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Pancreatic Neoplasms: HELP
Articles by Ping Chen
Based on 16 articles published since 2009
(Why 16 articles?)
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Between 2009 and 2019, Ping Chen wrote the following 16 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial High Dose Parenteral Ascorbate Inhibited Pancreatic Cancer Growth and Metastasis: Mechanisms and a Phase I/IIa study. 2017

Polireddy, Kishore / Dong, Ruochen / Reed, Gregory / Yu, Jun / Chen, Ping / Williamson, Stephen / Violet, Pierre-Christian / Pessetto, Ziyan / Godwin, Andrew K / Fan, Fang / Levine, Mark / Drisko, Jeanne A / Chen, Qi. ·Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, 66160, USA. · Integrative Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA. · Department of Internal Medicine, Hematology and Oncology Division, University of Kansas Medical Center, Kansas City, KS, 66160, USA. · National Institute of Diabetes, Digestive and Kidney Diseases, the National Institutes of Health, Bethesda, MD, 20892, USA. · Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA. · Integrative Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA. jdrisko@kumc.edu. · Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS, 66160, USA. qchen@kumc.edu. · Integrative Medicine, University of Kansas Medical Center, Kansas City, KS, 66160, USA. qchen@kumc.edu. ·Sci Rep · Pubmed #29215048.

ABSTRACT: Pancreatic cancer is among the most lethal cancers with poorly tolerated treatments. There is increasing interest in using high-dose intravenous ascorbate (IVC) in treating this disease partially because of its low toxicity. IVC bypasses bioavailability barriers of oral ingestion, provides pharmacological concentrations in tissues, and exhibits selective cytotoxic effects in cancer cells through peroxide formation. Here, we further revealed its anti-pancreatic cancer mechanisms and conducted a phase I/IIa study to investigate pharmacokinetic interaction between IVC and gemcitabine. Pharmacological ascorbate induced cell death in pancreatic cancer cells with diverse mutational backgrounds. Pharmacological ascorbate depleted cellular NAD+ preferentially in cancer cells versus normal cells, leading to depletion of ATP and robustly increased α-tubulin acetylation in cancer cells. While ATP depletion led to cell death, over-acetylated tubulin led to inhibition of motility and mitosis. Collagen was increased, and cancer cell epithelial-mesenchymal transition (EMT) was inhibited, accompanied with inhibition in metastasis. IVC was safe in patients and showed the possibility to prolong patient survival. There was no interference to gemcitabine pharmacokinetics by IVC administration. Taken together, these data revealed a multi-targeting mechanism of pharmacological ascorbate's anti-cancer action, with minimal toxicity, and provided guidance to design larger definitive trials testing efficacy of IVC in treating advanced pancreatic cancer.

2 Article Inhibition of pancreatic cancer stem cells by Rauwolfia vomitoria extract. 2018

Dong, Ruochen / Chen, Ping / Chen, Qi. ·Department of Pharmacology, Toxicology and Therapeutics, KU Integrative Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA. ·Oncol Rep · Pubmed #30272287.

ABSTRACT: The poor treatment outcomes of pancreatic cancer are linked to an enrichment of cancer stem cells (CSCs) in these tumors, which are resistant to chemotherapy and promote metastasis and tumor recurrence. The present study investigated an extract from the root of the medicinal plant Rauwolfia vomitoria (Rau) for its activity against pancreatic CSCs. In vitro tumor spheroid formation and CSC markers were tested, and in vivo tumorigenicity was evaluated in nude mice. Rau inhibited the overall proliferation of human pancreatic cancer cell lines with a 50% inhibitory concentration (IC50) ranging between 125 and 325 µg/ml, and showed limited cytotoxicity towards normal epithelial cells. The pancreatic CSC population, identified using cell surface markers or a tumor spheroid formation assay, was significantly reduced, with an IC50 value of ~100 µg/ml treatment for 48 h and ~27 µg/ml for long-term tumor spheroid formation. The levels of CSC-related gene Nanog and nuclear β-catenin were decreased, suggesting suppression of the Wnt/β-catenin signaling pathway. In vivo, 20 mg/kg of Rau administered five times per week by oral gavage significantly reduced the tumorigenicity of PANC-1 cells in immunocompromised mice. Taken together, these data showed that Rau preferentially inhibited pancreatic cancer stem cells. Further investigation is warranted to examine the potential of Rau as a novel treatment for pancreatic cancer.

