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The following is a summary of “GATA3 amplification is associated with high grade disease in non-invasive urothelial bladder cancer but unrelated to patient prognosis,” published in the February 2025 issue of BMC Urology by Plage et al. 

Researchers conducted a retrospective study to assess GATA3 binding protein (GATA3) gene copy number alterations in urothelial bladder cancer and their impact on tumor aggressiveness, prognosis, and protein expression. 

They analyzed tissue microarray of 2,700+ urothelial bladder cancers (pTa-pT4) using dual-labeling fluorescence in-situ hybridization (FISH) with probes for GATA3 (10p14) and centromere 10. They categorized GATA3 gains as elevation (ratio GATA3/centromere ≥ 2/≤4), low-level amplification (ratio > 4/≤12), and high-level amplification (ratio > 12) and classified deletions as homozygous or heterozygous. 

The results showed GATA3 copy number gain in 9.9% of 2,213 tumors, including 2.0% with elevation, 3.2% with low-level amplification, and 4.7% with high-level amplification. High-level amplification increased from pTa G2 low (0%) to pTa G3 (12% [CI 0.07;0.21]; P < 0.0001) but decreased in pT2-4 (5.4% [CI 0.07;0.21]; P < 0.0001). In muscle-invasive carcinomas, amplification was not linked to aggressiveness or survival. No homozygous deletion was detected, and heterozygous deletion was found in 1.1% of 1,432 pT2-4 tumors without association with progression. GATA3 copy number correlated with expression (P < 0.0001) but weakly; 2.3% of GATA3-negative cancers had deletions, and 42.1% of strong expression had high-level amplification. 

Investigators found high-level GATA3 amplification linked to pTa tumor progression, while GATA3 deletion was rare. They concluded neither drove GATA3 expression dysregulation.

Source: bmcurol.biomedcentral.com/articles/10.1186/s12894-025-01704-y