Abstract

Ovarian cancer represents a significant public health challenge, characterized by late-stage diagnosis and limited treatment options. Recent advancements in genomic research have uncovered a wealth of genetic variants associated with ovarian cancer susceptibility, shedding light on the underlying molecular mechanisms driving disease onset and progression. This abstract provides an overview of the genetic and functional mechanisms implicated in ovarian cancer susceptibility, focusing on the interplay of genetic variants, dysregulated pathways, and the tumor microenvironment. Through genome-wide association studies (GWAS) and functional annotation analyses, researchers have identified susceptibility loci and regulatory elements that modulate gene expression and cellular processes relevant to ovarian carcinogenesis.