A possible explanation includes the rapid divergence of chromosomally unstable high grade serous carcinomas after the early events during oncogenesis (typically loss of BRCA1 or BRCA2 and p53 loss) that results in heterogeneity within this group of tumors, such that no consistent pattern of miRNA upregulation emerged across the group as a whole, compared to the low grade tumors. Here, BRCA2 is linked to serous adenocarcinoma.