Expression of TP and TIE2 genes in normal ovary with corpus luteum and in ovarian cancer: correlation with ultrasound-derived peak systolic velocity

Citation
K. Hata et al., Expression of TP and TIE2 genes in normal ovary with corpus luteum and in ovarian cancer: correlation with ultrasound-derived peak systolic velocity, MOL HUM REP, 6(4), 2000, pp. 319-323
Citations number
29
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR HUMAN REPRODUCTION
ISSN journal
13609947 → ACNP
Volume
6
Issue
4
Year of publication
2000
Pages
319 - 323
Database
ISI
SICI code
1360-9947(200004)6:4<319:EOTATG>2.0.ZU;2-L
Abstract
Transvaginal colour and pulsed Doppler ultrasonography analyses of blood fl ow velocity have indicated that intra-tumoral peak systolic velocity (PSV) is a good indicator of ovarian malignancy. Therefore, we examined whether t here was an association between the expression of angiogenic genes, e.g, th ymidine phosphorylase (TP) and TIE2 and the PSV of blood flow in normal and cancerous ovaries. Initially, 40 patients were examined by transvaginal ul trasonography and 23 ovaries were surgically removed; 14 were normal with c orpora lutea (CL) and nine showed ovarian cancer. The ovarian tissue was di ssected according to areas of high blood velocity and gene expression was e xamined using the reverse transcriptase-polymerase chain reaction (RT-PCR). No significant differences were found between PSV in the normal ovary with CL and ovarian cancer (P = 0.95). TP gene expression was significantly hig her in ovarian cancer than in normal ovary with CL (P = 0.02), while TIE2 g ene expression was not significantly different (P = 0.186). There was a sig nificant correlation between TIE2 gene expression and PSV in the normal ova ry with CL (r = 0.633, P = 0.015), while TP expression was significantly co rrelated with the PSV in ovarian cancer (r = 0.757, P = 0.018). These resul ts indicate that there is a biological difference between physiological and pathological angiogenesis, TIE2 having a physiological role and TP being i nvolved in pathological angiogenesis.