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Young adult cancer has increased in incidence worldwide, but its molecular etiologies remain unclear. We systematically characterize genomic profiles of young adult tumors with ages of onset ≤50 years and compare them to later-onset tumors using over 6,000 cases across 14 cancer types. While young adult tumors generally show lower mutation burdens and comparable copy-number variation rates compared to later-onset cases, they are enriched for multiple driver mutations and copy-number alterations in subtype-specific contexts. Characterization of tumor immune microenvironments reveals pan-cancer patterns of elevated TGF-β response/dendritic cells and lower IFN-γ response/macrophages relative to later-onset tumors, corresponding to age-related responses to immunotherapy in several cancer types. Finally, we identify prevalent clinically actionable events that disproportionally affect young adult or later-onset cases. The resulting catalog of age-related molecular drivers can guide precision diagnostics and treatments for young adult cancer.
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•Gene-level mutations, CNVs, methylations, and fusions associated with young adult cases•Different rates of mutation/CNV-subtype pairs in young adult versus later-onset cases•Pan-cancer approach identifies consistent age-related tumor immune response•Young adult cases show different frequencies of actionable genomic drivers
In recent years, the incidence of multiple cancer types has risen among young adults under 50 years, but whether they show specific molecular etiology remains unclear. Lee et al. characterize the genomic and tumor microenvironment features distinguishing young adults from later-onset cancer and potential treatment implications.