Evidence map›Paper›PMID 21603317›Full record

ArticleWorld journal of clinical oncology2011

Tyrosine kinase inhibitors: Multi-targeted or single-targeted?

Fleur Broekman, Elisa Giovannetti, Godefridus J Peters

Abstract read
In one paragraph

Article in World journal of clinical oncology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

105 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. Neuropsychiatric Symptoms Mimicking Dementia in a Patient Treated With Imatinib.Annals of clinical and translational neurology · 2026
    Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
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  15. Article
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  17. ThePharmaceuticals (Basel, Switzerland) · 2025
    Article
  18. Kinase-Targeted Therapies for Glioblastoma.International journal of molecular sciences · 2025
    Review
  19. Article
  20. Article

45 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.

Fleur BroekmanFleur Broekman, Elisa Giovannetti, Godefridus J Peters, Department of Medical Oncology, VU University Medical Center, 1007 MB Amsterdam, The Netherlands.
Elisa Giovannetti
Godefridus J Peters

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Since in most tumors multiple signaling pathways are involved, many of the inhibitors in clinical development are designed to affect a wide range of targeted kinases. The most important tyrosine kinase families in the development of tyrosine kinase inhibitors are the ABL, SCR, platelet derived growth factor, vascular endothelial growth factor receptor and epidermal growth factor receptor families. Both multi-kinase inhibitors and single-kinase inhibitors have advantages and disadvantages, which are related to potential resistance mechanisms, pharmacokinetics, selectivity and tumor environment. In different malignancies various tyrosine kinases are mutated or overexpressed and several resistance mechanisms exist. Pharmacokinetics is influenced by interindividual differences and differs for two single targeted inhibitors or between patients treated by the same tyrosine kinase inhibitor. Different tyrosine kinase inhibitors have various mechanisms to achieve selectivity, while differences in gene expression exist between tumor and stromal cells. Considering these aspects, one type of inhibitor can generally not be preferred above the other, but will depend on the specific genetic constitution of the patient and the tumor, allowing personalized therapy. The most effective way of cancer treatment by using tyrosine kinase inhibitors is to consider each patient/tumor individually and to determine the strategy that specifically targets the consequences of altered (epi)genetics of the tumor. This strategy might result in treatment by a single multi kinase inhibitor for one patient, but in treatment by a couple of single kinase inhibitors for other patients.

Indexed as

Breakpoint cluster region-Abelson murine leukemia oncogene homolog 1Epidermal growth factor receptorJanus kinasePlatelet derived growth factorTargeted therapyTyrosine kinase inhibitorsVascular endothelial growth factor receptor

Identifiers

PMID21603317
PMCPMC3095472

What OpenQuestion holds

Textmetadata
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.