3 Article Extract of the Medicinal Plant Pao Pereira Inhibits Pancreatic Cancer Stem-Like Cell In Vitro and In Vivo. 2018

Dong, Ruochen / Chen, Ping / Chen, Qi. ·1 University of Kansas Medical Center, Kansas City, KS, USA. ·Integr Cancer Ther · Pubmed #29985062.

ABSTRACT: Pancreatic cancers are enriched with cancer stem-like cells (CSCs), which are resistant to chemotherapies, and responsible for tumor metastasis and recurrence. Here, we investigated the extract of a medicinal plant Pao Pereira (Pao) for its activity against pancreatic CSCs. Pao inhibited overall proliferation of human pancreatic cancer cell lines with IC

4 Article CSN5/Jab1 facilitates non-small cell lung cancer cell growth through stabilizing survivin. 2018

Li, Jie / Li, Yingjie / Wang, Bin / Ma, Yongfu / Chen, Ping. ·Department of Chest Surgery, The General Hospital of the People's Liberation Army, Beijing, China. Electronic address: lijieefy186@163.com. · Department of Cardio-thoracic Surgery, First Affiliated Hospital, General Hospital of the People's Liberation Army, Beijing, China. · Department of Chest Surgery, The General Hospital of the People's Liberation Army, Beijing, China. ·Biochem Biophys Res Commun · Pubmed #29596838.

ABSTRACT: CSN5/JAB1 is a critical subunit of the COP9 signalosome (CSN) and is essentially involved in diverse types of cancer, but little is known about the role of CSN5 in non-small cell lung cancer (NSCLC). In the current study, we found that CSN5 expression was higher in NSCLC tissues compared to the corresponding non-tumor tissues. High CSN5 expression level is closely correlated with tumor progression and poor survival in NSCLC patients. We also found that knockdown of CSN5 remarkably suppressed cell growth by inducing cell cycle arrest and apoptosis promotion in NSCLC cells. Mechanistic investigations revealed that CSN5 directly bound survivin and decreased its ubiquitination to enhance the protein stability of survivin. Additionally, our results confirmed that the tumor-promoting effects of CSN5 in NSCLC cells is at least partly through stabilization of survivin. Overall, our data suggested that CSN5 functions as an oncogenic gene in NSCLC, which could be a potential diagnostic and therapeutic target for NSCLC.

5 Article Targeting Epithelial-Mesenchymal Transition for Identification of Inhibitors for Pancreatic Cancer Cell Invasion and Tumor Spheres Formation. 2016

Polireddy, Kishore / Dong, Ruochen / McDonald, Peter R / Wang, Tao / Luke, Brendan / Chen, Ping / Broward, Melinda / Roy, Anuradha / Chen, Qi. ·Department of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, 3901 Rainbow Blvd., Kansas City, Kansas, United States of America. · High-Throughput Screening Core Facility, Structural Biology Center, University of Kansas, Lawrence, Kansas, United States of America. ·PLoS One · Pubmed #27764163.

ABSTRACT: BACKGROUND: Pancreatic cancer has an enrichment of stem-like cancer cells (CSCs) that contribute to chemoresistant tumors prone to metastasis and recurrence. Drug screening assays based on cytotoxicity cannot identify specific CSC inhibitors, because CSCs comprise only a small portion of cancer cell population, and it is difficult to propagate stable CSC populations in vitro for high-throughput screening (HTS) assays. Based on the important role of cancer cell epithelial-to-mesenchymal transition (EMT) in promoting CSCs, we hypothesized that inhibition of EMT can be a useful strategy for inhibiting CSCs, and therefore a feasible approach for HTS can be built for identification of CSC inhibitors, based on assays detecting EMT inhibition. METHODS: An immunofluorescent assay was established and optimized for HTS to identify compounds that enhance E-cadherin expression, as a hallmark of inhibition of EMT. Four chemical libraries containing 41,472 compounds were screened in PANC-1 pancreatic cancer cell line. Positive hits were validated for EMT and CSC inhibition in vitro using sphere formation assay, western blotting, immune fluorescence, and scratch assay. RESULTS: Initial hits were refined to 73 compounds with a secondary screening, among which 17 exhibited concentration dependent induction of E-cadherin expression. Six compounds were selected for further study which belonged to 2 different chemical structural clusters. A novel compound 1-(benzylsulfonyl) indoline (BSI, Compound #38) significantly inhibited pancreatic cancer cell migration and invasion. BSI inhibited histone deacetylase, increased histone 4 acetylation preferably, resulting in E-cadherin up-regulation. BSI effectively inhibited tumor spheres formation. Six more analogues of BSI were tested for anti-migration and anti-CSC activities. CONCLUSION: This study demonstrated a feasible approach for discovery of agents targeting EMT and CSCs using HTS, and identified a class of novel chemicals that could be developed as anti-EMT and anti-CSC drug leads.

