RT Journal Article SR Electronic T1 The Prognostic Role of ACO2 in Renal Cell Carcinoma JF Anticancer Research JO Anticancer Res FD International Institute of Anticancer Research SP 1503 OP 1511 DO 10.21873/anticanres.16299 VO 43 IS 4 A1 DAMIAN JAWORSKI A1 ADAM KOWALEWSKI A1 JUSTYNA DURŚLEWICZ A1 PAULINA ANTOSIK A1 MARTA SMOLIŃSKA A1 DARIUSZ GRZANKA A1 ŁUKASZ SZYLBERG YR 2023 UL http://ar.iiarjournals.org/content/43/4/1503.abstract AB Background/Aim: Renal cell carcinoma (RCC) continues to pose a challenge due to our limited understanding of its underlying pathophysiology. Aconitase 2 (ACO2) is a mitochondrial Fe–S cluster enzyme that catalyzes the stereospecific isomerization of citrate to isocitrate in the second step of the Krebs cycle. We investigated the relationship between ACO2 protein expression and the clinical course of RCC. Materials and Methods: Tumor samples were evaluated in a commercial tissue microarray for ACO2 expression using the H-score. The tissue microarrays contained a total of 96 cores from primary tumors, matched metastases, and matched adjacent tissues derived from 32 patients with RCC. The mean follow-up was 82.74 months. Correlation analysis of clinicopathological data and survival was performed. Expression levels of ACO2 mRNA were compared using publicly available data. Results: All the tissue samples showed cytoplasmic ACO2 expression, with median H-scores of 139.7, 130.3 and 166.7 in primary tumor, metastatic tissue, and matched control tissue, respectively. A significantly higher ACO2 expression was found in normal tissues compared to primary and metastatic RCC. The analysis demonstrated a significantly positive correlation between ACO2 expression in primary tumors and their metastases. The results also showed a significant correlation between the expression of ACO2 and worse overall survival among patients with RCC. Conclusion: ACO2 may be used as a prognostic factor in RCC. Significant alterations in ACO2 expression are thought to occur in the early stages of RCC carcinogenesis. Considering the physiological role of ACO2, its dysregulation may constitute an adaptive trait of RCC for escaping the equilibrium phase of immunoediting.