Xingbo Zhao

University of Jinan (Jinan, China), Chi-nan-shih, Shandong Sheng, China

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Publications (22)64.49 Total impact

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    ABSTRACT: The potential role of metformin in treating endometrial cancer remains to be explored. The current study investigated the role of metformin in 17β-estradiol-induced epithelial-mesenchymal transition (EMT) in endometrial adenocarcinoma cells. We found that 17β-estradiol promoted proliferation and migration, attenuated apoptosis in both estrogen receptor (ER) positive and ER negative endometrial adenocarcinoma cells (Ishikawa and KLE cells, respectively). Metformin abolished 17β-estradiol-induced cell proliferation and reversed 17β-estradiol-induced EMT in Ishikawa cells. In addition, metformin increased the expression of βKlotho, a fibroblast growth factors (FGFs) coreceptor, and decreased ERK1/2 phosphorylation in both Ishikawa and KLE cells. Decreased expression of βKlotho was noted in human endometrial adenocarcinomas, and plasmid-driven expression of βKlotho in Ishikawa cells abolished 17β-estradiol-induced EMT via inhibiting ERK1/2 signaling. βKlotho expression and metformin show synergetic effects on the proliferation and the EMT in Ishikawa cells. Furthermore, we demonstrated that the anti-EMT effects of metformin could be partly abolished by introducing Compound C, a specific AMPKα signaling inhibitor. In conclusion, metformin abolishes 17β-estradiol-induced cell proliferation and EMT in endometrial adenocarcinoma cells by upregulating βKlotho expression, inhibiting ERK1/2 signaling, and activating AMPKα signaling. Our study provides novel mechanistic insight into the anti-tumor effects of metformin.
    No preview · Article · Jan 2016 · Oncotarget
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    Hui Zhang · Qiufen Guo · Xia Wang · Chong Wang · Xingbo Zhao · Mingjiang Li
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    ABSTRACT: Fibroblast growth factor (FGF) 2-mediated signaling of the mitogen-activated protein kinase/RAS/extracellular signal-regulated kinase 1/2 pathway is a critical modulator in angiogenesis and is therefore essential for the pathogenesis of endometrial carcinoma. Human similar expression to FGFs (hSef) and Sprouty4 have each been reported to be negative regulators of FGF signaling. The aim of the present study was to investigate the expression of hSef and Sprouty4 in human endometrial adenocarcinoma. Using immunohistochemistry analysis, the expression of hSef and Sprouty4 was detected in human endometrial adenocarcinomas. Increased hSef expression was found to be present in endometrial adenocarcinomas. In addition, decreased hSef expression was identified in the blood vessels of endometrial adenocarcinoma samples. However, the expression of Sprouty4 was downregulated in human endometrial adenocarcinoma. Aberrant expression of hSef and Sprouty4 are involved in the pathogenesis of human endometrial adenocarcinoma.
    Preview · Article · Oct 2015 · Oncology letters
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    ABSTRACT: Sperm-associated antigen 9 (SPAG9), a recently characterized oncogene, may serve as a marker for the early diagnosis of endometrial cancer. However, whether SPAG9 can be a prognostic marker of complex atypical endometrial hyperplasia (CAEH) or grade 1 endometrioid adenocarcinoma (EA) treated with progestin is still unknown. Progestin therapy was performed in 27 women diagnosed with CAEH (19/27, CAEH group) or grade 1 EA (8/27, EA group). The expression of SPAG9 was measured in pre and post progestin-treated endometrial specimens by immunohistochemistry. The expression of SPAG9 was also examined by real-time polymerase chain reaction (PCR) and Western blot in Ishikawa cells and ECC-1 cells with or without progestin treatment. (1) CAEH showed a significantly better therapeutic efficacy than EA. (2) The expression of SPAG9 was lower in CAEH than in EA. (3) SPAG9 expression significantly declined in the endometrial tissues of women responding to progestin. (4) Significant downregulations of SPAG9 were validated by reverse transcription PCR (RT-PCR) and Western blot both in Ishikawa cells and ECC-1 cells treated with progestin. SPAG9 may be associated with the efficacy of progestin treatment in CAEH and grade 1 EA. It may help to distinguish CAEH from grade 1 EA and serve as a new prognostic marker of CAEH or grade 1 EA treated with progestin. © 2015 S. Karger AG, Basel.
