Lei Li

Sichuan University, Hua-yang, Sichuan, China

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Publications (35)33.1 Total impact

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    ABSTRACT: Mucinous minimal deviation adenocarcinoma (MDA) is a rare highly differentiated tumor of uterine cervix, of which the confusing histopathology resembling some benign lesions usually makes difficulty for pathologic diagnosis. The expression of forkhead box protein P1 (FOXP1) is found in some kinds of human tumors and is considered to be associated with the progression of the tumors. The purpose of this study is to detect the FOXP1 expression in MDA and evaluate its possible role in the diagnosis of MDA. Twenty-two MDA cases and 20 control cases consisting of 10 cases of lobular endocervical glandular hyperplasia and 10 cases of normal endocervical tissue were included in this study. All available clinical data were collected and immunostaining for FOXP1, carcinoembryonic antigen (CEA), human milk fat globule antigen 1 (HMFG1), estrogen receptor, and progesterone receptor were performed on these cases. The nuclear/cytoplasmic expression of FOXP1 was found in 18 of 22 MDA cases while in 1 of 20 control cases, which showed statistical significance (P = .000). The cytoplasmic CEA expression was found in 14 of 22 MDA cases and 2 of 20 control cases (P = .000), whereas cytoplasmic HMFG1 expression was found in 10 of 22 MDA cases and 4 of 20 control cases (P = .081). No statistical difference was found between FOXP1 and CEA expression (P = .083) or between FOXP1 and HMFG1 expression (P = .375) in MDA. Neither estrogen receptor nor PR expression was found in MDA. The significant expression of FOXP1 in MDA may be helpful to some extent in the pathologic diagnosis of cervical MDA. A widened observation range and further researches are needed to elucidate the potential mechanism.
    Annals of diagnostic pathology. 05/2014;
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    ABSTRACT: In this paper, we described a placenta with vesicular lesions in a 23-year-old woman (1-gravid) who visited our hospital at 13 weeks of gestation on prenatal routine examination. Ultrasound findings showed multiple vesicular lesions which gradually increased as the pregnancy advanced, and a live normal-appearing fetus which was confirmed of IUGR at 30 weeks of gestation in her uterus. Throughout gestation, the maternal serum β-human chorionic gonadotropin level keeps normal, but the serum alpha-fetoprotein was higher than average. The patient delivered an 1800-g female without obvious anomalies at 35 weeks 5 days of gestation due to premature rupture of membrane. The diagnosis of placental mesenchymal dysplasia was determined on the pathological examination and androgenetic/biparental mosaicism in the placenta was identified by immunohistochemical staining of p57kip2.
    International journal of clinical and experimental pathology. 01/2014; 7(8):5302-7.
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    ABSTRACT: To explore the association between clopidogrel resistance (CR) as assessed by whole blood electrical impedance aggregometry (EIA) and platelet parameters. The prospective study comprised 152 patients with coronary artery disease (CAD) on the therapy of clopidogrel. EIA employed adenosine diphosphate (ADP) as an inductor to measure platelet aggregation. CR was defined by spontaneous aggregation (electrical impedance ≥ 10 Ω). The subjects were divided into 2 groups of CR and clopidogrel sensitive (CS). Platelet parameters were measured by routine blood test. And their clinical data and outcomes were analyzed. The prevalence of CR was 10.5% (n = 16). The ratio of patients with diabetes in CR group was higher than that in CS group (7/16 vs 29/136, P = 0.046). Platelet counts and mean platelet volume (MPV) were also higher in CR group than those in CS group ((241 ± 58) ×10(9)/L vs (185 ± 56)×10(9)/L, (8.0 ± 0.8) fl vs (7.4 ± 0.9) fl, both P < 0.05). Logistic regression indicated each 10×10(9)/L increase in platelet and each 1 fl increase in MVP were associated with 0.376 and 1.015 folds increase in CR onset respectively (OR = 1.376, 95%CI 1.097 - 1.725, P = 0.006;OR = 2.015, 95%CI 1.148 - 3.537, P = 0.015). The patients with CR had more cardiovascular events during an average follow-up of 53 months (6/16 vs 23/136, P = 0.047). CAD patients with CR had higher incidence of cardiovascular events. Increased platelet counts and MPV levels are independent predictors for CR in CAD patients.
