be noninferior to Sorafenib. However, resistance to Lenvatinib is common, making the positive effects of Lenvatinib on a patient's survival null after resistance is acquired. Therefore, it is crucial to understand mechanisms related to Lenvatinib resistance. This review aims to piece together various mechanisms involved in Lenvatinib resistance and summarizes the research done so far investigating it.

Indexed as

Antineoplastic AgentsLiver NeoplasmsQuinolinesHumansPhenylurea CompoundsProtein Kinase InhibitorsReceptor Protein-Tyrosine KinasesVascular Endothelial Growth Factor AAntineoplastic AgentslenvatinibPhenylurea CompoundsProtein Kinase InhibitorsQuinolinesReceptor Protein-Tyrosine KinasesVascular Endothelial Growth Factor Alenvatinibliver cancerresistant mechanisms

Identifiers

PMID37671815
PMCPMC10840925
OpenAlexW4386467247

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.