    No preview · Article · Sep 2015 · Gynecologic and Obstetric Investigation
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    ABSTRACT: Epithelial mesenchymal transition (EMT) is involved in the pathogenesis of adenomyosis, and Notch signaling is crucial to EMT. The objective of this study was to explore Notch1/Numb/Snail signaling in adenomyosis. The expression levels of the members of the Notch1/Numb/Snail signaling cascade in normal endometria (proliferative phase: n = 15; secretory phase: n = 15; postmenopausal phase: n = 15) and adenomyotic endometria (proliferative phase: n = 15; secretory phase: n = 15) were determined by immunohistochemistry analysis. We found that the expressions of Notch1 and the EMT-related proteins N-cadherin, Snail and Slug were upregulated in the ectopic endometrium of adenomyosis compared with normal endometrium. Numb, a negative regulator of Notch signaling, was significantly decreased in adenomyosis. In addition, reduced immunoexpression of E-cadherin was observed in adenomyosis. We conclude that Notch1/Numb/Snail signaling plays an important role in the pathogenesis and development of adenomyosis.
    Preview · Article · Aug 2015 · Reproductive Biology and Endocrinology
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    ABSTRACT: Objective: To investigate the expression of CD56 in endometrial samples from patients with adenomyosis and its relationship with menstrual cycle phase and severity of dysmenorrhea. Study design: 40 patients with histologically proved adenomyosis (proliferative n=20; secretory n=20) and dysmenorrhea were examined in this study, control groups includes 20 patients with adenomyosis without dysmenorrhea (main complaint: menorrhagia) and 20 patients without adenomyosis who had undergone hysterectomy for non-endometrial pathology (no dysmenorrhea medical history). Immunohistochemical staining against CD56 was performed for the eutopic and ectopic endometrium from patients with adenomyosis and the control samples. The expression of CD56 was determined by calculating the H-score and the severity of dysmenorrhea was determined using the visual analogue scale. The menstrual cycle status and the disease severity were compared to the levels of staining. Result(s): CD56 was expressed mainly in the endometrial glandular epithelium in patients with adenomyosis and normal endometrium. The epithelial staining intensity of CD56 in ectopic lesions of adenomyosis with dysmenorrhea was obviously higher than in the corresponding eutopic endometrium and control groups (P<0.01). There were no statistical differences in the expression between normal endometrium, eutopic endometrium of adenomyosis with dysmenorrhea and adenomyostic samples without dysmenorrhea. For eutopic endometrium in adenomyosis with dysmenorrhea, expression was higher in the secretory phases than in the proliferative phase (P<0.05). The increased CD56 immunoreactivity correlated with the severity of dysmenorrhea (spearman rho=0.84, P<0.01). Conclusion(s): These findings suggest that the expression of CD56 in adenomyosis is positively associated with the severity of dysmenorrhea. Endometrial glandular epithelium is likely to secrete more CD56 and stimulating nerve growth in the stroma, which could then play a role in the pathogenesis of adenomoysis-related dysmenorrhea.
    No preview · Article · Aug 2015 · European journal of obstetrics, gynecology, and reproductive biology
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    ABSTRACT: In previous studies, we found that endometriotic stromal cells lose the ability to regulate cell survival signaling in endometriotic epithelial cells. Here, we invested the effect of Metformin on the stromal-epithelial cells crosstalk in endometriosis and explored the pathway that might be involved. We found that ectopic endometriotic stromal cells (ESC) expressed and secreted higher Wnt2 protein compared with normal endometrial stromal cells (NSC). Conditioned medium (CM) from ESC supplemented with Wnt2 antibody significantly inhibited the growth of normal endometrial epithelial cells (NEC), while CM from ESC per se showed no significant effect on the growth of NEC. Metformin decreased the expression and secretion of Wnt2 in ESC. CM from Metformin-pretreated ESC significantly inhibited the growth of NEC. In conclusion, Wnt2/β-catenin signaling was involved in stromal-epithelial cells interaction in endometriosis. Metformin might regulate the stroma-epithelium communication via Wnt2-mediated signaling in endometriosis. Copyright © 2015. Published by Elsevier Ireland Ltd.