    Zhonghua yi xue za zhi 03/2013; 93(12):916-20.
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    ABSTRACT: BACKGROUND: As an adipocytokine, resistin has been proposed as a link between inflammation, metabolic disorder and atherosclerosis. The aim of the study is to evaluate whether serum resistin is associated with acute coronary syndrome (ACS) and major adverse cardiovascular events (MACEs) among postmenopausal women with ACS undergoing percutaneous coronary intervention (PCI). METHODS: A total of 106 consecutive postmenopausal women who underwent coronary angiography for evaluation of suspected myocardial ischemia were enrolled. Pre-procedure serum resistin, inflammatory and metabolic biomarkers were measured. All participants were followed for seven years for MACEs, including cardiovascular death, recurrent nonfatal myocardial infarction, and re-PCI. RESULTS: Patients with ACS (n = 69) had significantly higher resistin levels than those without coronary artery disease (CAD) (n = 37) (4.61 (1.79 - 10.80) ng/ml vs. 2.36 (0.85 - 4.15) ng/ml, P = 0.002). Correlation analysis revealed positive correlations between resistin levels and inflammatory and metabolic factors (P < 0.05). A follow-up of a mean of 83.4 months showed that patients with ACS suffered more MACEs than those without (13.0% vs. 2.7%, P = 0.05). Adjusted for cardiovascular risks, inflammatory and metabolic factors, multiple Logistic regression analysis indicated that an elevated resistin level was an independent predictor of ACS onset (OR = 1.139, 95%CI 1.024 - 1.268, P = 0.017) and of MACEs after PCI (OR = 1.099, 95%CI 1.015 - 1.189, P = 0.019). To clarify the association between resistin levels and MACEs, ACS patients were divided into two subgroups on the basis of resistin levels. Compared with the low resistin subgroup (≤ 4.35 ng/ml, n = 32), patients in the high resistin subgroup (> 4.35 ng/ml, n = 37) were more prone to suffer MACEs (21.6% vs. 3.1%, P = 0.015). Kaplan-Meier analysis showed a significantly lower event-free survival rate in ACS patients with high resistin levels than in the low resistin subgroup (78.4% vs. 96.9%, Log rank 5.594, P = 0.018). CONCLUSION: An elevated serum resistin level is associated with ACS and cardiovascular events and acts as a predictor in progression of ACS in postmenopausal women.
    Chinese medical journal 03/2013; 126(6):1058-1062. · 0.90 Impact Factor
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    ABSTRACT: To assess the diagnostic accuracy of coronary flow reserve measured by transthoracic Doppler echocardiography (TTDE) associated with adenosine triphosphate (ATP) stress for detecting coronary stenosis in patients with chest pain. A total of 125 patients scheduled for elective coronary angiography (CAG) due to chest pain were recruited. ATP stress echocardiography were performed to measure CFR in left anterior descending (LAD) by TTDE with 2 days pre-CAG. Coronary flow reserve (CFR) was calculated as peak diastolic velocity during maximum hyperemia (PDV2) divided by baseline (PDV1). According to the coronary angiography results, all patients were divided into group A (stenosis < 50% in LAD, n = 57), group B (stenosis of 50% - 75% in LAD, n = 20) and group C (stenosis > 75% in LAD, n = 48). Then CFR was compared among three groups. The receiver operating characteristic curve (ROC) was used to assess the value of CFR for detecting LAD stenosis. CFR was significantly different among three groups (group A: 3.02 ± 0.85, group B: 2.49 ± 0.65, group C: 1.82 ± 0.56; all P < 0.01). With ROC analysis, CFR < 2.2 was the best cut-off value for diagnosing significant LAD stenosis (area under curve: 0.86 (95% CI 0.80 to 0.93)), with sensitivity of 81%, specificity of 83% and accuracy of 82%; CFR < 2.2 for diagnosing LAD stenosis > 50% (area under curve: 0.81 (95%CI 0.74 - 0.89, P < 0.01)), with a sensitivity of 59%, a specificity of 82% and an accuracy of 70%. CFR measured by TTDE associated with ATP stress is a valuable tool for screening significant stenosis in patients with chest pain. Its advantages are non-invasiveness, easy availability, safety and inexpensiveness.
