Beihua Kong

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

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Publications (116)332.15 Total impact

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    ABSTRACT: Calcium-sensing receptor (CaSR) is a G-protein‑ coupled receptor that senses blood calcium. In vivo, CaSR is required for normal epidermal differentiation by mediating calcium signaling. CaSR was confirmed to be a tumor suppressor in colon and breast cancer. The single-nucleotide polymorphism (SNP) rs17251221, located on the intron, is a genetic variation of the CaSR gene. We analyzed rs17251221 in ovarian cancer using an allelic discrimination assay. Cycling probes were used for genotyping 290 ovarian cancer patients and 312 age-matched cancer-free females. rs17251221 and clinicopathological characteristics of ovarian cancer were analyzed statistically. The AG and GG genotypes were confirmed to appear in fewer cancer cases than in controls and the genotype distribution between cases and controls was statistically significant. The AG+GG genotype was correlated with low ovarian cancer risk, while rs17251221 was not associated with clinicopathological variables including age at diagnosis, tumor size, histologic type, pathological subtype, lymph node metastasis, CA-125 expression, clinical stage, or degree of differentiation. The rs17251221 polymorphism genotype was not correlated with survival in ovarian cancer. These results suggest that the G allele of the CaSR rs17251221 polymorphism is protective against ovarian cancer and the homozygous GG genotype may be a protective genotype as well. The rs17251221 may play an important role in the development of ovarian cancer and could be used as a biomarker for predicting ovarian cancer.
    Oncology Reports 08/2015; 34(4). DOI:10.3892/or.2015.4179 · 2.30 Impact Factor
  • Li Yan · Xiaolin Liu · Aijun Yin · Yuyan Wei · Qifeng Yang · Beihua Kong
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    ABSTRACT: Although the anticancer effects of Huaier extract have been widely investigated, including anti-proliferate, anti-angiogenic and anti-metastatic activities, the mechanisms are not well understood. This study aimed to elucidate the inhibitory effect of Huaier extract on tumor growth in cervical cancer cells and its molecular mechanisms. Cell viability and motility were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony assays, migration, and invasive assays, respectively. The distribution of the cell cycle was analyzed by flow cytometry. Huaier inhibited cell viability of SiHa and C33A cells in a time- and dose-dependent manner; cell migration and invasiveness were also suppressed; Huaier was able to cause G2/M cell cycle arrest in C33A cells. The western blot results confirmed Huaier dose-dependently increased expression of phosphorylated c-Jun N-terminal kinase (JNK), p-38 and downregulated the expression of phosphorylated extracellular signal-regulated kinase (ERK) in a time- and dose-dependently manner. In vivo experiments showed that Huaier significantly suppressed the tumor volume of SiHa cell xenografts. These data suggest that Huaier may inhibit tumor proliferation in cervical cancer via the JNK/p38 signaling pathway.
    International Journal of Oncology 07/2015; 47(3). DOI:10.3892/ijo.2015.3094 · 3.03 Impact Factor
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    ABSTRACT: Due to a poor understanding of tumorigenesis, ovarian cancers remain the most lethal gynecologic malignancy and cause horrific deaths. In the last decade, a new dualistic model for ovarian cancer was proposed, wherein ovarian serous cancers are classified as either high-grade or low-grade, with each having different tumorigenic processes, and pathologic and clinical features. Surprisingly, both high- and low-grade ovarian serous cancers were recently found to originate not in the ovaries, but rather from the secretory cells of the fallopian tube, mostly from the tubal fimbriated ends. In this article, we review the evidentiary basis for the aforementioned paradigm shift in the cell origin of ovarian serous cancers, as well as its potential clinical implications.
