ArticleBMC medical genomics2021
Mutational signatures among young-onset testicular cancers.
Article in BMC medical genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Testicular sex cord-stromal tumors in mice with constitutive activation of PI3K and loss of Pten.Carcinogenesis · 2025Article
- TET2 gene mutation status associated with poor prognosis of transition zone prostate cancer: a retrospective cohort study based on whole exome sequencing and machine learning models.Frontiers in endocrinology · 2025Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIncidence of testicular cancer is highest among young adults and has been increasing dramatically for men born since 1945. This study aimed to elucidate the factors driving this trend by investigating differences in mutational signatures by age of onset.
methodsWe retrieved somatic variant and clinical data pertaining to 135 testicular tumors from The Cancer Genome Atlas. We compared mutational load, prevalence of specific mutated genes, mutation types, and mutational signatures between age of onset groups (< 30 years, 30-39 years, ≥ 40 years) after adjusting for subtype. A recursively partitioned mixture model was utilized to characterize combinations of signatures among the young-onset cases.
resultsMutational load was significantly higher among older-onset tumors (p < 0.05). There were no highly prevalent driver mutations among young-onset tumors. Mutated genes and types of nucleotide mutations were not significantly different by age group (p > 0.05). Signatures 1, 8 and 29 were more common among young-onset tumors, while signatures 11 and 16 had higher prevalence among older-onset tumors (p < 0.05). Among young-onset tumors, clustering of signatures resulted in four distinct tumor classes.
conclusionsSignature contributions differ by age with signatures 1, 8 and 29 were more common among younger-onset tumors. While these signatures are connected with endogenous deamination of 5-methylcytosine, late replication errors and chewing tobacco, respectively, additional research is needed to further elucidate the etiology of young-onset testicular cancer. Large studies of mutational signatures among young-onset patients are required to understand epidemiologic trends as well as inform targeted prevention and treatment strategies.
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