    No preview · Article · Jun 2015 · Molecular and Cellular Endocrinology
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    ABSTRACT: Objective: We previously found that Dual-specificity phosphatase 6 (Dusp6) over-expression enhanced the growth-promoting effect of estrogen in endometrial adenocarcinoma cells. The aim of this study was to explore the correlation of Dusp6 expression with progestin sensitivity in atypical endometrial hyperplasia (AEH) and earlier endometrial carcinomas (EC). Methods: Using immunohistochemistry study, we analyzed the expression of Dusp6 protein in AEH. Results: We found that progestin treatment was effective in 89% of AEH and 50% of EC. Before treatment, Dusp6 expression was significantly higher in progestin-sensitive AEH groups compared with progestin-resistant groups. After treatment, Dusp6 expression was significantly upregulated in progestin-sensitive groups, but not in progestin-resistant groups. Moreover, a high-dose of Dusp6 transfection significantly enhanced progestin-induced growth-inhibition in Ishikawa cells. Conclusions: Dusp6 could be a predicting marker for deciding the effectiveness of progestin therapy in AEH.
    No preview · Article · Nov 2014 · Gynecologic Oncology
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    ABSTRACT: Phosphatase and tensin homolog (PTEN) and protein phosphatase type 2A (PP2A) are negative modulators of PI3K/AKT/survivin signaling. To evaluate immunoexpression of PTEN, PP2A and survivin in adenomyosis, ectopic lesions from 28 patients with adenomyosis and endometria from 30 controls without adenomyosis were employed in the study. The expression of PTEN, PP2A and survivin was examined with the use of immunohistochemistry. We found a decreased expression of PP2A and PTEN in adenomyosis. The expression of PTEN showed great individual differences in adenomyosis, although expression of both PP2A and PTEN was lower in adenomyosis than in normal endometria. In contrast, the expression of survivin was higher in adenomyosis. Our results suggest the important role of the PI3K cascade in the pathogenesis and development of adenomyosis.
    No preview · Article · Sep 2014 · Reproductive biology
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    ABSTRACT: Objective: Basic fibroblast growth factor (FGF2)-mediated Extracellular signal-regulated kinases1/2 (ERK1/2) signaling is a critical modulator in angiogenesis. SPRY4 has been reported to be a feedback negative regulator of FGFs-induced ERK1/2 signaling. The aim of this study was to explore the role of SPRY4 in endometrial adenocarcinoma cell. Materials and methods: The effect of SPRY4 expression on FGF2-mediated ERK1/2 signaling was detected by luciferase assay and Western blot analysis. The growth of Ishikawa cells was detected using colony formation assay and cell number counting experiment. Results: We found that plasmid-driven SPRY4 expression efficiently blocked the activity of FGF2-induced ERK1/2 signaling in Ishikawa cells. SPRY4 expression significantly reduced the proliferation and 17β-estradiol-induced proliferation of Ishikawa cells. Conclusion: SPRY4 may function as a tumor suppressor in endometrial adenocarcinoma.
    No preview · Article · May 2014 · Gynecological Endocrinology
  • Qiufen Guo · Hui Zhang · Xingbo Zhao · Yibing Fu · Jie Zhang · Mingjiang Li
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    ABSTRACT: Dual-specificity phosphatase 6 (Dusp6), Sprouty4, and similar expression to FGF (Sef) are negative modulators of FGF2/ERK1/2 signaling. The objective of the study was to evaluate the expressions of Dusp6, Sprouty4, and Sef in eutopic endometria of patients with adenomyosis. Endometria from 30 women with adenomyosis and 29 women without adenomyosis were used in this study. The expressions of Dusp6, Sprouty4, and Sef were investigated by immunohistochemical analysis. We found that Dusp6, Sprouty4, and Sef expressions were present in endometrial epithelial cells of normal endometria and eutopic endometria of adenomyosis. Weak immunostainings were noted in stromal cells in both endometria. No cyclical change was noted either in normal endometria or in eutopic endometria of adenomyosis during menstrual cycle. By immunohistochemical analysis, we found that eutopic endometria of adenomyosis showed significantly decreased Dusp6, Sprouty4, and Sef expressions compared with normal endometria. By in situ hybridization analysis, we found that the mRNA expressions of Dusp6, Sprouty4, and Sef were downregulated in eutopic endometria of adenomyosis compared with normal endometria. We conclude that downregulation of Dusp6, Sprouty4, and Sef-negative modulators of FGF2/ERK1/2 signaling-was present in eutopic endometria of adenomyosis, which may play critical roles in the development of adenomyosis.
