ArticleMedicine2025
Comprehensive pan-cancer multi-omics analysis of ATAD2 in human cancers.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundATAD2, a member of the AAA + ATPase family and a known cancer/testicular antigen, has demonstrated oncogenic properties in various cancers. Despite its established role in cancer progression, a comprehensive pan-cancer analysis of its prognostic significance, therapeutic predictive potential, and immunological associations has not been conducted.
methodsWe performed a pan-cancer analysis of ATAD2 using data from The Cancer Genome Atlas (TCGA), assessing its expression profiles across different tumor types. We examined its correlations with survival prognosis, clinical outcomes, and cancer-associated signaling pathways. Additionally, we explored the relationship between ATAD2 expression and the tumor immune microenvironment, as well as its predictive value for responses to immunotherapy, targeted therapy, and chemotherapy.
resultsATAD2 was significantly upregulated in multiple tumor types, and its increased expression was associated with poor prognosis and adverse clinical outcomes. Further analysis revealed that ATAD2 expression was closely linked to cancer-related signaling pathways, tumor mutational burden, and microsatellite instability. Moreover, ATAD2 expression showed strong correlations with immune cell infiltration, immune-related gene expression, and responses to various treatment regimens, including immunotherapy, targeted therapy, and chemotherapy.
conclusionATAD2 is a critical biomarker for poor prognosis and treatment response across a wide range of cancers. Its ability to predict therapeutic responses, particularly for immunotherapy, targeted therapy, and chemotherapy, underscores its clinical significance. Further experimental studies and clinical trials are needed to explore ATAD2's role in cancer progression and its involvement in therapeutic resistance mechanisms.
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