Objective To assess the clinical effectiveness and safety of laparoscopy versus laparotomy for endometrial cancer. Methods The databases such as The Cochrane Library, PubMed, EMbase, Ovid, CNKI, WanFang Data, and VIP were searched to collect the randomized control trials (RCTs) about the clinical effectiveness and safety of laparoscopy and laparotomy for endometrial cancer. The retrieval time was from January 1998 to September 2012. Two reviewers independently screened the literature according to the inclusive and exclusive criteria, extracted the data, and assessed the methodological quality of included studies. Then the meta-analysis was performed by using RevMan 5.0 software. Results A total of 10 RCTs involving 6 993 patients were included. Meta-analysis showed that, compared with laparotomy, laparoscopy had lesser amount of intraoperative bleeding, lower decrease of hemoglobin before and 1-day after operation, shorter time of both waiting for postoperative gas and hospital stay, lower incidence of postoperative complications, longer operation time, and higher incidence of intraoperative complications. Additionally, there were no differences between the 2 groups in the number of pelvic and para-aortic lymph nodes removed during operation, as well as the postoperative recurrence and mortality rates in 3-5 year follow-up. Conclusion Compared with laparotomy, laparoscopy shows lesser amount of intraoperative bleeding, lower decrease of hemoglobin before and 1-day after operation, shorter time of both waiting for postoperative gas and hospital stay, lower incidence of postoperative complications. But laparotomy shows lower incidences of intraoperative complications, and shorter operation time. Both operations are similar in the number of pelvic and para-aortic lymph nodes removed during operation, as well as the postoperative recurrence and mortality rates in 3-5 year follow-up. For quantity limitation and low methodological quality of included studies, this conclusion still needs to be further proved by performing more high-quality and large scale RCTs.
Objective To systematically evaluate the correlation between coffee and risk of endometrial cancer. Methods Such databases as CBM, CNKI, WanFang data, PubMed, EMbase and The Cochrane Library (Issue 5, 2012) were searched to collect the prospective cohort studies about correlation between coffee and endometrial cancer. The retrieval time was by the end of May 2012, and the references of the included literature were also retrieved. Two evaluators independently screened the literature according to the inclusion and exclusion criteria, extracted the data, and assessed the quality, and then the statistical analysis was conducted by using Stata 12.0 software. Results A total of 10 cohort studies involving 4 484 patients with endometrial cancer were included. The results of meta-analysis showed that, compared with the women who didn’t drink coffee or drank in the lowest dose, the women who drank coffee in the highest dose had a decreased risk of endometrial cancer (RR=0.69, 95%CI 0.62 to 0.78), same as the women who drank coffee frequently (RR=0.83, 95%CI 0.77 to 0.89). The results of dose-response analysis revealed that, when there was an increase of 2 more cups of coffee per day, there was the risk of endometrial cancer decreased by 12%. Conclusion Drinking coffee frequently (more than 2 cups per day) can decrease the risk of endometrial cancer which can be significantly decreased when drinking in a big dose (more than 5 cups per day).
ObjectiveTo systematically review the value of human epididymis protein 4 (HE4) in early diagnosis of endometrial cancer. MethodsDatabases including The Cochrane Library (Issue 1, 2013), PubMed, MEDLINE (Ovid), CNKI, CBM and WanFang Data were electronically searched for relevant studies on HE4 versus the golden standard (pathological examination) in the diagnosis of endometrial cancer from inception to April 2013. Meanwhile, relevant journals were also manually searched. Two reviewers independently screened literature according to the inclusion and exclusion criteria, and evaluated the included studies using the QUADAS items. Then, meta-analysis was performed using RevMan 5.1 and Meta-DiSc 1.0. ResultsFinally, a total of 16 studies involving 2 299 women (1 088 endometrial cancer patients diagnosed according to the golden standard, of which, 504 with benign uterine disease and 707 with normal cervical) were included. The results of meta-analysis showed that, as for HE4 in early diagnosis of endometrial cancer (SEN=57%, 95%CI 0.54 to 0.60; SPE=92%, 95%CI 0.91 to 0.94; +LR=6.92, 95%CI 5.00 to 9.58;-LR=0.46, 95%CI 0.39 to 0.55; DOR=18.38, 95%CI 12.21 to 27.69; AUC=0.881 7). ConclusionThe current study indicates that serum HE4 is more sensitive and low specific when applied in patients with endometrial cancer, which is worth of being used in clinic. Due to the limitation of low quality of the included studies, more high quality trials are required to verify the above conclusion.