    Histology and histopathology 07/2015; DOI:10.14670/HH-11-645 · 2.10 Impact Factor
  • Zhao Li · Liping Sun · Zaijun Lu · Xuantao Su · Qifeng Yang · Xun Qu · Li Li · Kun Song · Beihua Kong
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    ABSTRACT: Nanoparticles are promising novel drug delivery carriers that allow tumor targeting and controlled drug release. In the present study, we prepared poly butyl-cyanoacrylate nanoparticles (PBCA-NP) entrapped with hypocrellin B (HB) to improve the effect of photodynamic therapy (PDT) in ovarian cancer. An ovarian cancer ascites model using Fischer 344 rats and PBCA-NP entrapped with HB (HB-PBCA-NP) were formed successfully. The pharmacodynamic characteristics and biodistribution of the HB-PBCA-NP system were evaluated by comparison with HB dimethyl sulfoxide (HB-DMSO) and testing at various time-points following intraperitoneal drug administration. HB-PBCA-NP-based PDT combined with cytoreductive surgery was then administrated to the tumor-bearing animals. Kaplan-Meier survival analysis was performed to assess the therapeutic effect of the nanoparticle system. The serum HB concentration peaked 4 h after drug administration in the nanoparticle system, and 1 h with HB-DMSO. The peak exposure time of tumor tissues was also extended (4 vs. 2 h), and PBCA-NP remained present for much longer than HB-DMSO. Although PDT combined with surgery prolonged the survival time significantly compared with surgery alone (84 days, P<0.05), there was no significant difference in the survival time of animals that received either HB-PBCA-NP- or HB-DMSO-based PDT after cytoreductive surgery (99 vs. 95 days, P=0.293). PBCA-NP exhibited potential advantages in controlled drug release and tumor targeting, which was beneficial for HB-based PDT. PDT combined with surgery prolonged the survival time, suggesting that this might be an alternative treatment option for ovarian cancer.
    International Journal of Oncology 07/2015; 47(3). DOI:10.3892/ijo.2015.3079 · 3.03 Impact Factor
  • Linyan Xie · Yan Yang · Xuming Sun · Xu Qiao · Qiao Liu · Kun Song · Beihua Kong · Xuantao Su
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    ABSTRACT: Conventional optical cytometric techniques usually measure fluorescence or scattering signals at fixed angles from flowing cells in a liquid stream. Here we develop a novel cytometer that employs a scanning optical fiber to illuminate single static cells on a glass slide, which requires neither microfluidic fabrication nor flow control. This static cytometric technique measures two dimensional (2D) light scattering patterns via a small numerical aperture (0.25) microscope objective for label-free single cell analysis. Good agreement is obtained between the yeast cell experimental and Mie theory simulated patterns. It is demonstrated that the static cytometer with a microscope objective of a low resolution around 1.30 μm has the potential to perform high resolution analysis on yeast cells with distributed sizes. The capability of the static cytometer for size determination with submicron resolution is validated via measurements on standard microspheres with mean diameters of 3.87 and 4.19 μm. Our 2D light scattering static cytometric technique may provide an easy-to-use, label-free, and flow-free method for single cell diagnostics. © 2015 International Society for Advancement of Cytometry. © 2015 International Society for Advancement of Cytometry.
    Cytometry Part A 06/2015; DOI:10.1002/cyto.a.22713 · 2.93 Impact Factor
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    ABSTRACT: Current research has strongly proposed that contrary to prior beliefs, many ovarian epithelial cancers (OECs) do not, as their name suggests, originate in the ovaries. Recent findings regarding both high-grade and low-grade serous carcinomas has implicated the fallopian tube as a cell source for these OECs, but until now, there has been little insight into the cellular source for clear cell and endometrioid carcinomas. In this commentary review article, we aimed to discuss the new findings that support the possible contribution from the fallopian tube in clear cell and endometrioid carcinomas. Specifically, we have provided results that showcased ovarian surface epithelia (OSE) and ovarian epithelial inclusions (OEIs) as having mesothelial and tubal origins and have strongly recognized the secondary müllerian system and the ability for tubal epithelia to implant upon the ovarian surface as contributing to fallopian tube-derived OEIs (F-OEIs). We have provided initial indications of these F-OEIs and their relationship to endometriosis and then clear cell and endometrioid carcinomas and subsequently offer our new proposal of a probable tubal origin. This new proposal is a paradigm that drastically changes the understanding behind the origin of these OECs and has significant clinical implications in the near future.