    No preview · Article · Mar 2014 · International journal of gynecological pathology: official journal of the International Society of Gynecological Pathologists
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    ABSTRACT: Dual-specificity phosphatase 6 (Dusp6) is a negative feedback mechanism of fibroblast growth factors (FGFs)/mitogen-activated protein kinase (MAPK)/ERK1/2 signaling. The aim of this study was to explore the expression of Dusp6 in human endometrial adenocarcinomas and the role of Dusp6 expression in the growth regulation of endometrial adenocarcinoma cell. We found that Dusp6 was over-expressed in human endometrial adenocarcinomas. In Ishikawa cells, plasmid-driven Dusp6 expression efficiently blocked the activity of FGF2-induced MAPK/ERK1/2 signaling. Unexpectedly, Dusp6 expression significantly enhanced the growth of Ishikawa cells. In Dusp6 forced-expression cells, 17β-estradiol stimulation increased the cell growth by all most threefolds. In addition, progesterone treatment reduced the cell growth to about half both in Ishikawa cells with and without forced-Dusp6-expression. Dusp6 over-expression is involved in the pathogenesis and development of human endometrial adenocarcinomas. Dusp6 functions as a negative regulator of FGF2/ERK1/2 signaling but enhances the growth and 17β-estradiol-induced cell growth in endometrial adenocarcinoma cell.
    No preview · Article · Feb 2013 · Molecular and Cellular Endocrinology
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    Xiaoyan Qin · Lei Yan · Xingbo Zhao · Chunyan Li · Yibing Fu
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    ABSTRACT: The aim of this study was to investigate the role of microRNA-21 (miR-21) in the regulation of phosphatase and tensin homolog deleted from chromosome-10 (PTEN) expression and proliferation of endometrioid endometrial cancer (EEC) cells. We performed a qRT-PCR assay with miR-21 and PTEN in 16 paired EEC tumor tissues and adjacent non-tumor endometrium. To investigate the regulation of PTEN by miR-21, we designed gain- and loss-of-function of miR-21 experiments in the KLE cell line by transfection with a synthetic miR-21 mimic and inhibitor. To validate the putative binding site of miR-21 in the 3' untranslated region (3'-UTR) of PTEN messenger RNA (mRNA), a dual-luciferase reporter assay was carried out. To evaluate the potential effect of miR-21 on EEC proliferation, we performed both overexpression experiments, using an miR-21 mimic, and inhibition assays, using an miR-21 inhibitor. miR-21 was overexpressed in EEC and was inversely correlated with PTEN protein expression (P<0.001). miR-21 regulated PTEN protein expression and cell proliferation in the KLE cell line and the direct binding of miR-21 to the PTEN 3'-UTR was confirmed using a dual-luciferase reporter assay. The upregulation of miR-21 led to a significant decrease in the PTEN protein expression level (P=0.007). The downregulation of miR-21 led to a significant increase in PTEN protein (P=0.002). The expression of luciferase in the wt-PTEN-3'-UTR-pGL3 group was downregulated in the presence of the miR-21 mimic (P=0.001). miR-21 was overexpressed in EEC. In conclusion, we demonstrated that the expression of PTEN protein, but not mRNA, was negatively directly regulated by miR-21 in the KLE cell line. The overexpression of miR-21 modulated EEC cell proliferation through the downregulation of PTEN.
    Preview · Article · Dec 2012 · Oncology letters
  • Peng Yu · Lei Yan · Hui Zhang · Xiaoyan Lin · Xingbo Zhao
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    ABSTRACT: To investigate the expression and humoral immune response of sperm-associated antigen 9 (SPAG9) in endometri al carcinoma. Sperm-associated antigen 9 gene expression levels were evaluated in endometrial carcinoma, endometrial hyperplasia, adjacent tissues, and normal endometrial tissues by reverse transcriptase-polymerase chain reaction, immunohistochemistry, and Western blot. Sperm-associated antigen 9 concentration in serum samples from 10 healthy women, 20 women with benign diseases, and 50 women with endometrial carcinoma was detected by enzyme-linked immunosorbent assay. (1) Sperm-associated antigen 9 antibodies were detected in approximately 72% of patients with endometrial cancer but not in healthy controls. (2) A significant difference has been found among pathological types and degrees (P < 0.05), and it was also found to be expressed in transferred lymph nodes. (3) Sperm-associated antigen 9 serum concentration (ng/mL) of patients with endometrial carcinoma is significantly higher than those of the healthy group (P < 0.05). Patients harboring grade 3 endometrial carcinoma were found to have significantly higher SPAG9 concentrations than those of grade 1/grade 2 (P = 0.003). SPAG9 is positively expressed in endometrial cancer, and with a high humoral immune response in patients. It may serve as a new type of endometrial cancer markers for early detection, diagnosis and treatment.
