Evidence map›Paper›PMID 27536065›Full record

ReviewDrug design, development and therapy2016

Receptor tyrosine kinase (c-Kit) inhibitors: a potential therapeutic target in cancer cells.

Maryam Abbaspour Babaei, Behnam Kamalidehghan, Mohammad Saleem, Hasniza Zaman Huri, Fatemeh Ahmadipour

Open access · goldAbstract readReview
In one paragraph

Review in Drug design, development and therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 1 pooled it
7.8field-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.

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

125 citing papers in PubMed, 1 synthesis or guideline pooled it, 245 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Molecular Mechanisms and Clinical Implications ofCurrent issues in molecular biology · 2025
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Stabilizing Tumor-Resident Mast Cells Restores T-Cell Infiltration and Sensitizes Sarcomas to PD-L1 Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Novel somatic Missense Mutations in Exon 11 of the KIT Gene are Detected in Melanoma.Asian Pacific journal of cancer prevention : APJCP · 2023
    Article
  19. Article
  20. Review

65 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

5 authors at 1 institution in 1 country.

Maryam Abbaspour BabaeiDepartment of Pharmacy, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Behnam KamalidehghanDepartment of Medical Genetics, National Institute of Genetic Engineering and Biotechnology (NIGEB), Shahrak-e Pajoohesh; Medical Genetics Department, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad SaleemDepartment of Urology; Department of Laboratory Medicine and Pathology, Masonic Cancer Center, University of Minnesota; Section of Molecular Therapeutics & Cancer Health Disparity, The Hormel Institute, Austin, MN, USA.
Hasniza Zaman HuriDepartment of Pharmacy, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia; Clinical Investigation Centre, University Malaya Medical Centre, Lembah Pantai, Kuala Lumpur, Malaysia.
Fatemeh AhmadipourDepartment of Pharmacy, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
University of Malaya · MY

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

c-Kit, a receptor tyrosine kinase, is involved in intracellular signaling, and the mutated form of c-Kit plays a crucial role in occurrence of some cancers. The function of c-Kit has led to the concept that inhibiting c-Kit kinase activity can be a target for cancer therapy. The promising results of inhibition of c-Kit for treatment of cancers have been observed in some cancers such as gastrointestinal stromal tumor, acute myeloid leukemia, melanoma, and other tumors, and these results have encouraged attempts toward improvement of using c-Kit as a capable target for cancer therapy. This paper presents the findings of previous studies regarding c-Kit as a receptor tyrosine kinase and an oncogene, as well as its gene targets and signaling pathways in normal and cancer cells. The c-Kit gene location, protein structure, and the role of c-Kit in normal cell have been discussed. Comprehending the molecular mechanism underlying c-Kit-mediated tumorogenesis is consequently essential and may lead to the identification of future novel drug targets. The potential mechanisms by which c-Kit induces cellular transformation have been described. This study aims to elucidate the function of c-Kit for future cancer therapy. In addition, it has c-Kit inhibitor drug properties and their functions have been listed in tables and demonstrated in schematic pictures. This review also has collected previous studies that targeted c-Kit as a novel strategy for cancer therapy. This paper further emphasizes the advantages of this approach, as well as the limitations that must be addressed in the future. Finally, although c-Kit is an attractive target for cancer therapy, based on the outcomes of treatment of patients with c-Kit inhibitors, it is unlikely that Kit inhibitors alone can lead to cure. It seems that c-Kit mutations alone are not sufficient for tumorogenesis, but do play a crucial role in cancer occurrence.

Indexed as

Antineoplastic AgentsCell ProliferationHumansLeukemia, Myeloid, AcuteMutationProto-Oncogene Proteins c-kitReceptor Protein-Tyrosine KinasesSignal TransductionAntineoplastic AgentsProto-Oncogene Proteins c-kitReceptor Protein-Tyrosine Kinasescancercancer therapyc-Kitoncogene

Identifiers

PMID27536065
PMCPMC4975146
OpenAlexW2506963569

What Socratic holds

Textmetadata
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 Socratic graph.