    American Journal of Cancer Research 06/2015; 5(3):869-79. · 4.17 Impact Factor
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    ABSTRACT: Successful human pregnancy requires the maternal immune system to recognize and tolerate the semi-allogeneic fetus. Myeloid-derived suppressor cells (MDSCs), which are capable of inhibiting T-cell responses, are highly increased in the early stages of pregnancy. Although recent reports indicate a role for MDSCs in fetal-maternal tolerance, little is known about the expansion of MDSCs during pregnancy. In the present study, we demonstrated that the trophoblast cell line HTR8/SVneo could instruct peripheral CD14(+) myelomonocytic cells toward a novel subpopulation of MDSCs, denoted as CD14(+)HLA-DR(-/low) cells, with suppressive activity and increased expression of IDO1, ARG-1, and COX2. After interaction with HTR8/SVneo cells, CD14(+) myelomonocytic cells secrete high levels of CCL2, promoting the expression of signal transducer and activator of transcription 3. We utilized a neutralizing monoclonal antibody to reveal the prominent role of CCL2 in the induction of CD14(+)HLA-DR(-/low) MDSCs. In combination, the results of the present study support a novel role for the cross-talk between the trophoblast cell line HTR8/SVneo and maternal CD14(+) myelomonocytic cells in initiating MDSCs induction, prompting a tolerogenic immune response to ensure a successful pregnancy.Cellular & Molecular Immunology advance online publication, 1 June 2015; doi:10.1038/cmi.2015.41.
    Cellular & molecular immunology 06/2015; DOI:10.1038/cmi.2015.41 · 4.11 Impact Factor
  • Lijie Wang · Beihua Kong
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    ABSTRACT: Studies investigating the association between matrix metalloproteinase-1 (MMP1) gene promoter 1607-base pair (bp) polymorphism and ovarian cancer risk have yielded conflicting results. We therefore carried out a meta-analysis of 754 ovarian cancer cases and 1184 controls from 5 published case-control studies. The strength of the association between MMP1 1607-bp polymorphism and ovarian cancer susceptibility was calculated using pooled odds ratios (ORs) with corresponding 95% confidence intervals (CIs). The results suggest that no statistically significant associations exist between MMP1 1607-bp polymorphisms and ovarian cancer risk in all 4 genetic models (2G2G vs 1G1G: OR, 1.08; 95% CI, 0.81-1.43; P = 0.23; 1G2G vs 1G1G: OR, 1.06; 95% CI, 0.82-1.36; P = 0.15; 1G2G + 2G2G vs 1G1G: OR, 1.05; 95% CI, 0.83-1.34; P = 0.16; 2G2G vs 1G1G + 1G2G: OR, 0.98; 95% CI, 0.80-1.20; P = 0.84). In summary, this meta-analysis showed that the MMP1 1607-bp polymorphism is not associated with ovarian cancer risk.
    International Journal of Gynecological Cancer 05/2015; 25(6). DOI:10.1097/IGC.0000000000000463 · 1.95 Impact Factor
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    ABSTRACT: Pseudo-Meigs' syndrome is a syndrome rarely caused by leiomyomas. Elevated CA125 usually suggests malignancy of the ovary. No reported case of pseudo-Meigs' syndrome presenting with necrosis and mucinous degeneration of uterine cellular leiomyomas (CLs) and an elevated CA125 level was found upon a PubMed search. A 37-year-old woman presenting with massive ascites, bilateral pleural effusions and a pelvic mass measuring 20x18x10 cm is described. The pre-operative serum CA125 was 920.4 U/ml. After total abdominal hysterectomy and partial omentumectomy, the final pathologic diagnosis was CL with focal hemorrhage, necrosis and mucinous degeneration. The ascites and pleural effusion disappeared, and the CA125 level returned to normal in one month. Benign leiomyoma accompanied by pseudo-Meigs' syndrome and elevated serum CA125 can mimic a pelvic malignancy.
    Oncology Reports 04/2015; 33(6). DOI:10.3892/or.2015.3912 · 2.30 Impact Factor
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    ABSTRACT: Struma ovarii is an uncommon ovarian teratoma comprised predominantly of mature thyroid tissue. The combination of pseudo-Meigs' syndrome, and elevation of CA 125 to the struma ovarii is a rare condition that can mimic ovarian malignancy. We reported a case of benign struma ovarii, presenting with the clinical features of advanced ovarian carcinoma: complex pelvic mass, gross ascites, bilateral pleural effusion and markedly elevated serum CA 125 levels. The patient underwent total abdominal hysterectomy and bilateral salpingo-oophorectomy. Ascites and pleural effusion were not evident and the CA 125 levels returned to normal following surgical excision. A systematic review of reported cases of coexistent benign struma ovarii, pseudo-Meigs' syndrome and elevated serum CA 125 was performed. Struma ovarii accompanied by pseudo-Meigs' syndrome and elevated serum CA 125 should be considered in the differential diagnosis of ovarian epithelial cancer.
