Evidence map›Paper›PMID 28638122›Full record

ArticleScientific reports2017

Synergistic effects of various Her inhibitors in combination with IGF-1R, C-MET and Src targeting agents in breast cancer cell lines.

Aryan Stanley, G Hossein Ashrafi, Alan M Seddon, Helmout Modjtahedi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 94 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Gene Copy Number Dictates Extracellular Vesicle Cargo.International journal of molecular sciences · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Pyrotinib is effective in both trastuzumab-sensitive and primary resistant HER2-positive breast tumors.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2024
    Article
  15. Article
  16. Article
  17. Review
  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

4 authors at 1 institution in 2 countries.

Aryan StanleyKingston University London, School of Life Science, London, United Kingdom.
G Hossein AshrafiKingston University London, School of Life Science, London, United Kingdom.
Alan M SeddonKingston University London, School of Life Science, London, United Kingdom.
Helmout ModjtahediKingston University London, School of Life Science, London, United Kingdom. H.Modjtahedi@kingston.ac.uk.ORCID 0000-0002-5509-7415
Kingston University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Overexpression of HER2 has been reported in around 25% of human breast cancers. Despite recent advances in HER2 targeted therapy, many patients still experience primary and secondary resistance to such treatments, the mechanisms for which are poorly understood. Here, we investigated the sensitivity of a panel of breast cancer cell lines to treatment with various types of HER-family inhibitors alone or in combination with other tyrosine kinase inhibitors or chemotherapeutic agents. We found that treatment with the second-generation irreversible HER-family inhibitors, particularly afatinib and neratinib, were more effective than treatment with the first-generation reversible inhibitors in inhibiting growth, migration and downstream cell signalling in breast cancer cells. Of the three HER2 overexpressing cell lines in this panel, SKBr3 and BT474 were highly sensitive to treatment with HER-family inhibitors, while MDA-MB-453 was comparatively resistant. Combinations of HER-family inhibitors with NVP-AEW541, dasatinib or crizotinib (inhibitors of IGF-1R, Src and c-Met/ALK, respectively) led to synergistic effects in some of the cell lines examined. In particular, treatment with a combination of Src and HER-family member inhibitors resulted in synergistic growth inhibition of MDA-MB453 cells, implicating Src as a mediator of resistance to HER2-targeting agents. Our results suggest that combining HER-family inhibitors with other TKIs such as dasatinib may have therapeutic advantages in certain breast cancer subtypes and warrants further investigation.

Indexed as

AfatinibAntineoplastic AgentsBreast NeoplasmsCell CycleCell EnlargementCell Line, TumorCell MovementCrizotinibDasatinibErb-b2 Receptor Tyrosine KinasesFemaleHumansPhosphorylationProtein Kinase InhibitorsProto-Oncogene Proteins c-metPyrimidinesAfatinibAntineoplastic AgentsCrizotinibDasatinibERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesneratinibNVP-AEW541Protein Kinase InhibitorsProto-Oncogene Proteins c-metPyrimidinesPyrrolesQuinolinesReceptor, IGF Type 1src-Family Kinases

Identifiers

PMID28638122
PMCPMC5479850
OpenAlexW2627019357

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.