ObjectiveTo systematically review the diagnostic value between serum human epididymis protein 4 (HE4) and carbohydrate antigen 125 (CA125) for endometrial cancer (EC). MethodsWe electronically searched databases including PubMed, The Cochrane Library, Web of Science, ScienceDirect, EBSCO, CNKI and VIP to collect diagnostic accuracy studies of serum HE4 and/or CA125 versus golden standard (pathology) for EC from inception to August 2014. Two reviewers independently screened literature, extracted data and assessed the risk bias of included studies by QUADAS-2 tool. Then, meta-analysis was performed by Meta-Disc 1.4 software. ResultsA total of 20 studies involving 4 351 participants were included. The results of meta-analysis showed that:the pooled sensitivity (Sen), specificity (Spe), positive likelihood ratio (+LR), and negative likelihood ratio (-LR), and diagnostic odds ratio (DOR) of HE4 in the diagnosis of EC were 0.56 (95%CI 0.54 to 0.58), 0.89 (95%CI 0.88 to 0.90), 6.19 (95%CI 4.31 to 8.88), 0.49 (95%CI 0.44 to 0.56), and 14.27 (95%CI 9.50 to 21.42), respectively. The area under the curve (AUC) of SROC was 0.855 9. The pooled Sen, Spe, +LR,-LR, and DOR of CA125 in the diagnosis of EC were 0.33 (95%CI 0.31 to 0.34), 0.80 (95%CI 0.78 to 0.82), 2.07 (95%CI 1.45 to 2.95), 0.83 (95%CI 0.76 to 0.91), and 2.65 (95%CI 1.63 to 4.32), respectively. The SROC AUC was 0.657 5. ConclusionCompared with CA125, HE4 has higher diagnostic accuracy for EC. Due to limited quality and quantity of the included studies, more high quality studies are needed to verify the above conclusion.
Objective To explore the role of estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) in estrogen-induced proliferation of endometrial cancer, and explore whether metformin inhibits the proliferation of endometrial cancer cells through ERα and ERβ. Methods Stable transfected Ishikawa cells were constructed by lentivirus. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell proliferation were detected by methyl thiazolyl tetrazolium assay. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell cycle were detected by flow cytometry. In addition, quantitative real-time polymerase chain reaction and Western blotting assays were used to detect changes in the expression of cyclinD1 and P21 involved in cell cycle regulation. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell proliferation were observed by adding metformin to estrogen treatment. Results Down-regulation of ERα inhibited the proliferation and cell cycle of Ishikawa cells (P<0.05). Down-regulation of ERα also inhibited the expression of cyclinD1 and promoted the expression of P21 (P<0.05). Down-regulation of ERα counteracted the effect of estrogen-induced cell proliferation, cell cycle, and the expression changes of cyclinD1 and P21 (P<0.05). Down-regulation of ERβ promoted the proliferation and cell cycle of Ishikawa cells (P<0.05). Down-regulation of ERβ also promoted the expression of cyclinD1 and inhibited the expression of P21 (P<0.05). Down-regulation of ERβ enhanced the effect of estrogen-induced cell proliferation, cell cycle, and the expression changes of cyclinD1 and P21 (P<0.05). Metformin inhibited the proliferation of estrogen-induced Ishikawa cells (P<0.05), while in the down-regulated ERα Ishikawa cells or down-regulated ERβ Ishikawa cells, the inhibition of metformin on Ishikawa cells disappeared (P<0.05). Conclusions ERα may promote estrogen-induced proliferation of endometrial cancer cells, while ERβ may inhibit estrogen-induced proliferation of endometrial cancer cells. In addition, ERα and ERβ may also mediate the inhibitory effect of metformin on endometrial cancer cells.