6 Article MiR-377 inhibits the proliferation of pancreatic cancer by targeting Pim-3. 2016

Chang, Weihua / Liu, Menggang / Xu, Jianhua / Fu, Hangwei / Zhou, Bo / Yuan, Tao / Chen, Ping. ·Department of Hepatobiliary Surgery, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, No.10, Changjiangzhilu Road, Yu Zhong District, Chongqing, 400042, People's Republic of China. · Department of Hepatobiliary Surgery, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, No.10, Changjiangzhilu Road, Yu Zhong District, Chongqing, 400042, People's Republic of China. yuantaotmmu@163.com. · Department of Hepatobiliary Surgery, Daping Hospital and Research Institute of Surgery, The Third Military Medical University, No.10, Changjiangzhilu Road, Yu Zhong District, Chongqing, 400042, People's Republic of China. chenpingsyd@126.com. ·Tumour Biol · Pubmed #27638830.

ABSTRACT: MicroRNAs (miRNAs) play important roles in the regulation of various tumor biological processes including proliferation and apoptosis. MiR-377 has been implicated in many types of cancer, whereas its expressional feature and potential biological function in pancreatic ductal adenocarcinoma (PDAC) remains unclear. In this study, we scanned the global miRNA expression profiles in PDAC from The Cancer Genome Atlas (TCGA) and found miR-377 was down-regulated significantly in PDAC. Then, its expression was measured in both pancreatic cancer tissues and cells; the data showed that miR-377 was de-regulated and inversely correlated with pathologic parameters of tumor growth or metastasis. We generated PDAC cell lines with stable overexpression or inhibition of miR-377, and our results indicated that miR-377 up-regulation significantly promoted cell viability, proliferation, and migration in PDAC cells, and also induced cell apoptosis and cell cycle arrest simultaneously. Binding-site predictions by bioinformatics showed that Pim-3 might be a potential target of miR-377. Luciferase reporter assay ulteriorly identified that miR-377 suppressed Pim-3 expression by binding the 3'-UTR. In tumor tissues, we also showed that the Pim-3 expression was inversely correlated with that of miR-377. Furthermore, stable ectopic miR-377 expression in pancreatic cancer cell lines suppressed Pim-3 expression, leading to the attenuation of Bad phosphorylation level at its Ser

7 Article Long non-coding RNA UCA1 promotes the tumorigenesis in pancreatic cancer. 2016

Chen, Ping / Wan, Daiwei / Zheng, Dingcheng / Zheng, Qi / Wu, Feng / Zhi, Qiaoming. ·Department of General Surgery, Ningbo No. 2 Hospital, Ningbo 315000, China. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. · Department of General Surgery, Ningbo No. 2 Hospital, Ningbo 315000, China. Electronic address: gastroclinical@sina.com. · Department of General Surgery, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China. Electronic address: strexboy@163.com. ·Biomed Pharmacother · Pubmed #27562722.

ABSTRACT: The contribution of long non-coding RNAs (lncRNAs) to tumorigenesis and metastasis of pancreatic cancer (PC) remains largely unknown. Urothelial cancer-associated 1 (UCA1), which is an originally identified lncRNA in bladder cancer, has be proved to play a pivotal role in bladder cancer progression and embryonic development. In this study, we detected the mRNA expression of UCA1 in 128 PC patients by qRT-PCR, and found that UCA1 expression was significantly, up-regulated in tumor tissues than that in matched adjacent non-tumor tissues (p<0.05). Clinicopathological analysis demonstrated that UCA1 expression in PC significantly correlated with malignant potential factors such as tumor size (p=0.021), depth of invasion (p=0.033), CA19-9 level (p=0.034) and tumor stage (p=0.013). Cox proportional hazards regression analysis also confirmed that high UCA1 expression was an independent prognostic biomarker of PC (p=0.046), which led to an obviously shorter 5-year overall survival (OS) compared to those patients with low UCA1 expressions (p=0.018). Furthermore, we effectively down-regulated UCA1 mRNA expression by transfecting RNA interfere fragments into SW-1990 cells, and our results in vitro indicated that down-regulation of UCA1 could effectively inhibit the cell proliferative activities, induce apoptotic rate and cause cell cycle arrest in PC cells (p<0.05). Meanwhile, UCA1 expression negative-correlated with p27 in PC tissues (r

