ULK4 (Unc-51 Like Kinase 4)

DNAH11 rs4487645 A/C genotype (OR = 1.35; 95% CI: 1.24-1.46; p < 0.00001; I2 = 0%), ULK4 rs1052501 G/G genotype (OR = 1.21; 95% CI: 0.98-1.50; p = 0.08; I2 = 64%), ULK4 rs1052501 A/G genotype (OR = 1.23; 95% CI: 1.13-1.34; p < 0.00001; I2 = 0%), DTNB rs6746082 A/A genotype (OR = 1.10; 95% CI: 1.01-1.20; p = 0.03; I2 = 45%), and VDR rs1544410 A/G genotype (OR = 1.87; 95% CI: 1.04-3.36; p = 0.04; I2 = 0%) increased multiple myeloma risk. Our study concludes that DNAH11, ULK4, DTNB, and VDR may serve as predictive biomarkers for MM risk.

This study provides novel insights into CESC prognosis, immunotherapy, and drug development, contributing to the clinical treatment for CESC.

Finally, we observed that the CDKN2A SNP correlated with levels of CD4EMCD45ROCD27 cells (p = 9.3 × 10). These results suggest that genetic variants within these six loci influence MM risk through the modulation of specific subsets of immune cells, as well as vitamin D3, MCP-2, and IL20-dependent pathways.

This study reports the consistent association of genetic polymorphisms within the ULK4, ATG5, CDKN2A, IKBKE, CD46 and PARK2 loci in modulating MM risk and provides new insights into the functional role of ULK4, IKBKE, CD46, and CDKN2A polymorphisms in disease pathogenesis. Additional studies are still necessary to confirm the functional impact of these SNPs on the risk of developing MM and to identify the biological mechanisms behind the ATG5 association.