Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Lei Zhao
Based on 12 articles published since 2010
(Why 12 articles?)
||||

Between 2010 and 2020, Le Zhao wrote the following 12 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article IL-29 Exhibits Anti-Tumor Effect on Pan-48 Pancreatic Cancer Cells by Up-regulation of P21 and Bax. 2019

Balabanov, Dean / Zhao, Lei / Zhu, Ziwen / Hunzeker, Zachary E / Tonner, Hannah M / Ding, Vivi A / Wakefield, Mark R / Bai, Qian / Fang, Yujiang. ·Department of Microbiology & Immunology, Des Moines University, Des Moines, IA, U.S.A. · Department of Respiratory Medicine, the 2nd People's Hospital of Hefei and Hefei Hospital Affiliated to Anhui Medical University, Hefei, P.R. China. · Department of Surgery, University of Missouri School of Medicine, Columbia, MO, U.S.A. · Department of Microbiology & Immunology, Des Moines University, Des Moines, IA, U.S.A. yujiang.fang@dmu.edu. ·Anticancer Res · Pubmed #31262873.

ABSTRACT: BACKGROUND/AIM: Pancreatic cancer is the most lethal cancer of the digestive system. IL-29 is a new member of the IFNλ family and well-known for its strong antiviral activity. However, its direct effect on pancreatic cancer is still unclear. This study was performed to investigate if IL-29 has any direct effect on Pan-48 pancreatic cancer cells. MATERIALS AND METHODS: Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the effects of IL-29 on cell survival, proliferation, and apoptosis of Pan-48 pancreatic cancer cells. RT-PCR and IHC were subsequently performed to explore IL-29's potential molecular mechanisms. RESULTS: The percentage of colonies of Pan-48 cells was decreased following the addition of IL-29. This was consistent with a decreased optical density (OD) value of cancer cells. Furthermore, the relative caspase-3 activity in cancer cells was increased after the addition of IL-29, indicating increased apoptosis of cancer cells. The anti-proliferative effect of IL-29 on cancer cells correlated with increased expression of the anti-proliferative molecule p21. The pro-apoptotic effect of IL-29 on cancer cells correlated with an increased expression of the pro-apoptotic molecule Bax. CONCLUSION: IL-29 constrains Pan-48 pancreatic cell growth via up-regulation of p21 and Bax. Our study suggests a potential use of IL-29 in immunotherapy for pancreatic cancer treatment.

2 Article Correlation Between Dual-Energy Computed Tomography Single Scan and Computed Tomography Perfusion for Pancreatic Cancer Patients: Initial Experience. 2019

Bao, Jiaqi / Liu, Aishi / Zhao, Changhong / Hao, Fenʼe / Su, Xiulan / Bao, Lili / Zhao, Lei. ·Departments of Radiology, and. · Clinical Research Center, The Affiliated Hospital of Inner Mongolia Medical University. · Department of Preclinical Medicine, Inner Mongolia Medical University, Inner Mongolia, China. ·J Comput Assist Tomogr · Pubmed #31162238.

ABSTRACT: OBJECTIVE: The objective of this study was to evaluate the role and limit of iodine maps by dual-energy computed tomography (CT) single scan for pancreatic cancer. METHODS: Thirty patients with suspected solitary pancreatic cancer were enrolled in this study and underwent CT perfusion and iodine maps. The parameters of pancreatic cancer and normal pancreatic tissue were calculated. Pearson correlation and paired t test were used for evaluating 2 techniques. RESULTS: Iodine concentration had a moderate positive correlation with blood flow or blood volume (P < 0.05 for both). All values of iodine concentration and blood flow, iodine concentration, and blood volume had significant positive correlations (P < 0.001 for both). The mean effective dose for CT perfusion and iodine maps had significant difference (8.61 ± 0.00 mSv vs 1.13 ± 0.14 mSv, P < 0.001). CONCLUSIONS: Iodine maps had the potential to replace routine CT perfusion for pancreatic cancer with low radiation dose.