8 Article Direct TGF-β1 signaling between activated platelets and pancreatic cancer cells primes cisplatin insensitivity. 2013

Chen, Hongxu / Lan, Xiang / Liu, Menggang / Zhou, Bo / Wang, Baoling / Chen, Ping. ·Department of Hepatobiliary Surgery, Daping Hospital, The Third Military Medical University, 10 Changjiangzhilu Daping, Chongqing 400042, P.R., China. ·Cell Biol Int · Pubmed #23584798.

ABSTRACT: The exact mechanisms underlying chemotherapy insensitivity in pancreatic cancer remain largely unclear. The dynamic cross talk between tumors and their microenvironment is an important determinant of cancer chemosensitivity. However, whether additional signals provided during the intravascular transit of tumor cells affect the sensitivity of pancreatic cancer cells to chemotherapy is unknown. We have found that activated platelet-cancer cell interactions are sufficient to prime cisplatin (CDDP) insensitivity in pancreatic cancer cells. Activated platelet-derived TGF-β1 rather than direct platelet-tumor cell contacts stimulates PI3K/Akt and MEK/Erk signaling in pancreatic cancer cells, resulting in reduction of CDDP sensitivity in these cells. Therefore, the platelet-tumor cell interactions and the relevant signaling pathways that prime CDDP insensitivity may be potential targets for adjuvant chemotherapy for pancreatic cancer.

9 Article Genome-wide screening reveals an EMT molecular network mediated by Sonic hedgehog-Gli1 signaling in pancreatic cancer cells. 2012

Xu, Xuanfu / Zhou, Yingqun / Xie, Chuangao / Wei, Shu-mei / Gan, Huizhong / He, Shengli / Wang, Fan / Xu, Ling / Lu, Jie / Dai, Weiqi / He, Lei / Chen, Ping / Wang, Xingpeng / Guo, Chuanyong. ·Department of Gastroenterology, The Tenth People's Hospital of Shanghai, Tongji University, Shanghai, China. ·PLoS One · Pubmed #22900095.

ABSTRACT: AIMS: The role of sonic hedgehog (SHH) in epithelial mesenchymal transition (EMT) of pancreatic cancer (PC) is known, however, its mechanism is unclear. Because SHH promotes tumor development predominantly through Gli1, we sought to understand its mechanism by identifying Gli1 targets in pancreatic cancer cells. METHODS: First, we investigated invasion, migration, and EMT in PC cells transfected with lentiviral Gli1 interference vectors or SHH over-expression vectors in vitro and in vivo. Next, we determined the target gene profiles of Gli1 in PC cells using cDNA microarray assays. Finally, the primary regulatory networks downstream of SHH-Gli1 signaling in PC cells were studied through functional analyses of these targets. RESULTS: Our results indicate there is decreased E-cadherin expression upon increased expression of SHH/Gli1. Migration of PC cells increased significantly in a dose-dependent manner within 24 hours of Gli1 expression (P<0.05). The ratio of liver metastasis and intrasplenic miniature metastasis increased markedly upon activation of SHH-Gli1 signals in nude mice. Using cDNA microarray, we identified 278 upregulated and 59 downregulated genes upon Gli1 expression in AsPC-1 cells. The data indicate that SHH-Gli1 signals promote EMT by mediating a complex signaling network including TGFβ, Ras, Wnt, growth factors, PI3K/AKT, integrins, transmembrane 4 superfamily (TM4SF), and S100A4. CONCLUSION: Our results suggest that targeting the molecular connections established between SHH-Gli1 signaling and EMT could provide effective therapies for PC.

