SynthesisFrontiers in endocrinology2026
A scoping review of imatinib-induced testicular toxicity and male fertility impairment.
Synthesis in Frontiers in endocrinology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- Platelet-Derived Growth Factor Receptor Alpha in Male Reproductive Health and Oxidative Stress: Stromal Homeostasis, Injury, and Research Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Imatinib, the first-generation tyrosine kinase inhibitor (TKI), has been widely adopted as frontline therapy for chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST). Growing evidence indicates potential gonadotoxic effects, raising concerns about its long-term impact on male fertility. Objective: This scoping review was undertaken to synthesize preclinical and clinical evidence on imatinib-induced reproductive toxicity in males, with emphasis on mechanisms, dose- and age-dependent susceptibility, and reversibility of testicular injury. Methods: A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science following PRISMA-ScR guidelines. Twenty studies published between 2003 and 2025 were included. Results: Across animal and human studies, inhibition of Proto-oncogene c-KIT (c-KIT) and Platelet-Derived Growth Factor Receptor (PDGFR) signaling was consistently observed, leading to germ cell apoptosis, impaired spermatogonial proliferation, and disruption of the blood-testis barrier (BTB). Dose-dependent reductions in testosterone and sperm density were documented, with partial recovery after drug discontinuation in several models. However, neonatal exposure was more often associated with persistent or irreversible testicular damage. Conclusion: Imatinib exerts gonadotoxic effects through inhibition of c-KIT/PDGFR signaling, disruption of the BTB, and dysregulation of the hypothalamic-pituitary-gonadal axis in a dose- and age-dependent manner. Although partial recovery is possible after withdrawal, neonatal and prepubertal exposures carry a high risk of irreversible impairment. These findings highlight the need for systematic fertility counseling and preservation in adolescent and reproductive-age males, in line with the 2025 European LeukemiaNet (ELN) recommendations.
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Registered trials
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.