3 Article Rosmarinic inhibits cell proliferation, invasion and migration via up-regulating miR-506 and suppressing MMP2/16 expression in pancreatic cancer. 2019

Han, Yongguang / Ma, Ligang / Zhao, Le / Feng, Weisheng / Zheng, Xiaoke. ·College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China. Electronic address: hyg1207@hactcm.edu.cn. · College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China. Electronic address: maligang@qq.com. · College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China. Electronic address: zhaole1983@126.com. · College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China. Electronic address: fwsh@hactcm.edu.cn. · College of Pharmacy, Henan University of Chinese Medicine, Zhengzhou, 450046, China. Electronic address: zhengxk.2006@163.com. ·Biomed Pharmacother · Pubmed #31060006.

ABSTRACT: Pancreatic cancer is the fourth leading cause of cancer-related deaths worldwide. However, therapeutic strategies for the treatment of pancreatic cancer are still limited. Therefore, it is urgent for us to develop novel effective therapies for pancreatic cancer. In this study, we explored the effects of rosmarinic acid on pancreatic progression and explored the underlying molecular mechanisms. Rosmarinic acid significantly suppressed cell viability, cell growth, cell invasion and migration as well as epithelial mesenchymal transition (EMT) of pancreatic cancer cells, and induced cell apoptosis in pancreatic cells. In addition, rosmarinic acid significantly up-regulated the expression of miR-506 in pancreatic cancer cells, and knockdown of miR-506 attenuated the suppressive effects of rosmarinic acid on cell growth, cell invasion and migration and EMT, and prevented the enhanced effects of rosmarinic acid on cell apoptosis in pancreatic cancer cells. Mechanistically, the luciferase reporter assay showed that miR-506 targeted the 3' untranslated region of matrix metalloproteinase (MMP)-2/16, and miR-506 overexpression and rosmarinic acid treatment suppressed the expression of MMP2/16 in pancreatic cancer cells. Overexpression of MMP2/16 attenuated the inhibitory effects of rosmarinic acid on pancreatic cell invasion and migration. In vivo studies showed that rosmarinic acid dose-dependently suppressed tumor growth of pancreatic cancer cells, and increased the expression of miR-506, while suppressed the expression of MMP2/16 and Ki-67 in dissected tumor tissues from xenograft nude mice. Collectively, our results for the first time revealed the anti-tumor effects of rosmarinic acid in pancreatic cancer, and the anti-tumor effects of rosmarinic acid were via regulating the miR-506/MMP2/16 axis in pancreatic cancer.

4 Article IL-39 acts as a friend to pancreatic cancer. 2018

Manning, Alicia A / Zhao, Lei / Zhu, Ziwen / Xiao, Huaping / Redington, Chase G / Ding, Vivi A / Stewart-Hester, Theodore / Bai, Qian / Dunlap, Jacob / Wakefield, Mark R / Fang, Yujiang. ·Department of Microbiology & Immunology, Des Moines University College of Osteopathic Medicine, Des Moines, IA, 50312, USA. · Department of Respiratory Medicine, The 2nd People's Hospital of Hefei and Hefei Hospital Affiliated to Anhui Medical University, Hefei, China. · Department of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA. · Department of Microbiology & Immunology, Des Moines University College of Osteopathic Medicine, Des Moines, IA, 50312, USA. yujiang.fang@dmu.edu. · Department of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA. yujiang.fang@dmu.edu. · Department of Microbiology, Immunology & Pathology, Des Moines University College of Osteopathic Medicine, Des Moines, IA, 50312, USA. yujiang.fang@dmu.edu. ·Med Oncol · Pubmed #30506430.

