Abstract A068: Downregulation of MEIS2 in Multiple Cancers and Its Correlation with Improved Overall Survival: A Potential Prognostic Biomarker

Abstract

The homeobox transcription factor MEIS2 is a crucial regulator of developmental processes, including embryogenesis and neurogenesis. However, its role in cancer progression and prognosis remains poorly understood across various human malignancies. This study evaluated the expression profile of MEIS2 in different cancer types and investigated its potential utility as a robust prognostic biomarker for overall survival. We analyzed MEIS2 expression levels across multiple primary cancer datasets—including adrenocortical carcinoma (ACC), bladder urothelial carcinoma (BLCA), breast invasive carcinoma (BRCA), cervical squamous cell carcinoma (CESC), acute myeloid leukemia (LAML), and ovarian serous cystadenocarcinoma (OV)—using public data from the Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases. Expression differences between tumor and normal tissues were evaluated using two-tailed t-tests. Survival outcomes were determined via Kaplan-Meier analysis and Mantel-Haenszel hazard ratios, comparing cohorts split into high and low MEIS2 expression ($n = 60$ per group). Statistical variance across distinct clinical subgroups (M0–M7) was evaluated using Tukey’s multiple comparison test. MEIS2 expression was significantly downregulated in malignant tissues compared to corresponding normal controls across all six analyzed cancer types. The most pronounced transcriptomic reductions were observed in ACC ($p = 7.55 \times 10^{-31}$) and BRCA ($p = 8.72 \times 10^{-157}$). Kaplan-Meier survival analysis demonstrated that high MEIS2 expression is strongly associated with a significantly prolonged median survival compared to low expression (1,374 days vs. 336 days; Hazard Ratio = 2.27, 95% CI: 1.43–3.61, $p < 0.0001$). Furthermore, multiple comparison tests across subgroup presentations (M0–M7) revealed significant baseline differences in MEIS2 retention (e.g., M0 vs. M1–M4, $p < 0.0001$), establishing a distinct link to advanced clinical progression. Our findings demonstrate that MEIS2 is consistently downregulated across various malignancies and serves as a robust prognostic biomarker for overall survival. These results suggest a potential tumor-suppressive role for MEIS2, highlighting its promise for future clinical stratification and as a potential target for innovative therapeutic strategies in oncology.