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Objective:Small cell neuroendocrine carcinoma of the ovary is a kind of ovarian cancer with a very low incidence.Its clinical manifestations are not obvious.The diagnosis should be based on the pathology and neuroendocrine indicators, and its primary nature should be determined.The main treatment is operation combined with platinum based chemotherapy.The survival period is related to clinical stage and treatment plan.The patient was hospitalized for 2 days because of the aggravation of abdominal distention and pain for half a year.The diagnosis of adnexal mass was confirmed by pathology.After three cycles of neoadjuvant chemotherapy (etoposide+ cisplatin), the patients underwent abdominal " total hysterectomy+ greater omentum resection+ appendectomy+ right pelvic wall peritoneal biopsy+ mesenteric biopsy" . After the operation, the patients received three cycles of EP chemotherapy, and they have been followed up for 15 months.
ABSTRACT
Objective@#Small cell neuroendocrine carcinoma of the ovary is a kind of ovarian cancer with a very low incidence.Its clinical manifestations are not obvious.The diagnosis should be based on the pathology and neuroendocrine indicators, and its primary nature should be determined.The main treatment is operation combined with platinum based chemotherapy.The survival period is related to clinical stage and treatment plan.The patient was hospitalized for 2 days because of the aggravation of abdominal distention and pain for half a year.The diagnosis of adnexal mass was confirmed by pathology.After three cycles of neoadjuvant chemotherapy (etoposide+ cisplatin), the patients underwent abdominal " total hysterectomy+ greater omentum resection+ appendectomy+ right pelvic wall peritoneal biopsy+ mesenteric biopsy" . After the operation, the patients received three cycles of EP chemotherapy, and they have been followed up for 15 months.
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Objective To investigate the relationship between fibrosis and M2 macrophages in endometriosis. Methods BALB/c mice model of endometriosis was established by intraperitoneal injection. The growth of ectopic lesions in mice was observed on the 7th,14th and 21th day after modeling. Masson staining was used to observe the degree of fibrosis and immunohistochemical method to detect the expression of CD206 and CD68 of mice. Image-Pro-Plus 6.0 was used for semi quantitative analysis of staining and the correlation between the degree of fibrosis and the expression of M2 macrophages was explored. Results The success rate of the establishment of endometriosis model by intraperitoneal injection was 100%. There was a positive correlation between fibrosis and the expression of M2 macrophages in endometriosis mice model. Conclusions The mice model of endometriosis can be established successfully by intraperitoneal injection and M2macrophages may promote fibrosis in endometriosis.
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By reviewing the reports of clinical study on herbs of promoting the circulation of Qi to remove blood stasis in treating adenomyosis in recent years, therapeutic mechanism and clinical effects of the treatment were summed up, in order to provide literature reference for the therapy.
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Objective To investigate the effects of miR-135a on HOXA10 expression,proliferation and apoptosis of SKOV3 cells.Methods (1) Through computer-aided algorithms,the predicted target gene of miR-135a (HOXA10)were determined.(2) miR-135a mimics,miR-135a inhibitor and negative control were transfected into SKOV3 cells,respectively.Reverse transcription (RT)-PCR,western blot analysis were used to examine the expression levels of HOXA10 at different times (24,48 and 72 hours).(3) A luciferase reporter assay was used to confirm the direct regulation between miR-135a and HOXA10.(4) SKOV3 cells proliferation at different times (24,48 and 72 hours) was detected by methyl thiazolyl tetrazolium(MTT) assay [quantified by absorbance(A)].Western blot was used to examine the expression of apoptosis-associated protein bcl-2,bax and caspase-3 in SKOV3 cells after 48 hours transfection.Results (1) HOXA10 was predicted to be the target gene of miR-135a by computer-aided algorithms.(2) RT-PCR shown that HOXA10 mRNA levels were decreased over time (24,48 and 72 hours) after miR-135a mimics transfectionin SKOV3 cells (0.94 ±0.04 vs 0.78 ±0.03 vs 0.70 ±0.03,P ＜0.05).While,the expression of HOXA10 mRNA was increased over time after miR-135a inhibitor transfection (1.14 ± 0.05 vs 1.16 ±0.03 vs 2.60 ±0.08,P ＜0.05).After transfected with miR-135a mimics or miR-135a inhibitor over 48 and 72 hours,the HOXA10 expression levels in SKOV3 cells were significantly lower or higher than each control group,respectively (all P ＜ 0.01).Western blot analysis of HOXA10 expression in SKOV3 cells confirmed the results of RT-PCR detected.(3) After cotransfection of miR-135a plasmid and pMIR-REPORT luciferase plasmid containing HOXA10,luciferase reporter assays showed that the luciferase activity reduced by 67.8％ (P ＜0.01).(4) MTT showed that SKOV3 cells growth after miR-135a mimics transfection for 48 and 72 hours were significantly lower than those in control group (0.38 ± 0.03 vs 0.52 ± 0.05,0.67 ±0.05 vs 0.75 ± 0.06 ; respectively,all P ＜ 0.05).While,SKOV3 cells transfected with miR-135a inhibitor for 72 hours grew significantly faster than that in control group (0.95 ± 0.05 vs 0.75 ± 0.06,P ＜ 0.01).After miR-135a mimics transfection,the level of bcl-2 protein was significantly lower than that in control group (0.28 ±0.06 vs 0.76 ±0.09,P ＜0.01).The activity of caspase-3 was significantly higher than that in control group (115.0 ± 2.4 vs 95.4 ± 2.1,P ＜ 0.01).While,there was no statistical difference of bax expression (P =0.142).However,after miR-135a inhibitor transfection,the expression level of bcl-2 protein was significantly higher than that in control group (0.92 ± 0.03 vs 0.76 ± 0.09,P =0.037) and the activity of caspase-3 was significantly lower than that in control group (59.5 ± 4.1 vs 95.4 ± 2.1,P ＜ 0.01).There was also no statistical difference of bax expression (P =0.066).Conclusion miR-135a may play an important role in cell proliferation and apoptosis of ovarian cancer cells by regulating HOXA10 and its downstream pathways.