    No preview · Article · Dec 2011 · International Journal of Gynecological Cancer
  • Min Shi · Hui Zhang · Mingjiang Li · Jing Xue · Yibing Fu · Lei Yan · Xingbo Zhao
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    ABSTRACT: Stroma-tumor communication plays an important role in the genesis of neoplasia. In the current study, we investigated the effect of normal stromal cells on the survival and apoptosis signaling of endometrial cancer cells and further explored the possible mechanism implied in this communication. Using primarily cultured normal endometrial stromal cells and an endometrial adenocarcinoma cell line, Ishikawa cells, we established a 2D-coculture system to observe the stromal cell-tumor cell crosstalk in endometrial carcinomas. Using methyl thiazolyl tetrazolium (MTT) assays, cell counting and colony formation assays, we analyzed the effect of stomal cells on the growth and proliferation of Ishikawa cells under different conditions. Using western blot analysis, we determined the effect of stromal cells on the activity of PI3K/AKt/Survivin signaling in Ishikawa cells under different conditions. Using immunohistochemistry analysis, we determined the expression of Survivin in normal endometria and endometrial adenocarcinomas. We found that the paracrine factors from normal endometrial stromal cells grown on Matrigel repeatedly and significantly decreased hormone-stimulated activity of PI3K/AKt/Survivin signaling in Ishikawa cells, which were proved to be increased in endometrial adenocarcinoma and essential in hormone-induced cell growth in Ishikawa cells. Paracrine factors from normal endometrial stromal cells can inhibit hormone-stimulated cell proliferation in Ishikawa cells by regulating cell survival and apoptosis through PI3K/AKt/Survivin signaling.
    No preview · Article · Jul 2011 · Gynecologic Oncology
  • Lei Yan · Xingbo Zhao · Xiaoyan Qin

    No preview · Article · Jul 2011 · European journal of obstetrics, gynecology, and reproductive biology
  • Hui Zhang · Xingbo Zhao · Lei Yan · Mingjiang Li
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    ABSTRACT: Fibroblast growth factors (FGF) axis, and in particular FGF2 axis, is an important mitogenic stimulus in endometrial carcinogenesis. hSef is a key inhibitory regulator of FGF signaling and aberrant hSef expression is reported to be present in various human carcinomas. The objective of this study was to investigate the role of hSef in the growth and proliferation of endometrial adenocarcinoma cells and to explore the mechanism that may be involved. Using western blot analysis, we determined the expression of hSef in Ishikawa cells under different conditions. Using luciferase reporter assays and western blot analysis, we detected the effect of hSef on MAPK/ERK-mediated FGF2 signaling. Using MTT, cell counting and colony formation assays, we analyzed the growth and proliferation of Ishikawa cells under different conditions. We found that the hSef expression was positively regulated by FGF2-induced MAPK/ERK signaling and inversely, hSef expression efficiently inhibited the activity of FGF2-induced MAPK/ERK signaling, indicating the presence of hSef-mediated negative feedback mechanism for FGF signaling in endometrial cancer cells. In addition, we found that MAPK/ERK signaling was essential for the growth and proliferation of endometrial cancer cells in vitro, and hSef expression significantly reduced the cell proliferation. hSef expression can inhibit the growth and proliferation of endometrial cancer cells via acting on the FGF2/MAPK/ERK signaling.
    No preview · Article · Jun 2011 · Gynecologic Oncology
  • Lei Yan · Changting Zuo · Deying Wei · Xingbo Zhao
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    ABSTRACT: Citation Yan L, Zuo C, Wei D, Zhao X. Some severe maternal diseases might be caused by fetal-versus-maternal disease (FVMD). Am J Reprod Immunol 2010; 63: 189–192 Pregnancy-related disease is a common challenging clinical problem. From our review and clinical experience, we hypothesize that many severe pregnancy-related complications might be caused by a fetal-versus-maternal disease (FVMD), based on the fact that maternal disease is related to immunity and that fetal cells are present in maternal blood. Fetus is a semi-antigen and can be considered as a tumor or graft. The pathophysiology of FVMD must be complex. We speculate it to be a three-step process: impaired maternal immunological function, fetal T-cell activation and injury of target organs. More experiments and research will be needed to prove our hypothesis.