ABSTRACT: Pancreatic cancer is the most lethal digestive cancer and the fourth leading cause of cancer death in the US. IL-39, a heterodimer of p19 and EBI3, is a newly found cytokine and its role in the pathogenesis of neoplasia has not been studied yet. This study was designed to investigate the direct role of IL-39 in the growth of pancreatic cancer. Clonogenic survival assay, cell proliferation, and caspase-3 activity kits were used to evaluate the direct effects of IL-39 on cell survival, proliferation and apoptosis of the widely studied pancreatic cancer cell line MiaPaCa-2. We further investigated the possible molecular mechanisms by using RT-PCR and IHC. The percentage of colonies of pancreatic cancer cells increased significantly in the presence of IL-39. This was paralleled with the increase in the OD value of cancer cells in the presence of IL-39. Interestingly, the relative caspase-3 activity in cancer cells decreased significantly in the presence of IL-39. Furthermore, the pro-tumor effect of IL-39 on pancreatic cancer cells correlated with decreased anti-proliferative molecule p21.The anti-apoptotic effect of IL-39 correlated with decreased pro-apoptotic molecule TRAILR1. These results suggest that IL-39 favors growth of pancreatic cancer by promoting growth and inhibiting apoptosis of cancer cells. This suggests that IL-39 acts as a friend to pancreatic cancer. Thus, inhibition of effect of IL-39 on cells might be a promising strategy to treat pancreatic cancer.

5 Article A blockade of PD-L1 produced antitumor and antimetastatic effects in an orthotopic mouse pancreatic cancer model via the PI3K/Akt/mTOR signaling pathway. 2017

Zhao, Lei / Li, Cheng / Liu, Fei / Zhao, Yonghong / Liu, Jun / Hua, Ye / Liu, Jinyang / Huang, Jiapeng / Ge, Chunlin. ·Department of Pancreatic and Biliary Surgery, The First Hospital of China Medical University. · Department of Immunology, College of Basic Medical Sciences, China Medical University, Shenyang, Liaoning, People's Republic of China. ·Onco Targets Ther · Pubmed #28442920.

ABSTRACT: BACKGROUND: Pancreatic cancer is one of the most aggressive and intractable malignant tumors, and most deaths from pancreatic cancer are related to metastases. It has been demonstrated in vitro that overexpression of programmed death-ligand 1 (PD-L1) correlates with a lack of phosphatase and tensin homologue (PTEN) expression in pancreatic cancer tissue. This loss of PTEN expression may aberrantly activate the phosphatidylinositol 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) pathway, and thereby promote tumor cell survival, proliferation, and disease progression. In this study, we investigated the potential therapeutic effect of blockading PD-L1 expression on the progression of pancreatic cancer and its spontaneous liver metastases in vivo by inhibiting the PI3K/Akt/mTOR signaling pathway. METHODS: We investigated the effect of blockading PD-L1 in an orthotopic pancreatic cancer mouse model. The pancreatic tumor weights and inhibition ratios were determined after treatment with antimouse PD-L1 antibody for 5 weeks. We used immunohistochemistry methods to investigate PD-L1 expression in pancreatic cancer tissue and spontaneous liver metastasis tissue. The levels of mRNA and protein expression for various components involved in the PI3K/Akt/mTOR signaling pathway as well as for matrix metalloproteinases-2 and -9 (MMP2 and MMP9) were measured by reverse transcription polymerase chain reaction (RT-PCR) and Western blot methods, respectively. RESULTS: Blockading PD-L1 significantly inhibited tumor growth and decreased the levels of PD-L1 expression in tumor tissue. Furthermore, the levels of PTEN mRNA and protein expression were elevated, while the levels of phospho-Akt (p-Akt) and phospho-mTOR (p-mTOR) protein were decreased in pancreatic cancer and liver metastasis tissues after establishing a PD-L1 blockade. In addition, a PD-L1 blockade decreased the levels of MMP2 and MMP9 mRNA and protein expression in tumor tissues. CONCLUSION: Our results suggest that a blockade of PD-L1 may inhibit the growth and metastasis of pancreatic cancer by modulating the PI3K/Akt/mTOR pathway.