    Oncology letters 02/2015; 9(4). DOI:10.3892/ol.2015.2927 · 1.55 Impact Factor
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    ABSTRACT: Ovarian cancer is a highly invasive cancer with poor prognosis. Previous studies have revealed lots of connections between the invasiveness and epithelial-mesenchymal transition (EMT), which is common during the progression of ovarian cancer. MDC1, a mediator of DNA damage checkpoint, has recently been implicated as a potential oncogene. Here, in this article, we studied the role of MDC1 in ovarian cancer metastasis. First, in tissue samples, we found that high expression level of MDC1 was correlated with poor prognosis. Furthermore, MDC1 overexpression in ovarian cancer cells significantly increased migration and invasion. In contrast, silencing MDC1 reversed these processes. Consistently, nude mice xenograft confirmed that silencing MDC1 suppressed tumor metastasis in vivo. We further demonstrated that MDC1 induced EMT through modulation EMT markers such as E-cadherin, N-cadherin, and vimentin. Taken together, our findings suggest that MDC1 promotes ovarian cancer metastasis through the induction of EMT.
    Tumor Biology 01/2015; 36(6). DOI:10.1007/s13277-015-3063-5 · 3.61 Impact Factor
  • Liping Sun · Li Li · Zhao Li · Shuhui Hong · Qifeng Yang · Xun Qu · Beihua Kong
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    ABSTRACT: Ovarian cancer causes more deaths than any other malignant tumor of the female reproductive system. This is because the condition usually goes undetected until the late stages. The purpose of the present study is to identify alterations in the serum proteome profile during the development of ovarian cancer and to provide an experimental basis for discovering new and valuable serum biomarkers for the early detection of ovarian carcinoma. Surface-enhanced laser desorption/ionization-time of flight (SELDI-TOF-MS) was used to profile changes in the serum proteome of Fischer 344 rats with ovarian cancer during the progress of tumor development. Sera were collected from the rats on day A (1 week before injection of tumor cells), day B (4 weeks after injection), and day C (6 weeks after injection). Each sample was subjected to SELDI-TOF-MS testing. Peak detection and alignment and selection of peaks with the highest discriminatory power were performed using proteinchip biomarker software. Decision tree analyses were performed using biomarker pattern software. Finally, 3 peaks were found to be the most valuable ones (3759, 4659 and 9318 Da). The expression frequency of m/z 3759-Da peaks was downregulated and another two frequencies (4659 and 9318 Da) were upregulated, and the levels of expression of these three proteins showed the same tendency as the expression frequency during the development of ovarian cancer. The total accuracy rate of diagnosis at 4 and 6 weeks post-injection was 94.7 and 97.3%, respectively. Profiling the serum proteome changes during the process of the cancer development using SELDI-TOF-MS may provide useful information regarding carcinogenesis and facilitate discovery of novel serum biomarkers for early detection.
    International Journal of Oncology 12/2014; 45(6):2495-501. DOI:10.3892/ijo.2014.2675 · 3.03 Impact Factor
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    ABSTRACT: Background: Uterine smooth muscle tumors (USMTs) constitute a group of histologic, genetic, and clinical heterogeneous tumors that include at least 6 major histologically defined tumor types: leiomyoma (ULM), mitotically active leiomyoma (MALM), cellular leiomyoma (CLM), atypical leiomyoma (ALM), uncertain malignant potential (STUMP), and leiomyosarcoma (LMS). Apart from ULM and LMS, the nature of these variants is not well defined. Methods: A total of 167 cases of different USMT variants were collected, reviewed, and diagnostically confirmed based on the World Health Organization and Stanford schemes. These included 38 cases of LMS, 18 cases of STUMP, 42 cases of ALM, 22 cases of CLM, 7 cases of MALM, and 40 cases of ULM. Molecular analysis included selected microRNAs (miRNAs), oncogenes, and tumor suppressors that are highly relevant to USMT. Results: Overall, 49% (17/35) of LMS cases and 7% (1/14) of STUMP cases died due to their USMT, but no deaths were attributed to ALM. miRNA profiling revealed that ALM and LMS shared similar miRNA signatures. P53 mutations and PTEN deletions were significantly higher in LMS, ALM, and STUMP compared with other USMT variants (P < .01). In contrast, MED12 mutations were extremely common in ULM and MALM (> 74%) but were significantly less common (< 15%) in CLM, ALM, STUMP, and LMS (P < .01). Conclusion: Six types of USMT have different gene mutation fingerprints. ALM shares many molecular alterations with LMS. Our findings suggest that ALM may be a precursor lesion of LMS or have similar genetic changes during its early stage.