10 Article Anti-cancer effect of pharmacologic ascorbate and its interaction with supplementary parenteral glutathione in preclinical cancer models. 2011

Chen, Ping / Stone, Jennifer / Sullivan, Garrett / Drisko, Jeanne A / Chen, Qi. ·Program in Integrative Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA. ·Free Radic Biol Med · Pubmed #21672627.

ABSTRACT: Two popular complementary, alternative, and integrative medicine therapies, high-dose intravenous ascorbic acid (AA) and intravenous glutathione (GSH), are often coadministered to cancer patients with unclear efficacy and drug-drug interaction. In this study we provide the first survey evidence for clinical use of iv GSH with iv AA. To address questions of efficacy and drug-drug interaction, we tested 10 cancer cell lines with AA, GSH, and their combination. The results showed that pharmacologic AA induced cytotoxicity in all tested cancer cells, with IC(50) less than 4 mM, a concentration easily achievable in humans. GSH reduced cytotoxicity by 10-95% by attenuating AA-induced H(2)O(2) production. Treatment in mouse pancreatic cancer xenografts showed that intraperitoneal AA at 4 g/kg daily reduced tumor volume by 42%. Addition of intraperitoneal GSH inhibited the AA-induced tumor volume reduction. Although all treatments (AA, GSH, and AA+GSH) improved survival rate, AA+GSH inhibited the cytotoxic effect of AA alone and failed to provide further survival benefit. These data confirm the pro-oxidative anti-cancer mechanism of pharmacologic AA and suggest that AA and GSH administered together provide no additional benefit compared with AA alone. There is an antagonism between ascorbate and glutathione in treating cancer, and therefore iv AA and iv GSH should not be coadministered to cancer patients on the same day.

11 Article Cyclopamine reverts acquired chemoresistance and down-regulates cancer stem cell markers in pancreatic cancer cell lines. 2011

Yao, Jie / An, Yong / Wie, Ji-shu / Ji, Zhen-ling / Lu, Zi-peng / Wu, Jun-li / Jiang, Kui-rong / Chen, Ping / Xu, Ze-kuan / Miao, Yi. ·Department of General Surgery, The First Affiliated Hospital of Yangzhou University, Yangzhou, P R China. ·Swiss Med Wkly · Pubmed #21630164.

ABSTRACT: BACKGROUND: The hedgehog (Hh) pathway has been implicated in the pathogenesis of cancer including pancreatic ductal adenocarcinoma (PDAC). Recent studies have suggested that Hh plays an important role in maintaining the cancer stem cell (CSCs) pool. Gemcitabine-resistant pancreatic cancer cells highly express some of the CSCs markers. However, the expression level of Hh members in gemcitabine-resistant pancreatic cancer cells remains unknown. The aim of this study was to verify the expression of HH members, such as Shh, Ptc, SMO and Gli-1 in gemcitabine-resistant PDAC cell lines, and to explore a new strategy to overcome chemoresistance in PDAC. MATERIAL AND METHODS: Quantitative real-time RT-PCR (Q-PCR) and western blot were used to evaluate the relative expression level of HH members in SW1990, CFPAC-1 cells and gemcitabine-resistant SW1990, CFPAC-1 cells. The change of cancer stem cell markers and the expression level of HH members before and after cyclopamine treatment was evaluated using flow cytometry and Q-PCR, western blot, respectively. Cell apoptosis after cyclopamine treatment was measured by flow cytometry. RESULTS: CD44, CD133 and the expression level of HH members, including Shh, SMO, Gli-1, were found to be highly expressed in gemcitabine-resistant cells, which were significantly down-regulated by cyclopamine treatment. Flow cytometry analysis showed increased cell apoptosis after cyclopamine treatment. CONCLUSION: Gemcitabine-resistant pancreatic cancer cells highly express CSCs markers and some of the HH members, and inhibition of HH by cyclopamine is an effective method of reversing gemcitabine resistance in pancreatic cancer.

12 Article Pharmacologic ascorbate synergizes with gemcitabine in preclinical models of pancreatic cancer. 2011

Espey, Michael Graham / Chen, Ping / Chalmers, Brian / Drisko, Jeanne / Sun, Andrew Y / Levine, Mark / Chen, Qi. ·Molecular and Clinical Nutrition Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892, USA. ·Free Radic Biol Med · Pubmed #21402145.

