ArticleThe Journal of clinical endocrinology and metabolism2026
Hypothalamic-pituitary deficiency after radiation in childhood cancer survivors is associated with rare variants in TNS2.
Article in The Journal of clinical endocrinology and metabolism, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Hypothalamic-pituitary deficiency after radiation in childhood cancer survivors is associated with rare variants in TNS2.The Journal of clinical endocrinology and metabolism · 2026Article
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18 authors.
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Abstract
contextRadiation to the hypothalamic-pituitary (HP) region (HP-RT) is a strong risk factor for HP deficiency among childhood cancer survivors (survivors). However, there is inter-individual variability in developing HP deficiency after similar HP-RT dose exposures.
objectivesTo assess the genetic contribution to developing deficiencies of GH (GHD), LH/FSH (LH/FSHD), thyroid-stimulating hormone deficiency (thyroid-stimulating hormone deficiency [TSHD]), and ACTH (adrenocorticotropic hormone deficiency [ACTHD]) among survivors exposed to HP-RT.
methodsEligible participants included 5-year survivors exposed to HP-RT (n = 809; median follow-up 31.9 years) from the St. Jude Lifetime Cohort. We assessed the association between rare variants from whole-exome sequencing data (minor allele frequency [MAF] < 0.01, predicted to be pathogenic by functional prediction tools) and HP deficiency rate (total counts/person-year) among 801 survivors by the exact Poisson test. Genome-wide association analysis (GWAS) was conducted among 606 survivors of European ancestry with available whole-genome sequence data, targeting variants with MAF ≥ 0.01. The replication population was 1328 survivors from the Childhood Cancer Survivor Study (CCSS).
resultsCarriers of rare variants in TNS2, a ubiquitously expressed protein-coding gene including in brain, had significantly higher rates of HP deficiencies (rate ratio 2.72 [95% CI 1.81-4.09], P = 1.5 × 10-5) compared to non-carriers, which was replicated in the CCSS. This was also observed in individual HP deficiencies: LH/FSHD (3.31 [1.28-7.99]), TSHD (5.29 [2.42-11.34]), and ACTHD (3.97 [1.05-12.31]). There were no statistically significant variants in GWAS.
conclusionTNS2 may contribute to radiation-induced HP deficiencies. With further validation, screening for TNS2 variants has potential to help identify individuals who would benefit from surveillance and intervention following HP-RT.
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