    Cancer 10/2014; 120(20). DOI:10.1002/cncr.28900 · 4.89 Impact Factor
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    ABSTRACT: High-grade serous ovarian carcinoma (HGSOC), the most common and aggressive subtype of epithelial ovarian cancer, is characterized by TP53 mutations and genetic instability. Using miRNA profiling analysis, we found that miR-145, a p53 regulated miRNA, was frequently down-regulated in HGSOC. miR-145 down-regulation was further validated in a large cohort of HGSOCs by qPCR. Overexpression of miR-145 in ovarian cancer cells significantly suppressed proliferation, migration and invasion in vitro and inhibited tumor growth and metastasis in vivo. Metadherin (MTDH) was subsequently identified as a direct target of miR-145, and was found to be significantly up-regulated in HGSOC. Furthermore, overexpression of MTDH rescued the inhibitory effects of miR-145 in ovarian cancer cells. Finally, we found that high level of MTDH expression correlated with poor prognosis of HGSOC. Therefore, lack of suppression of MTDH by miR-145 when p53 is dysfunctional leads to increased tumor growth and metastasis of HGSOC. Our study established a new link between p53, miR-145 and MTDH in the regulation of tumor growth and metastasis in HGSOC.
    Oncotarget 10/2014; 5(21). DOI:10.18632/oncotarget.2522 · 6.36 Impact Factor
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    ABSTRACT: Silent information regulator 1 (SIRT1) is involved in a number of cellular regulatory mechanisms affecting cellular life span, stress resistance, apoptosis and cellular metabolism. Recent studies have revealed that SIRT1 plays a dual role as a tumor suppressor and a tumor promoter in multiple stages of carcinogenesis. Increased lipogenesis has been found in cancer cells, sterol regulatory element binding protein 1 (SREBP1) are nuclear lipogenic transcription factors, which mainly regulate lipogenic processes by activating genes involved in fatty acid and triglyceride biosynthesis. In the present study, we detected expression of SIRT1 in endometrial cancer (EC) and illustrated the relationship between SIRT1 and SREBP1, which indicated that SIRT1 could stimulate endometrial tumor growth through the lipogenic pathway. Gene expression levels of SIRT1 were assayed using quantitative real-time PCR and protein expression levels were detected by western blotting. RNA interference was conducted in order to explore the subsequent effect on tumor cells and on the expression of SREBP1. Expression levels of SIRT1 in EC were found to be significantly higher than in normal endometrium. Knockdown of SIRT1 could downregulate expression of SREBP1 and suppress cell proliferation. These results demonstrated that SIRT1 may play a role as a tumor promoter in EC and can promote endometrial tumor growth by promoting lipogenesis. Our findings suggest that targeting SIRT1 may provide a theoretical basis for the management of EC.