ABSTRACT: Conventional treatment approaches have had little impact on the course of pancreatic cancer, which has the highest fatality rate among cancers. Gemcitabine, the primary therapeutic agent for pancreatic carcinoma, produces minimal survival benefit as a single agent. Therefore, numerous efforts have focused on gemcitabine combination treatments. Using a ratio design, this study established that combining pharmacologically achievable concentrations of ascorbate with gemcitabine resulted in a synergistic cytotoxic response in eight pancreatic tumor cell lines. Sensitization was evident regardless of inherent gemcitabine resistance and epithelial-mesenchymal phenotype. Our analysis suggested that the promiscuous oxidative actions of H(2)O(2) derived from pharmacologic ascorbate can culminate in synergism independent of the cancer cell's underlying phenotype and resistance to gemcitabine monotherapy. Gemcitabine-ascorbate combinations administered to mice bearing pancreatic tumor xenografts consistently enhanced inhibition of growth compared to gemcitabine alone, produced 50% growth inhibition in a tumor type not responsive to gemcitabine, and demonstrated a gemcitabine dose-sparing effect. These data support the testing of pharmacologic ascorbate in adjunctive treatments for cancers prone to high failure rates with conventional therapeutic regimens, such as pancreatic cancer.

13 Article Side population in the pancreatic cancer cell lines SW1990 and CFPAC-1 is enriched with cancer stem-like cells. 2010

Yao, Jie / Cai, Hui-Hua / Wei, Ji-Shu / An, Yong / Ji, Zhen-Ling / Lu, Zi-Peng / Wu, Jun-Li / Chen, Ping / Jiang, Kui-Rong / Dai, Cun-Cai / Qian, Zhu-Yin / Xu, Ze-Kuan / Miao, Yi. ·Laboratory of General Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, P.R. China. ·Oncol Rep · Pubmed #20372854.

ABSTRACT: In this study, we first sought to determine the existence of side population (SP) cells in pancreatic cancer cell lines. Furthermore, we compared the biological characteristics of SP and non-SP cells. The presence of side population cells in pancreatic cancer cell lines was detected by Hoechst 33342 staining and FACS analysis. Cell cycle distribution was analyzed using flow cytometry. SP and non-SP cells were exposed to various concentrations of gemcitabine; drug sensitivity was examined using the MTT assay and flow cytometry using Annexin-V and PI staining. To compare the tumorigenic ability in vivo, groups of nude mice were orthotopically inoculated with varying numbers of SP and non-SP cells. The percentages of CD44+CD24+ and CD133+ in SP and non-SP cells were also detected by FACS analysis. The SP fraction was detected in BxPc-3, CFPAC-1, MIA PaCa-2, PANC-1 and SW1990 pancreatic cancer cell lines. Cell cycle analysis revealed that the SP cells contained more cells in the G1 phase and fewer cells in the S phase when compared with the non-SP cells. The SP cells exhibited increased tumorigenetic ability following in vivo transplantation into BALB/C nude mice and increased chemoresistance following in vitro exposure to gemcitabine. FACS analysis showed that the SP cells contained more CD44+CD24+ and CD133+ cells than the non-SP cells. In conclusion, these observations suggest that SP cells in the pancreatic cancer cell lines possess the property of cancer stem cells. SP cells may therefore be novel specific targets for the effective treatment of pancreatic cancer.

14 Article Postoperative pancreatic leakage might improve the survival of patients with carcinoma of head of pancreas. 2009

Liu, Hongming / Liu, Menggang / Yuan, Tao / Tang, Chun / Chen, Ping. ·Third Military Medical University, Department of Hepatobiliary Surgery, Daping Hospital, Chongqing 400042, PR China. ·Med Hypotheses · Pubmed #19375240.

ABSTRACT: The pancreatic leakage is a lethal postoperative complication to the patients after duodenopancreatectomy for carcinoma of head of pancreas. However, we found that the patients who survived this lethal postoperative complication could potentially acquire a longer survival time comparing with those without postoperative pancreatic leakage. We surmise pancreatic enzyme can destroy tumor cell directly by its strong corrosive action. On the other hand, pancreatic leakage can lead to severe bacterial infection which cause serial inflammatory reaction and immunological reaction. We hypothesize that celiac infection after pancreatic leakage might prevent cancer cellstransfuse to liver along duodenohepatic ligament. Our hypothesis might provide a novel therapeutic strategy for patients who underwent radical duodenopancreatectomy. For instance, the exogenous infection or controlling pancreatic leakage may be reasonable and deserve further study. With the aid of animal model of carcinoma of head of pancreas, this hypothesis could be partially or fully confirmed.

