Aitokallio-Tallberg A, Viinikka L, Ylikorkala O
Cancer Lett. 1987 Feb;34(2):201-6. doi: 10.1016/0304-3835(87)90011-5.
The production of the antiaggregatory and vasodilatory prostacyclin (PGI2) in patients with gynaecological tumours was studied by assaying urinary 6-keto-prostaglandin F1a (= 6-keto-PGF1a), a hydration product of PGI2), by radioimmunoassay following high performance liquid chromatography (HPLC) in 59 patients with gynaecological tumours and 12 non-tumourous control women. Urinary 6-keto-PGF1a excretion in patients with cervical cancer (28.3 +/- 3.6 pmol/mmol creatinine, mean +/- S.E., n = 12), endometrial cancer (22.8 +/- 3.7 pmol/mmol creatinine, n = 12, uterine fibroids (26.0 +/- 3.5 pmol/mmol creatinine, n = 12) benign ovarian cysts (22.4 +/- 1.8 pmol/mmol creatinine, n = 12) did not differ from that in the control women (29.9 +/- 3.6 pmol/mmol creatinine, n = 12). However, patients with ovarian cancer excreted increased amounts of 6-keto-PGF1a (55.4 +/- 10.4 pmol/mmol creatinine, n = 11, P less than 0.05), although this bore no relation to tumour histology, clinical stage or the outcome of the patients. Thus, ovarian cancer is accompanied by increased PGI2 production, perhaps in the kidneys and/or in the cancer tissue.
通过高效液相色谱法（HPLC）后采用放射免疫分析法测定尿中6-酮-前列腺素F1α（PGI2的水合产物），对59例妇科肿瘤患者和12例非肿瘤对照女性进行研究，以探讨妇科肿瘤患者抗聚集和血管舒张性前列环素（PGI2）的产生情况。宫颈癌患者（28.3±3.6 pmol/mmol肌酐，均值±标准误，n = 12）、子宫内膜癌患者（22.8±3.7 pmol/mmol肌酐，n = 12）、子宫肌瘤患者（26.0±3.5 pmol/mmol肌酐，n = 12）、良性卵巢囊肿患者（22.4±1.8 pmol/mmol肌酐，n = 12）的尿6-酮-PGF1α排泄量与对照女性（29.9±3.6 pmol/mmol肌酐，n = 12）相比无差异。然而，卵巢癌患者排泄的6-酮-PGF1α量增加（55.4±10.4 pmol/mmol肌酐，n = 11，P<0.05），尽管这与肿瘤组织学、临床分期或患者预后无关。因此，卵巢癌伴随着PGI2产生增加，可能发生在肾脏和/或癌组织中。
