ArticleEndocrine2026
Association of ADAM17 expression with CD4 + and CD8 + tumor-infiltrating lymphocytes in adrenocortical carcinoma and benign adrenal adenoma.
Article in Endocrine, 2026. 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
backgroundAdrenocortical carcinoma (ACC) is a rare and aggressive endocrine malignancy. Although immune checkpoint signaling and tumor-infiltrating lymphocytes (TILs) have been implicated in ACC biology, the role of ADAM10 and ADAM17 in the adrenocortical tumor immune microenvironment remains poorly understood. This study aimed to evaluate the expression of ADAM10, ADAM17, PD-L1, CD4, and CD8 in ACC and benign adrenal adenoma (BAA) tissues.
methodsThis retrospective study included 21 patients with histopathologically confirmed ACC and 39 patients with BAA. Immunohistochemical staining for ADAM10, ADAM17, PD-L1, CD4, and CD8 was performed on formalin-fixed paraffin-embedded tissue samples. ADAM10 and ADAM17 expression were assessed using H-scores, while CD4 + and CD8 + TIL counts were quantified by cell counting. Comparative and correlation analyses were conducted.
resultsACC tissues exhibited significantly higher CD4 + and CD8 + TIL counts than BAA tissues (p = 0.010 and p = 0.006, respectively). No significant differences were observed between the groups regarding ADAM10, ADAM17, or PD-L1 expression (all p > 0.05). ADAM17 H-scores showed significant positive correlations with both CD4 + and CD8 + TIL counts in ACC and BAA. No significant associations were found between ADAM10, ADAM17, or PD-L1 expression and Ki-67 index, tumor size, or ENSAT stage.
conclusionsIn this cohort, ACC tissues showed higher CD4 + and CD8 + TIL counts than BAA tissues. Although ADAM10, ADAM17, and PD-L1 expression did not differ significantly between malignant and benign tumors, ADAM17 expression was positively associated with TIL count. These findings warrant further investigation of the potential relationship between ADAM17 and the immune microenvironment of adrenocortical tumors.
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