    Oncology Reports 10/2014; 32(6). DOI:10.3892/or.2014.3521 · 2.30 Impact Factor
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    ABSTRACT: Pharmacokinetics and bio-distribution are crucial factors affecting the performance of an intravenous drug. In this study, we explore the combined use of glucose and polyethylene glycol (PEG) ligands to further improve gold nanoparticle (GNP) pharmacokinetics and bio-distribution, with the aim of using the drug for in-vivo radiotherapy. The inclusion of PEG was found to significantly prolong the half-life period, where PEG-Glu-GNPs achieved 6.17 +/- 3.71 h, compared to 1.23 +/- 0.14 h for Glu-GNPs and 1.07 +/- 0.22 h for uncoated GNPs. Our data indicates that nanoparticle size impacts cell uptake performance, with 20 nm being the optimal diameter for cancer treatment applications. Although PEG-Glu-GNPs mainly distributed in the spleen, liver, lung, and kidneys, the concentration of PEG-Glu-GNPs in tumour tissue was 20 times higher than healthy cells in the uterus and ovaries, reaching 9.22 +/- 2.41 microg/g cancer tissue at 48 h after injection. This difference in uptake holds promise for selective tumor targeting which can in turn lead to more effective radiotherapy through the interaction of X-rays and GNPs. Specifically tumor size after 47 days of treatment had reduced to (769 +/- 92) mm3 compared to (1432 +/- 269) mm3 using X-rays alone and (3514 +/- 1818) mm3 without any treatment. Moreover, the mice remained healthy without statistically significant weight loss. Results of our pharmacokinetic and bio-distribution study as well as therapeutic data for PEG-Glu-GNPs in our tumor bearing animal model demonstrate that PEG-Glu-GNPs provide excellent in-vivo stability, tumor targeting function, and radiotherapeutic enhancement effects, providing useful insights for further clinical studies.
    Journal of Biomedical Nanotechnology 07/2014; 10(7):1205-16. DOI:10.1166/jbn.2014.1855 · 5.34 Impact Factor
  • G. Feng · B. Kong · J. Xing · J. Chen
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    ABSTRACT: Aim To describe how pegylated glucose-coated gold nanoparticles (PEG-Glu-GNPs) can help improve computed tomography (CT) imaging. Materials and methods PEG-Glu-GNPs were designed for use as an imaging nanoprobe to act an effective contrast agent for both CT and PET scans. Twelve BALB/c mice were divided into two groups: mice with injected with PEG-Glu-GNPs and control mice. The mice were examined using high-resolution micro-CT at different time intervals (24 h, 7 days, and 15 days) after the injection of the particles. Greyscale density and CT attenuation values were determined to trace the excretion of the particles over time. Results Tumour contours were easily distinguished from surrounding tissue in mice injected with PEG-Glu-GNPs but not controls. This distinction was still visible at 7 days, but not at 15 days post-injection. Conclusion Molecular imaging technology has enabled the development of a new generation of imaging probes. These sophisticated probes can visualize biological processes or enable early diagnosis of diseases in vivo. Compared to conventional CT images and PET scans, PEG-Glu-GNPs significantly improved image quality at the cellular and molecular level, which can significantly aid the early detection of cancer or cancer metastases.
    Clinical Radiology 07/2014; 69(11). DOI:10.1016/j.crad.2014.05.112 · 1.76 Impact Factor
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    ABSTRACT: Serous endometrial intraepithelial carcinoma is often associated with extrauterine disease. It is currently unclear where does the extrauterine disease come from. This study addressed this issue. A total of 135 samples from 21 serous endometrial intraepithelial carcinoma patients were studied. Cellular lineage relationships between intrauterine and extrauterine serous carcinomas were determined by TP53-mutation analysis and correlated to the clinicopathologic features. There were three conditions contributing the extrauterine disease: metastasis from serous endometrial intraepithelial carcinoma (n=10) showed identical TP53 mutation between intrauterine lesions and extrauterine disease, cases of adnexal origin (n=5) had discordant TP53 mutations, and the mixed cellular origin cases (n=6) with both identical and discordant mutation status. Patients with extrauterine disease from serous endometrial intraepithelial carcinoma metastasis typically had small tumor masses (<2 cm) in extrauterine sites and without finding of serous tubal intraepithelial carcinoma, while extrauterine disease with adnexal or tubal origin commonly had larger tumor masses in extrauterine sites including ovary and omentum and serous tubal intraepithelial carcinoma. The majority of extrauterine diseases associated with serous endometrial intraepithelial carcinoma are metastasized from the endometrium. Serous endometrial intraepithelial carcinoma is frequently associated with serous cancers of adnexal or tubal origin, indicating that endometrial and adnexal or tubal serous cancers may share similar etiologies. TP53-mutation analysis provides a strong linkage for cellular lineage analysis. Tumor size in extrauterine disease and presence of serous tubal intraepithelial carcinoma or not are useful clinicopathologic features to determine primary cancer site, which helps in clinical management.Modern Pathology advance online publication, 13 June 2014; doi:10.1038/modpathol.2014.76.