15 Retraction Association between single-nucleotide polymorphisms of OGG1 gene and pancreatic cancer risk in Chinese Han population. 2014

Chen, Hongxu / Zhou, Bo / Lan, Xiang / Wei, Dong / Yuan, Tao / Chen, Ping. ·Department of Hepatobiliary Surgery, Daping Hospital, The Third Military Medical University, No. 10 Changjiangzhilu Daping, Chongqing, 400042, People's Republic of China. ·Tumour Biol · Pubmed #23999824.

ABSTRACT: The purpose of this study was to test the association between single-nucleotide polymorphisms (SNPs) of 8-oxoguanine DNA glycosylase (OGG1) gene and susceptibility to pancreatic cancer (PC). A total of 347 PC patients and 364 healthy subjects were enrolled in this case-control study. The c.269C>A genetic variant was investigated using the created restriction site-polymerase chain reaction method. The c.627T>C genetic variant was identified by the polymerase chain reaction-restriction fragment length polymorphism method. Our data indicated that the alleles and genotypes frequencies of these two SNPs were statistically different in PC cases and controls. As for c.269C>A, the AA genotype was statistically associated with decreased PC susceptibility compared to CC wild genotype (odds ratio (OR) = 0.44, 95% confidence interval (CI) 0.27-0.73, P = 0.001). As for c.627T>C, statistically significant decreased PC susceptibility was detected in CC genotype compared to TT wild genotype (OR = 0.57, 95% CI 0.35-0.94, P = 0.028). The allele A of c.269C>A and allele C of c.627T>C might be associated with a protection from PC (for c.269C>A, A versus (vs.) C, OR = 0.69, 95% CI 0.55-0.86, P < 0.001; for c.627T>C, C vs. T, OR = 0.72, 95% CI 0.58-0.91, P = 0.005). Results from this study indicate that the c.269C>A and c.627T>C SNPs of OGG1 gene are associated with PC susceptibility in Chinese Han ethnicity.

16 Retraction Association of XRCC1 gene single nucleotide polymorphisms and susceptibility to pancreatic cancer in Chinese. 2014

Chen, Hongxu / Tang, Chun / Liu, Menggang / Zhou, Bo / Kuang, Yi / Yuan, Tao / Chen, Ping. ·Department of Hepatobiliary Surgery, Daping Hospital, The Third Military Medical University, No. 10 Changjiangzhilu Daping, Chongqing, 400042, People's Republic of China. ·Tumour Biol · Pubmed #23893380.

ABSTRACT: The human X-ray repair cross-complementing group 1 gene (XRCC1) is an important candidate gene for affecting pancreatic cancer (PC) risk. The objective of this study was to detect whether the c.1471G > A and c.1686C > G polymorphisms of XRCC1 gene influence PC risk. The association of XRCC1 genetic variants with PC risk was analyzed in 328 PC patients and 350 controls by the polymerase chain reaction-restriction fragment length polymorphism and created restriction site-polymerase chain reaction method. Our data suggested that the genotypes and alleles from these two genetic variants were statistically associated with PC risk. For c.1471G > A, the AA genotype was associated with the decreased risk of developing PC compared to GG wild genotype (odds ratio (OR) = 0.43, 95% confidence intervals (CI) 0.26-0.70, chi-squared (χ(2)) = 11.91, P = 0.001). For c.1686C > G, the risk of PC was significantly lower for GG genotype in comparing to CC wild genotype (OR = 0.48, 95% CI 0.29-0.81, χ(2) = 7.98, P = 0.005). The A allele of c.1471G > A and G allele of c.1686C > G genetic variants could contribute to decrease the risk of PC (for c.1471G > A: A vs G, OR = 0.65, 95% CI 0.52-0.82, χ(2) = 13.71, P < 0.001, for c.1686C > G: G vs C, OR = 0.70, 95% CI 0.55-0.88, χ(2) = 9.42, P = 0.002). Our findings indicate that the c.1471G > A and c.1686C > G polymorphisms of XRCC1 gene are associated with PC risk in Chinese population.