    Zhonghua yi xue za zhi 02/2013; 93(6):432-5.
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    ABSTRACT: Despite outstanding antiplatelet properties of aspirin and clopidogrel, some patients taking these drugs continue to suffer complications. Antiplatelet resistance appears to be a new prognostic factor in acute coronary syndrome patients for clinical events associated with stent thrombosis (ST). However, there is no optimal method to identify it and assess its correlation to clinical outcomes. This study sought to evaluate the predictive value of antiplatelet resistance assessed by whole blood impedance aggregometry for the risk of early ST in patients with acute coronary syndrome who underwent coronary stenting. Platelet responses to aspirin and clopidogrel in 86 patients with acute coronary syndrome were measured by whole blood impedance aggregometry. Spontaneous platelet aggregation was defined as antiplatelet resistance identified by the increased electrical impedance. The clinical endpoint was early stent thrombosis during 30-day follow-up after coronary stenting. The prevalence of aspirin resistance, clopidogrel resistance and dual resistance of combined clopidogrel and aspirin resistance were 19.8%, 12.8% and 5.8% respectively. Diabetes, female and higher platelet counts were more frequently detected in clopidogrel-resistant and dual-resistant patients. During 30-day follow-up, the patients with clopidogrel resistance and dual resistance had higher incidence of early stent thrombosis (18.2% vs. 1.3%, 40.0% vs. 1.2%, P < 0.05). Binary Logistic Regression analysis indicated that dual resistance remained an independent predicator for early stent thrombosis (odds ratio 34.064, 95%CI 1.919 - 604.656, P = 0.016). Antiplatelet resistance assessed by whole blood impedance aggregometry is paralleled to clinical events, and dual antiplatelet resistance is an independent predicator for early stent thrombosis in patients with acute coronary syndrome. As a physiological assessment of platelet reactivity, whole blood impedance aggregometry is a convenient and accurate option for measuring antiplatelet resistance and hence predicting early stent thrombosis.
    Chinese medical journal 02/2013; 126(4):626-33. · 0.90 Impact Factor
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    ABSTRACT: PNAS-4, a novel pro-apoptotic gene, was activated during the early response to DNA damage. Previous studies have shown that hPNAS-4 can inhibit tumor growth when over-expressed in ovarian cancer cells. However, the underlying action mechanism remains elusive. In this work, we found that hPNAS-4 expression was significantly increased in SKOV3 cells when exposed to cisplatin, methyl methanesulfonate or mitomycin C, and that its overexpression could induce proliferation inhibition, S phase arrest and apoptosis in A2780s and SKOV3 ovarian cancer cells. The S phase arrest caused by hPNAS-4 was associated with up-regulation of p21. p21 is p53-dispensable and correlates with activation of ERK, and activation of the Cdc25A-Cdk2-Cyclin E/Cyclin A pathway, while the pro-apoptotic effects of hPNAS-4 were mediated by activation of caspase-9 and -3 other than caspase-8, and accompanied by release of AIF, Smac and cytochrome c into the cytosol. Taken together, these data suggest a new mechanism by which hPNAS-4 inhibits proliferation of ovarian cancer cells by inducing S phase arrest and apoptosis via activation of Cdc25A-Cdk2-Cyclin E/Cyclin A axis and mitochondrial dysfunction-mediated caspase-dependent and -independent apoptotic pathways. To our knowledge, we provide the first molecular evidence for the potential application of hPNAS-4 as a novel target in ovarian cancer gene therapy.