    No preview · Article · Mar 2010 · American Journal Of Reproductive Immunology
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    ABSTRACT: To explore the stroma-epithelium interactions in endometriosis and to identify the possible signalling pathways involved in this cross-talk. Laboratory study via primary cultured endometrial stromal and epithelial cells. University Hospital. Fifteen patients with endometriosis confirmed by histopathology were recruited in the study, and 12 women free of endometriosis were used as control group. Specific NFkappaB inhibitor 1-Pyrrolidinecarbodithioic acid ammonium salt (PDTC) was used in cell cultures. The expression and secretion of MMP-2, MMP-9, TIMP-1, TIMP-2 and the DNA-binding activity of NFkappaB in normal endometrial stromal cells or in co-cultures with normal or endometriotic epithelial cells from patients with endometriosis. Endometrial epithelial cells induced MMP-9 and MMP-2 expression in normal stromal cells in vitro. In co-cultures with endometriotic epithelial cells, normal endometrial stromal cells expressed and secreted higher MMP-2 (p < 0.05) and MMP-9 (p < 0.05). Specific inhibition of NFkappaB pathway in stromal cells abolished this induction effect by epithelial cells. Endometriotic epithelial cells induce MMPs expression and secretion in normal endometrial stromal cells via an NFkappaB-dependent pathway in vitro. This cross-talk between epithelial cells and stromal cells may facilitate the implantation and extension of the ectopic foci and favour the development of the disease.
    No preview · Article · Nov 2009 · Gynecological Endocrinology
  • Hui Zhang · Xingbo Zhao · Shu Liu · Jijun Li · Zeqing Wen · Mingjiang Li
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    ABSTRACT: The objective of this study was to explore the mechanism of phosphatase and tensin homolog (PTEN) loss in endometriosis. We found that aberrant PTEN expression and mitogen-activated protein kinases (MAPK)/ERK, phosphoinositide 3-kinase (PI3K)/AKt, and nuclear factor-kappaB (NFkappaB) signaling overactivities coexisted in endometriosis. In vitro, 17beta-estradiol rapidly activated the 3 pathways in endometriotic cells and specific inhibitions on the 3 pathways respectively blocked 17beta-estradiol-induced cell proliferation. 17beta-estradiol suppressed PTEN transcription and expression in endometriotic cells which was abolished by specific NFkappaB inhibition. CONCLUSION(S): Total/nuclear PTEN-loss and MAPK/ERK, PI3K/AKt, and NFkappaB signal overactivities coexist in endometriosis. In vitro, 17beta-estradiol can promotes cell proliferation in endometriosis by activating PI3K/AKt pathway via an NFkappaB/PTEN-dependent pathway. For the first time we propose the possibility of the presence of a positive feedback-loop: 17beta-estradiol-->high NFkappaB-->low PTEN-->high PI3K-->high NFkappaB, in endometriosis, which may finally promote the proliferation of ectopic endometrial epithelial cells and in turn contributes to the progression of the disease.
    No preview · Article · Nov 2009 · Molecular and Cellular Endocrinology
  • Lei Yan · Yongjie Tian · Yibing Fu · Xingbo Zhao
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    ABSTRACT: To report a case of successful pregnancy after treatment for endometrial stromal sarcoma. Case report. Gynecology department at a provincial hospital affiliated with a university. A 25-year-old woman (gravida 0, para 0) with a misdiagnosis of myoma who received a pathologic diagnosis of endometrial stromal sarcoma after the first surgery. Second fertility-preserving surgery and chemotherapy. Successful pregnancy and follow-up visit. After the conservative treatment, the patient entered complete remission. She conceived naturally and delivered at 39 weeks' gestation by caesarean section approximately 40 months after the surgery. Endometrial stromal sarcoma is a rare uterine tumor with a poor prognosis. This case shows that successful pregnancy is possible after effective conservative treatment by local surgical resection and adjunct chemotherapy.
    No preview · Article · Oct 2009 · Fertility and sterility