Evidence map›Paper›PMID 35490363›Full record

ReviewBosnian journal of basic medical sciences2022

Role and significance of c-KIT receptor tyrosine kinase in cancer: A review.

Emana Sheikh, Tony Tran, Semir Vranic, Arkene Levy, R Daniel Bonfil

Open access · goldAbstract readReview
In one paragraph

Review in Bosnian journal of basic medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 2 pooled it
7.0field-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

75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 87 citations in OpenAlex.

  1. Pooled it
  2. Molecular Basis of Hydatidiform Moles-A Systematic Review.International journal of molecular sciences · 2024
    Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. The Mutational Landscape of Acute Myeloid Leukemia and Its Impact.International journal of molecular sciences · 2026
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

15 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 2 institutions in 2 countries.

Emana SheikhOMS-III, Dr. Kiran C. Patel College of Osteopathic Medicine, Nova Southeastern University, Fort Lauderdale, Florida, USA.
Tony TranDr. Kiran C. Patel College of Osteopathic Medicine, Nova Southeastern University, Fort Lauderdale, Florida, USA.
Semir VranicCollege of Medicine, QU Health, Qatar University, Doha, Qatar.
Arkene LevyDepartment of Medical Education, Dr. Kiran C. Patel College of Allopathic Medicine, Nova Southeastern University, Fort Lauderdale, Florida, USA.
R Daniel BonfilDepartment of Medical Education, Dr. Kiran C. Patel College of Allopathic Medicine, Nova Southeastern University, Fort Lauderdale, Florida, USA.
Nova Southeastern University · USQatar University · QA

Funding

Bone-induced c-kit in Prostate Cancer Cells: Implications for Bone MetastasisR21CA162232 · NCI · WAYNE STATE UNIVERSITY · PI BONFIL, RICARDO DANIEL · 2011 to 2012
$364k
NCI NIH HHS R21 CA162232
6 · The paper itself

Abstract

c-kit is a classical proto-oncogene that encodes a receptor tyrosine kinase (RTK) that responds to stem cell factor (SCF). C-KIT signaling is a critical regulator of cell proliferation, survival, and migration and is implicated in several physiological processes, including pigmentation, hematopoiesis and gut movement. Accumulating evidence suggests that dysregulated c-KIT function, caused by either overexpression or mutations in c-kit, promotes tumor development and progression in various human cancers. In this review, we discuss the most important structural and biological features of c-KIT, as well as insights into the activation of intracellular signaling pathways following SCF binding to this RTK. We then illustrate how different c-kit alterations are associated with specific human cancers and describe recent studies that highlight the contribution of c-KIT to cancer stemness, epithelial-mesenchymal transition and progression to metastatic disease in different experimental models. The impact of tyrosine kinase inhibitors in treating c-KIT-positive tumors and limitations due to their propensity to develop drug resistance are summarized. Finally, we appraise the potential of novel therapeutic approaches targeting c-KIT more selectively while minimizing toxicity to normal tissue.

Indexed as

NeoplasmsCell ProliferationHumansProtein Kinase InhibitorsProto-Oncogene Proteins c-kitStem Cell FactorKIT protein, humanProtein Kinase InhibitorsProto-Oncogene Proteins c-kitStem Cell Factor

Identifiers

PMID35490363
PMCPMC9519160
OpenAlexW4225264853

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.