    Apoptosis 01/2013; · 4.07 Impact Factor
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    ABSTRACT: Progestins, particularly medroxyprogesterone acetate (MPA), have for a long time been used as conservative treatment for young patients with clinical stage I, grade I endometrial carcinoma. However, more than 30% of patients with endometrial adenocarcinoma display resistance to endocrine therapies at the time of presentation and most cancer patients that initially respond to progestin treatment will at some point develop resistance, resulting in tumor progression. The cellular mechanisms underlying acquired resistance to progestin are poorly understood. In order to investigate the molecular mechanisms whereby human endometrial adenocarcinoma develops resistance to progestin therapy, we have undertaken to develop human endometrial adenocarcinoma cell lines that are resistant to the growth-inhibitory effects of progestins in vitro. A progestin-resistant subcell line of Ishikawa cells was developed from Ishikawa human endometrial adenocarcinoma cells by stepwise selection in increasing concentrations of the synthetic progestin, MPA, over ten months. The doubling time of the progestin-resistant cells (34.18±3.15 h) grown routinely in the medium containing 10 μM MPA was not significantly different from the doubling time of the parent Ishikawa cells (35.14±2.68 h) grown in the absence of MPA (t=-0.331, P=0.762). Moreover, the effect of treatment with MPA shifted from suppression of growth and invasiveness, as observed in the parent Ishikawa cells, to stimulation of growth and invasiveness in the progestin-resistant Ishikawa cells. The positive rates of estrogen receptor a (ERα) and progesterone receptor B (PRB) of the progestin-resistant Ishikawa cells were significantly reduced, whilst the positive rate of ERβ was significantly enhanced compared to the parent Ishikawa cells. These differences were statistically significant (P<0.05). Our results indicate that long-term treatment with MPA in Ishikawa cells may give rise to a resistance effect to MPA. When the resistant subtype is acquired, treatment with MPA enhances cancer cell proliferation and invasiveness. The imbalance of ER and PR subtypes may contribute to the mechanisms involved in progestin resistance. Determination of the subtypes of ER and PR may provide important additional information on the hormone sensitivity of endometrial carcinoma.
    Oncology letters 01/2013; 5(1):139-144. · 0.24 Impact Factor
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    ABSTRACT: To study the clinicopathologic features of primitive neuroectodermal tumor (PNET) in female genital tract. Six cases of PNET arising in female genital tract were retrospectively reviewed. The clinicopathologic features, immunohistochemical findings and EWS gene translocation study results were analyzed. The age of patients ranged from 10 to 27 years (mean = 20 years). The sites of involvement included ovary (1 case), uterus (1 case), vulva (2 cases) and vagina (2 cases). The greatest diameter of the tumor ranged from 2 to 10 cm (mean = 5.4 cm). The tumor had nodular appearance and showed grayish-pink fleshy cut surface, accompanied by foci of hemorrhage and necrosis. Histologically, the tumor was composed of malignant small round cells with indistinct cell borders, hyperchromatic nuclei, dense chromatin, tiny nucleoli and scanty cytoplasm. The tumor cells were arranged in sheets or lobules. Homer-Wright rosettes were identified in 1 case. Immunohistochemical study showed that the tumor cells were positive for CD99, FLI-1 and CD56 (6/6). Focal expression of vimentin (5/6), NSE (5/6), nestin (4/6), synaptophysin (4/6), S-100 protein (2/6) and chromogranin A (1/6) was also demonstrated. EWS gene translocation was detected in 5 cases studied. Follow-up information was available in 2 patients (7 and 17 months of follow up, respectively). One of them died of tumor metastasis 17 months after diagnosis. The other patient was still alive. PNET arising in female genital tract is rare. It mainly involves ovary, uterus, vulva and vagina. Immunohistochemical study using a panel of antibodies and fluorescence in-situ hybridization play an important role in definitive diagnosis of this rare malignancy.
    Zhonghua bing li xue za zhi Chinese journal of pathology 11/2012; 41(11):729-32.
  • Rui Qiao, Lei Li, Jie Zhang
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    ABSTRACT: Several medicines are currently used to inhibit the platelet activity. We aim to monitor the residual platelet activity (RPA) despite antiplatelet therapy and assess its relationship with major adverse events. The impedance platelet aggregation was employed to determine RPA. Totally, 202 patients with acute coronary syndrome (ACS) were followed up for 10 months for major clinical events of myocardial infarction, cerebrovascular accident (CVA), and all cause mortality, and RPA after clopidogrel loading was assessed in 30 patients. The RPA at 2 hours after 300 mg clopidogrel loading was 1 Ω (± 2.3 Ω) induced by adenosine diphosphate. Residual platelet activity of patients who experienced death, MI, or CVA was significantly higher than those who did not experience (P < .05). Cutoff values of RPA showed optimal negative predictive values (96%-97%) and poor positive predictive values (16%-29%). Therefore, RPA monitored by whole blood impedance platelet aggregation may have high exclusionary predictive value for the occurrence of major clinical events in patients with ACS.
