Prevalence,patterns,risk factors and outcomes of peritoneal metastases after laparoscopic hepatectomy for hepatocellular carcinoma:a multicenter study from China

Background:We aim to investigate the prevalence,patterns,risk factors,and outcomes of peritoneal metastases(PM)after curative laparoscopic hepatectomy(LH)for hepatocellular carcinoma(HCC).Methods:A multicenter cohort of 2,138 HCC patients who underwent curative LH from August 2010 to December 2016 from seven hospitals in China was retrospectively analyzed.The incidence of PM following LH was evaluated and compared with that in open hepatectomy(OH)after 1:1 propensity score matching(PSM).Results:PM prevalence was 5.1%(15/295)in the early period[2010-2013],2.6%(47/1,843)in the later period[2014-2016],and 2.9%(62/2,138)in all LH patients,which was similar to 4.0%(59/1,490)in the OH patients.The recurrence patterns,timing,and treatment did not significantly vary between the LH and OH patients(P>0.05).Multivariate logistic regression revealed that tumor diameter>5 cm,non-anatomical resection,presence of microvascular invasion,and lesions<2 cm from major blood vessels were independent risk factors of PM after LH.Of the 62 cases with PM,26(41.9%)had PM only,34(54.9%)had intrahepatic recurrence(IHR)and PM,and 2(3.2%)had synchronous extraperitoneal metastases(EPM).Patients with resectable PM had a 5-year overall survival(OS)of 65.0%compared to 9.0%for unresectable PM(P=0.001).Conclusions:The prevalence,patterns and independent risk factors of PM were identified for HCC patients after LH.LH was not associated with increased incidence of PM in HCC patients for experienced surgeons.Surgical re-excision of PM was associated with prolonged survival.

Influence of gonadotropin-releasing hormone agonist on the effect of chemotherapy upon ovarian cancer and the prevention of chemotherapy-induced ovarian damage:an experimental study with nu/nu athymic mice

Background and objective:Gonadotropin-releasing hormone (GnRH) plays an important role in the regulation of ovarian function and ovarian cancer cell growth. In this study, we determined whether administration of the GnRH agonist (GnRHa), triporelin, prior to cisplatin treatment affects cisplatin and/or prevents cisplatin-induced ovarian damage. Methods:nu/nu mice were injected with ovarian cancer OVCAR-3 cells intraperitoneally. After two weeks, the mice were treated with saline (control), cisplatin, GnRHa, or cisplatin plus GnRHa for four weeks. At the end of the experimental protocol, blood, tumor, ovary, and uterine tissues were resected for hematoxylin and eosin (H&E) staining, immunohistochemical analyses of Ki67, nuclear factor-κB (NF-κB), and caspase-3, transmission electron microscopy of apoptosis, or enzyme-linked immunosorbent assay (ELISA) analyses of anti-Mullerian hormone (AMH). Results:Cisplatin treatment effectively inhibited tumor growth in mice treated with human ovarian cancer cells; however the treatment also induced considerable toxicity. Immunohistochemical analyses showed that Ki67 expression was reduced in cisplatin-treated mice compared to control (P<0.05), but there was no statistically significant differences between cisplatin-treated mice and cisplatin plus GnRHa-treated mice (P>0.05), while expressions of NF-κB and caspase-3 were reduced and induced, respectively, in cisplatin-treated mice and cisplatin plus GnRHa-treated mice. Apoptosis occurred in the GnRHa, cisplatin, and cisplatin plus GnRHa-treated mice, but not in control mice. Ovaries exposed to GnRHa in both GnRHa mice and cisplatin-treated mice (combination group) had significantly more primordial and growth follicles and serum levels of AMH than those in the control mice and cisplatin-treated mice (P<0.05). Conclusions:Administration of GnRHa to mice significantly decreased the extent of ovarian damage induced by cisplatin, but did not affect the anti-tumor activity of cisplatin.