In the subgroup analysis, RFA demonstrated comparable RFS in treating less than 3 cm tumor (P=0.22) located in noncentral bisection (SII, SIII, SVI, SVII) and tumor between 3 cm and 5 cm (P=0.07) located in central bisections (SIV, SV, SVIII).
Gene expression analysis showed that TCEB2 gene was significantly upregulated in the OC tumors with acquired resistance compared with the sensitive tumors.
It has been demonstrated that von Hippel-Lindau disease (VHL) tumor-suppressor gene product possesses the SOCS box that forms a complex with Elongin B and C and Cullin-2, and it functions as a ubiquitin ligase.
The von Hippel-Lindau (VHL) tumour suppressorgene product is believed to be involved in the down-regulation of transcriptional elongation by preventing the association of elongin B and C with the catalytic subunit elongin A. Alterations in the human VHL gene lead to VHL disease which is associated with various rare neoplasias, including haemangioblastoma of the central nervous system, retinal angioma, clear cell renal carcinoma and pheochromocytoma.
Germline mutations in VHL patients, as well as somatic mutations in different tumors, including hemangioblastomas, have been identified, its ability to act as a tumor suppressor in vivo has been confirmed, and interaction with transcription factors Elongin B and C leading to inhibition of transcriptional elongation has been demonstrated.