6 Article IL-33 acts as a foe to MIA PaCa-2 pancreatic cancer. 2017

Fang, Yujiang / Zhao, Lei / Xiao, Huaping / Cook, Kathryn M / Bai, Qian / Herrick, Elizabeth J / Chen, Xuhui / Qin, Chenglu / Zhu, Ziwen / Wakefield, Mark R / Nicholl, Michael B. ·Department of Microbiology, Immunology and Pathology, College of Osteopathic Medicine, Des Moines University, Des Moines, IA, 50312, USA. yujiang.fang@dmu.edu. · Department of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA. yujiang.fang@dmu.edu. · Department of Infectious Disease, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China. · Department of Microbiology, Immunology and Pathology, College of Osteopathic Medicine, Des Moines University, Des Moines, IA, 50312, USA. · The Affiliated Hospital of Xiangnan University, Chenzhou, Hunan, China. · Department of Surgery, University of Missouri School of Medicine, Columbia, MO, 65212, USA. · Luohu Hospital, Shenzhen, China. · Department of Surgery, South Texas Veterans Health Care System, 7400 Merton Minter Blvd, San Antonio, TX, 78229, USA. ·Med Oncol · Pubmed #28058630.

ABSTRACT: IL-33 is a member of the IL-1 family of cytokines, and no study has been performed to address its direct anti-tumor effect. This study is designed to investigate whether IL-33 has any direct effect on pancreatic cancer. Clonogenic survival assay, immunohistochemistry, TUNEL staining, proliferation, caspase-3 activity kits and RT-PCR were used to evaluate the effects of IL-33 on cell survival, proliferation and apoptosis of a pancreatic cancer cell line, MIA PaCa-2. We found that the percentage of colonies of MIA PaCa-2 cells, PCNA+ cells and the OD value of cancer cells were all decreased in the presence of IL-33. TUNEL+ cells and the relative caspase-3 activity in cancer cells were increased in the presence of IL-33. We further found that its anti-proliferative effect on cancer cells correlated with downregulation of pro-proliferative molecules cdk2 and cdk4 and upregulation of anti-proliferative molecules p15, p21 and p53. Its pro-apoptotic effect correlated with downregulation of anti-apoptotic molecule FLIP and upregulation of pro-apoptotic molecule TRAIL. These results suggest that IL-33 presents significant anti-tumor effects by inhibition of proliferation and induction of apoptosis of MIA PaCa-2 pancreatic cancer cells. Thus, strength of IL-33/ST2 signal pathway might be a promising way to treat pancreatic cancer.

7 Article Expression profile of long non-coding RNAs in pancreatic cancer and their clinical significance as biomarkers. 2015

Wang, Yingxue / Li, Zhihua / Zheng, Shangyou / Zhou, Yu / Zhao, Lei / Ye, Huilin / Zhao, Xiaohui / Gao, Wenchao / Fu, Zhiqiang / Zhou, Quanbo / Liu, Yimin / Chen, Rufu. ·Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Department of Hepatopancreatobiliary Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China 510120. · Department of Medical Oncology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China 510120. · Department of Radiation Oncology, Sun Yat-Sen University Cancer Center, Guangzhou, China 510060. · Department of Radiation Oncology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China 510120. ·Oncotarget · Pubmed #26447755.

ABSTRACT: Long non-coding RNAs (lncRNAs) have shown great potential as powerful and non-invasive tumor markers. However, little is known about their value as biomarkers in pancreatic cancer (PC). We applied an Arraystar Human LncRNA Microarray which targeting 7419 lncRNAs to determine the lncRNA expression profile in PC and to screen the potential biomarkers. The most increased lncRNAs in PC tissues were HOTTIP-005, XLOC_006390, and RP11-567G11.1. Increased HOTTIP-005 and RP11-567G11.1 expression were poor prognostic factors for patients with PC (n = 144, p < 0.0001). The expression patterns of HOTTIP splice variants in PC were also detected. HOTTIP-005 and HOTTIP-001 were the first and second most increased HOTTIP splice variants, respectively. Plasma HDRF and RDRF (HOTTIP-005 and RP11-567G11.1 derived RNA fragments in plasma/serum) were present in stable form. Their levels were significantly increased in the patients with PC as compared to the healthy controls (n = 127 and 122 respectively, p < 0.0001) and the high levels were derived from PC. HDRF and RDRF levels are promising indicators for distinguishing patients with PC from those without PC. This study identified HOTTIP-005 and RP11-567G11.1 and their plasma fragments with the potential to be used as prognostic and diagnostic biomarkers of PC. Further large-scale prospective studies are needed to confirm our findings.