    Clinical and Applied Thrombosis/Hemostasis 10/2012; · 1.02 Impact Factor
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    ABSTRACT: To evaluate the predictive value of antiplatelet resistance assessed by whole blood electronic impedance aggregometry (EIA) for the risk of recurrent cardiac ischemic events in patients with acute myocardial infarction (AMI) who underwent coronary stenting. We enrolled 109 patients with AMI, 72 (66.1%) men and 37 (33.9%) women with mean age (63 ± 12) years, who were treated with aspirin and clopidogrel daily after coronary stenting. EIA used arachidonic acid (AA) and adenosine diphosphate (ADP) as inductors to measure platelet aggregation inhibited by aspirin and clopidogrel respectively. The subjects were divided into four groups: pure aspirin resistant group (AR, electrical impedance > 0 Ω), pure clopidogrel resistant group (CR, electrical impedance ≥ 10 Ω), dual resistant group (DR) and dual sensitive group (DS). The primary outcomes were recurrent cardiac ischemic events during the 12-month follow-up. Antiplatelet resistance occurred more often in patients with type 2 diabetes (P = 0.027). The platelet counts (PLT) were higher in antiplatelet resistant groups than DS group (P = 0.013). During the 12-month follow-up, the antiplatelet resistant patients had a higher incidence of recurrent cardiac ischemic events and stent thrombosis (ST) than the patients without (12.5%, 10.0%, 50.0% vs 3.8%, P = 0.036; 6.3%, 10.0%, 50.0% vs 1.3%, P = 0.000; respectively). Binary Logistic regression indicated that dual resistance remained an independent predicator of recurrence cardiac ischemic events and ST (OR 5.99, 95%CI 1.05 - 34.34, P = 0.045; OR 6.36, 95%CI 1.13 - 35.78, P = 0.036; respectively). As a physiological assessment of platelet reactivity, EIA is a convenient and accurate option for measuring aspirin resistance. Antiplatelet resistance assessed by EIA is paralleled to clinical events. Dual resistance is an independent predicator for ST and recurrence cardiac ischemic events in patients with AMI.
    Zhonghua yi xue za zhi 10/2012; 92(38):2677-80.
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    ABSTRACT: This study aimed to transfer the hPNAS-4 gene, a novel apoptosis-related human gene, into Lewis lung cancer (LL2) and observe its radiosensitive effect on radiation therapy in vitro and in vivo. The hPNAS-4 gene was transfected into LL2 cells, and its expression was detected via western blot. Colony formation assay and flow cytometry were used to detect the growth and apoptosis of cells treated with irradiation/PNAS-4 in vitro. The hPNAS-4 gene was transferred into LL2-bearing mice through tail vein injection of the liposome/gene complex. The tumor volumes were recorded after radiation therapy. Proliferating cell nuclear antigen (PCNA) immunohistochemistry staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay were performed to detect the tumor cell growth and apoptosis in vivo. The hPNAS-4 gene was successfully transferred into LL2 cells and tumor tissue, and its overexpressions were confirmed via western blot analysis. Compared with the control, empty plasmid, hPNAS-4, radiation, and empty plasmid plus radiation groups, the hPNAS-4 plus radiation group more significantly inhibited growth and enhanced apoptosis of LL2 cells in vitro and in vivo (P<.05). The hPNAS-4 gene was successfully transferred into LL2 cells and tumor tissue and was expressed in both LL2 cell and tumor tissue. The hPNAS-4 gene therapy significantly enhanced growth inhibition and apoptosis of LL2 tumor cells by radiation therapy in vitro and in vivo. Therefore, it may be a potential radiosensitive treatment of radiation therapy for lung cancer.
