Evidence map›Paper›PMID 28256196›Full record

ArticleBMB reports2017

Afatinib ameliorates osteoclast differentiation and function through downregulation of RANK signaling pathways.

Hye Jung Ihn, Ju Ang Kim, Yong Chul Bae, Hong-In Shin, Moon-Chang Baek, Eui Kyun Park

Open access · goldAbstract read
In one paragraph

Article in BMB reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Bone Effects of Anti-Cancer Treatments in 2024.Calcified tissue international · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Roles of Mitogen-Activated Protein Kinases in Osteoclast Biology.International journal of molecular sciences · 2018
    Review
  13. Review
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

6 authors at 2 institutions in 2 countries.

Hye Jung IhnDepartments of Oral Pathology and Regenerative Medicine, Kyungpook National University, Daegu 41940, Korea.
Ju Ang KimDepartments of Oral Pathology and Regenerative Medicine, Kyungpook National University, Daegu 41940, Korea.
Yong Chul BaeAnatomy and Neurobiology, School of Dentistry, Kyungpook National University, Daegu 41940, Korea.
Hong-In ShinDepartments of Oral Pathology and Regenerative Medicine, Kyungpook National University, Daegu 41940, Korea.
Moon-Chang BaekDepartment of Molecular Medicine, CMRI, School of Medicine, Kyungpook National University, Daegu 41944, Korea.
Eui Kyun ParkDepartments of Oral Pathology and Regenerative Medicine, Kyungpook National University, Daegu 41940, Korea.
Regenerative Medicine Institute · MXKyungpook National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-small-cell lung cancer (NSCLC) is the third most common cancer that spreads to the bone, resulting in osteolytic lesions caused by hyperactivation of osteoclasts. Activating mutations in epidermal growth factor receptor-tyrosine kinase (EGF-TK) are frequently associated with NSCLC, and afatinib is a first-line therapeutic drug, irreversibly targeting EGF-TK. However, the effects of afatinib on osteoclast differentiation and activation as well as the underlying mechanism remain unclear. In this study, afatinib significantly suppressed receptor activator of nuclear factor κB (RANK) ligand (RANKL)-induced osteoclast formation in bone marrow macrophages (BMMs). Consistently, afatinib inhibited the expression of osteoclast marker genes, whereas, it upregulated the expression of negative modulator genes. The bone resorbing activity of osteoclasts was also abrogated by afatinib. In addition, afatinib significantly inhibited RANKL-mediated Akt/protein kinase B and c-Jun N-terminal kinase phosphorylation. These results suggest that afatinib substantially suppresses osteoclastogenesis by downregulating RANK signaling pathways, and thus may reduce osteolysis after bone metastasis. [BMB Reports 2017; 50(3): 150-155].

Indexed as

AfatinibAnimalsBone Marrow CellsBone ResorptionCell DifferentiationDown-RegulationErbB ReceptorsJNK Mitogen-Activated Protein KinasesMacrophagesMiceNF-kappa BOsteoclastsPhosphorylationQuinazolinesRANK LigandReceptor Activator of Nuclear Factor-kappa BAfatinibErbB ReceptorsJNK Mitogen-Activated Protein KinasesNF-kappa BQuinazolinesRANK LigandReceptor Activator of Nuclear Factor-kappa B

Identifiers

PMID28256196
PMCPMC5422028
OpenAlexW2609573012

What OpenQuestion holds

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LicenceCC BY-NC
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.