    Modern Pathology 06/2014; 28(1). DOI:10.1038/modpathol.2014.76 · 6.19 Impact Factor
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    Cunzhong Yuan · Xiaoyan Liu · Shi Yan · Cunfang Wang · Beihua Kong
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    ABSTRACT: This meta-analysis aims to examine whether the XRCC3 polymorphisms are associated with ovarian cancer risk. Eligible case-control studies were identified through search in PubMed. Pooled odds ratios (ORs) were appropriately derived from fixed effects models. We therefore performed a meta-analysis of 5,302 ovarian cancer cases and 8,075 controls from 4 published articles and 8 case-control studies for 3 SNPs of XRCC3. No statistically significant associations between XRCC3 rs861539 polymorphisms and ovarian cancer risk were observed in any genetic models. For XRCC3 rs1799794 polymorphisms, we observed a statistically significant correlation with ovarian cancer risk using the homozygote comparison (T2T2 versus T1T1: OR = 0.70, 95% CI = 0.54-0.90, P = 0.005), heterozygote comparison (T1T2 versus T1T1: OR = 1.10, 95% CI = 1.00-1.21, P = 0.04), and the recessive genetic model (T2T2 versus T1T1+T1T2: OR = 0.67, 95% CI = 0.52-0.87, P = 0.002). For XRCC3 rs1799796 polymorphisms, we also observed a statistically significant correlation with ovarian cancer risk using the heterozygote comparison (T1T2 versus T1T1: OR = 0.91, 95% CI = 0.83-0.99, P = 0.04). In conclusion, this meta-analysis shows that the XRCC3 were associated with ovarian cancer risk overall for Caucasians. Asian and African populations should be further studied.
    BioMed Research International 06/2014; 2014:648137. DOI:10.1155/2014/648137 · 3.17 Impact Factor
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    ABSTRACT: High-grade serous ovarian carcinoma (HGSOC) is a fatal disease, and its grave outcome is largely due to widespread metastasis at the time of diagnosis. Current chemotherapies reduce tumor burden, but they do not provide long term benefits for cancer patients. The aggressive tumor growth and metastatic behavior characteristic of these tumors demand novel treatment options such as anti-microRNA treatment which is emerging as a potential modality for cancer therapy. MicroRNA-182 (miR-182) overexpression contributes to aggressive ovarian cancer, largely by its negative regulation of multiple tumor suppressor genes involved in tumor growth, invasion, metastasis, and DNA instability. In this study, we examined the therapeutic potential of anti-miR-182 utilizing the animal orthotopic model to mimic human ovarian cancer using ovarian cancer cells SKOV3 (intrabursal xenografts) and OVCAR3 (IP injection). These models provide a valuable model system for the investigation of ovarian cancer therapy in vivo. Through a combination of imaging, histological, and molecular analyses, we found that anti-miR-182 treatment can significantly reduce tumor burden (size), local invasion, and distant metastasis compared to its control in both models. The bases of anti-miR-182 treatment are mainly through the restoration of miR-182 target expression, including but not limited to BRCA1, FOXO3a, HMGA2 and MTSS1. Overall, our results strongly suggest that anti-miR-182 can potentially be used as a therapeutic modality in treating HGSOC.
    Molecular Cancer Therapeutics 05/2014; 13(7). DOI:10.1158/1535-7163.MCT-13-0982 · 5.68 Impact Factor

Publication Stats

974 Citations
332.15 Total Impact Points


  • 2009–2015
    • University of Jinan (Jinan, China)
      Chi-nan-shih, Shandong Sheng, China
    • University of Texas Health Science Center at San Antonio
      • Department of Pathology
      San Antonio, Texas, United States
  • 2002–2015
    • Shandong University
      • School of Medicine
      Chi-nan-shih, Shandong Sheng, China
  • 2014
    • Northwestern University
      • Department of Obstetrics and Gynecology
      Evanston, Illinois, United States
  • 2013
    • Huazhong University of Science and Technology
      Wu-han-shih, Hubei, China
    • The University of Arizona
      • Department of Obstetrics and Gynecology
      Tucson, Arizona, United States
  • 2011–2012
    • University of Alberta
      • Department of Biomedical Engineering
      Edmonton, Alberta, Canada