    International journal of radiation oncology, biology, physics 07/2012; 84(4):e533-40. · 4.59 Impact Factor
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    ABSTRACT: The forkhead box protein P1 (FOXP1) expression resulted from chromosome translocation was found in MALT lymphoma, and its nuclear expression in diffuse large B cell lymphoma has been believed to be a poor prognostic factor. In our study, FOXP1 expression was investigated in its relationship to the occurrence of large tumor cells, clinical features, and prognosis in a series of 115 MALT lymphomas divided into two groups with or without the large tumor cells. All cases were morphologically reviewed, and FOXP1 expression was detected both in mRNA and protein levels by real-time PCR, immunochemical staining, and Western blot hybridization. All available clinical data were collected. In the MALT lymphoma with large cells, FOXP1 expression was higher at both mRNA (P = 0.008) and protein (P = 0.000) levels than that in group without large cells, and most large tumor cells showed FOXP1 positivity. It was also found that cases beyond Ann Arbor stage I have a higher FOXP1 expression rate than cases in stage I (P = 0.01), moreover, FOXP1-positive group has more plasmacytic differentiation (P = 0.025), deeper filtrating depth in digestive tract (P = 0.039), and a higher Ki67 proliferation index (P = 0.022). However, no statistical significance was identified in the involved anatomic sites and prognosis. Our data demonstrated the close relationship between FOXP1 nuclear expression and the occurrence of large tumor cells in MALT lymphoma, which suggested the possibility of large cell transformation of FOXP1-positive cases. And FOXP1 positivity was associated with enhanced invasion and proliferation ability of tumor cells. In the thyroid cases, the FOXP1 positivity showed a poorer prognosis (P = 0.043), but the significance was not found in the overall survival analysis (P = 0.1123).
    Medical Oncology 06/2012; · 2.14 Impact Factor
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    ABSTRACT: Despite progress made in the treatment of hepatocellular carcinoma (HCC), there is no curable treatment. Novel therapies are therefore needed. In our previous study on the design and synthesis of a small molecular inhibitor targeting Aurora kinase, we discovered a novel thienopyridine derivative compound (1g, TP58) which displayed the most potent and relatively specific inhibition of the proliferation of HepG2 human hepatoma cells in vitro. However, the molecular mechanism remains to be elucidated. Herein, in vitro and in vivo studies were conducted to further verify its antitumor activity against HCC. cDNA microarray and two-dimensional protein gel electrophoresis technology were utilized to elucidate the mechanism of HCC-specific inhibition of TP58. Flow cytometry analysis displayed that TP58 can significantly induce G0/G1 arrest in HepG2 cells. Sixteen genes involved in cell cycle regulation were found to be dysregulated following TP58 treatment using microarray technology. Nine proteins whose expression was altered (corresponding to 10 spots identified as differentially expressed) were identified by proteomic analysis. Further study showed that TP58 can modulate the expression of some liver-enriched transcription factors (LETFs) and liver-specific marker genes, such as hepatic nuclear factor (HNF-4) and α-fetoprotein (AFP). These findings may help explain the mechanism of HCC-specific antitumor activity of TP58 and provide some useful insight for anti-HCC drug design and future use of thienopyridine derivatives in HCC therapy.
    Oncology Reports 04/2012; 28(1):225-31. · 2.30 Impact Factor
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    ABSTRACT: Noxa is an important proapoptotic protein in the intrinsic pathway of cell apoptosis. Experiments were carried out to investigate whether Noxa could, therefore, enhance the cytotoxic effect of gemcitabine in human ovarian cancer cell lines (A2780 and COC1). In this study, the combined treatment of Noxa and gemcitabine, in vitro, significantly inhibited the proliferation of A2780 and COC1 cells, as verified by MTT assay, Hoechst staining, and flow cytometric analysis. Moreover, the combination of Noxa and gemcitabine inhibited tumor growth and prolonged the survival of nude mice in vivo. The combined treatment also inhibited the growth of tumor xenografts through the inhibition of proliferation and the induction of apoptosis, as observed in immunohistochemical anti-PCNA staining and TdT-mediated dUTP-biotin nick-end labeling (TUNEL) assay. Our data suggest that Noxa exhibited potent proapoptotic activity against human ovarian cancer cells, and the combination of Noxa and gemcitabine showed a more significant cytotoxic effect against ovarian cancer cells in comparison with either of these agents alone. To our knowledge, we have provided the first evidence that Noxa can enhance therapeutic responses of ovarian cancer cells to gemcitabine, and that it could be potentially useful as a chemosensitizer in ovarian cancer therapy.
    Cancer Biotherapy & Radiopharmaceuticals 04/2012; 27(4):259-66. · 1.44 Impact Factor
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    ABSTRACT: To summarize the clinical and pathological features of all reported Langerhans cell histiocytosis (LCH) cases of female genital tract and to provide our additional three cases, and the emphasis is put on the pathological diagnosis to remind both gynecologists and pathologists of this rare disease. Literatures available are reviewed and the routine hematoxylin and eosin stained sections and immunohistochemical stained sections are studied for the diagnosis of our cases. Only 18 female genital tract LCH cases have been previously reported in medical literatures. The three cases we provide are diagnosed as LCH by both morphology and immunochemical staining after biopsy. All the patients presented papulous or ulcerative lesions on vulva or cervix, and the following systemic laboratory and radiologic examinations demonstrated no other affected site. After various treatments based on surgery and chemotherapy, most patients showed no signs of local or systemic recurrence. 'Pure' LCH of female genital tract without any other spreading is a quite rare disease and it might be misrecognized as some other diseases, so both gynecologists and pathologists should keep it in mind when encountered with such cases. The three patients we reported appeared to be the first cases having 'pure' lesion of female genital tract in China.
    Archives of Gynecology 01/2012; 285(1):99-103. · 0.91 Impact Factor
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    ABSTRACT: Ovarian cancer is the most common cause of death from gynecologic malignancy. Deregulation of p53 and/or p73-associated apoptotic pathways contribute to the platinum-based resistance in ovarian cancer. NOXA, a pro-apoptotic BH3-only protein, is identified as a transcription target of p53 and/or p73. In this study, we found that genetic variants of Bcl-2 proteins exist among cisplatin-sensitive and -resistant ovarian cancer cells, and the responses of NOXA and Bax to cisplatin are regulated mainly by p53. We further evaluated the effect of NOXA on cisplatin. NOXA induced apoptosis and sensitized A2780s and SKOV3 cells to cisplatin in vitro and in vivo. The effects were mediated by elevated Bax expression, enhanced caspase activation, release of Cyt C and Smac into the cytosol. Furthermore, gene silencing of Bax or Smac significantly attenuated NOXA and/or cisplatin-induced apoptosis in chemosensitive A2780s cells, whereas overexpression of Bax or addition of Smac-N7 peptide significantly increased NOXA and/or cisplatin-induced apoptosis in chemoresistant SKOV3 cells. To our knowledge, these data suggest a new mechanism by which NOXA chemosensitized ovarian cancer cells to cisplatin by inducing alterations in the Bax/Smac axis. Taken together, our findings show that NOXA is potentially useful as a chemosensitizer in ovarian cancer therapy.
    PLoS ONE 01/2012; 7(5):e36722. · 3.73 Impact Factor
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    ABSTRACT: A 78-year-old man presented with an eight-hour history of chest distress. Electrocardiograph and serum cardiac enzymes were suggestive of acute inferior myocardial infarction with right ventricular infarction. The patient, who underwent emergency percutaneous coronary intervention, suffered from thrombocytopenia presenting with cerebral infarction and myocadial reinfarction during haparin exposure. The laboratory test for heparin-induced thrombocytopenia (HIT) specific antibodies (heparin-platelet factor, PF4) was positive. The case was diagnosed as arteries thrombosis due to heparin-induced thrombocytopenia; the patient died after cessation of heparin.
    Chinese medical journal 11/2011; 124(22):3830-3. · 0.90 Impact Factor
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    ABSTRACT: To assess the prognostic values for in-hospital event rate of tissue Doppler imaging (TDI) parameter (E/Em) after acute myocardial infarction. A total of 289 patients with acute myocardial infarction were retrospectively examined. Their clinical data and echocardiograms were obtained. Clinical events were recorded. Patients were divided into two groups according to the value of ratio of early transmitral flow velocity to early diastolic velocity of mitral annulus (E/Em): Group E/Em < 10 (n = 152) and Group E/Em ≥ 10 (n = 137). Clinical characteristics, echocardiographic parameters and the rate of cardiac events were compared. Predictors of heart failure were identified by multivariate Logistic regression analysis. On echocardiography, the patients with an E/Em ratio ≥ 10 had statistically larger left atrial diameter [(39.1 ± 6.2) vs (36.0 ± 4.4) mm, P = 0.000] and left ventricular end diastolic diameter [(52.3 ± 7.3)vs (49.2 ± 5.2) mm, P = 0.000]. Worse systolic functions were found in group E/Em ≥ 10: left ventricular ejection fraction (LVEF) [(48.3 ± 11.7)% vs (56.7 ± 9.7)%, P = 0.000]. Systolic velocities of mitral annulus (Sm) [(6.6 ± 1.7) vs (8.6 ± 2.2) cm/s, P = 0.000]. Em [(6.4 ± 1.9) vs (9.4 ± 2.4) cm/s, P = 0.000] was statistically lower than that of E/Em < 10 group. Killip classes on admission were statistically higher in group E/Em ≥ 10 than those of the other group [(1.7 ± 0.9) vs (1.2 ± 0.6), P = 0.000]. So were as the ratio of heart failure (38.5% vs 13.8%, P = 0.000) and in-hospital mortality rate (4.4% vs 0.8%, P = 0.000). Logistic regression analysis demonstrated that the independent risk factors of heart failure included the value of E/Em and LVEF. Early E/Em is probably a powerful predictor for left ventricular remodeling and in-hospital heart failure in patients after acute myocardial infarction.
    Zhonghua yi xue za zhi 09/2011; 91(34):2380-3.
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    ABSTRACT: Ovarian cancer is the number one cause of death from gynecologic malignancy. A defective p53 pathway is a hallmark of ovarian carcinoma. The p53 mutation correlates significantly with resistance to platinum-based chemotherapy, early relapse and shortened overall survival in ovarian cancer patients. PUMA (p53 upregulated modulator of apoptosis), a BH3-only Bcl-2 family protein, was recently identified as a transcriptional target of p53 and a potent apoptosis inducer in various cancer cells. In this study, we showed that the induction of PUMA by cisplatin was abolished in p53-deficient SKOV3 cells. Elevated expression of PUMA-induced apoptosis and sensitized A2780s and SKOV3 ovarian cancer cells to cisplatin, and the combination of PUMA and low-dose cisplatin, significantly suppressed xenograft tumor growth in vivo through enhanced induction of apoptosis compared with treatment with PUMA or cisplatin alone. The effects of PUMA were mediated by enhanced caspase activation and release of cytochrome c and Smac (second mitochondria-derived activator of caspase) into the cytosol. Furthermore, PUMA chemosensitized intrinsically resistant SKOV3 cells to cisplatin through downregulation of B-cell lymphoma-extra large (Bcl-x(L)) and myeloid cell leukemia sequence 1 (Mcl-1). PUMA-mediated Bcl-x(L) downregulation mainly happened at the transcription level, whereas PUMA-induced Mcl-1 down-regulation was associated with caspase-dependent cleavage and proteasome-mediated degradation. To our knowledge, these data suggest a new mechanism by which overexpression of PUMA enhances sensitivity of SKOV3 cells to cisplatin by lowering the threshold set simultaneously by Bcl-x(L) and Mcl-1. Taken together, our findings indicate that PUMA is an important modulator of therapeutic responses of ovarian cancer cells and is potentially useful as a chemosensitizer in ovarian cancer therapy.
    Molecular Medicine 08/2011; 17(11-12):1262-74. · 4.47 Impact Factor

Publication Stats

36 Citations
33.10 Total Impact Points


  • 2005–2014
    • Sichuan University
      • • State Key Laboratory of Biotherapy
      • • Department of Pathology
      • • Department of Obstetrics and Gynecology
      Hua-yang, Sichuan, China
  • 2007–2013
    • Peking University Third Hospital
      Peping, Beijing, China