8 Article Association between E-cadherin (CDH1) polymorphisms and pancreatic cancer risk in Han Chinese population. 2015

Zhao, Lei / Wang, Ying-Xue / Xi, Mian / Liu, Shi-Liang / Zhang, Peng / Luo, Li-Ling / Liu, Meng-Zhong. ·Department of Radiation Oncology, Sun Yat-Sen University Cancer Center Guangzhou, China ; State Key Laboratory of Oncology in South China, Sun Yat-Sen University Cancer Center Guangzhou, China. · Department of Hepatobiliary Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University Guangzhou, China. ·Int J Clin Exp Pathol · Pubmed #26191293.

ABSTRACT: This study was designed to investigate the associations between E-cadherin (CDH1) gene polymorphisms and pancreatic cancer (PC) risk predisposition. We undertook a case-control study to analyze three E-cadherin polymorphisms (+54T>C, -160C>A and -347G→GA) in an Han Chinese population, by extraction of genomic DNA from the peripheral blood of 368 patients with PC and 376 control participants and performed E-cadherin genotyping using DNA sequencing. Overall, no statistically significant association was observed in +54T>C. Nevertheless, -347G→GA genotype was at increased risk of PC (P=0.022; odds ratio (OR)=1.128, CI 95%: 1.017-1.251). Furthermore, -347GA/GA genotype pancreatic cancers were more significantly common in cases of advanced T stage, lymph node metastasis and clinical pathological stage than G or G/GA genotypes PC. However, -160C>A genotype demonstrated a protective effect in PCs (P=0.017; OR=0.883, CI 95%: 0.798-0.977). In conclusion, polymorphism in -347G→GA was observed to be associated with susceptibility of PC. However, -160C>A polymorphism indicated to play a protective role in susceptibility to PC. Nevertheless, further investigation with a larger sample size is needed to support our results.

9 Article Combination doxorubicin and interferon-α therapy stimulates immunogenicity of murine pancreatic cancer Panc02 cells via up-regulation of NKG2D ligands and MHC class I. 2014

Wang, Wen-Jia / Qin, Si-Hao / Zhang, Ji-Wei / Jiang, Yue-Yao / Zhang, Jin-Nan / Zhao, Lei. ·Institute of Pharmacy, Jilin University, Changchun, Jilin, China E-mail : zjghospital@sina.com. ·Asian Pac J Cancer Prev · Pubmed #25520086.

ABSTRACT: BACKGROUND: Pancreatic adenocarcinoma is a malignant gastrointestinal cancer with significant morbidity and mortality. Despite severe side effects of chemotherapy, the use of immunotherapy combined with chemotherapy has emerged as a common clinical treatment. In this study, we investigated the efficacy of the combined doxorubicin and interferon-α (IFN-α) therapy on murine pancreatic cancer Panc02 cells in vitro and in vivo and underlying mechanisms. MATERIALS AND METHODS: A Panc02-bearing mouse model was established to determine whether doxorubicin and interferon-α (IFN-α) could effectively inhibit tumor growth in vivo. Cytotoxicity of natural killer (NK) cells and cytotoxic T lymphocytes (CTLs) was evaluated using a standard LDH release assay. To evaluate the relevance of NK cells and CD8 T cells to the combination therapy-mediated anti-tumor effects, they were depleted in tumor-bearing mice by injecting anti-asialo-GM-1 antibodies or anti-CD8 antibodies, respectively. Finally, the influence of doxorubicin+interferon-α (IFN-α) on the ligands of NK and T cells was assessed by flow cytometry. RESULTS: The combination therapy group demonstrated a significant inhibition of growth of Panc02 in vivo, resulting from activated cytotoxicity of NK cells and CTLs. Depleting CD8 T cells or NK cells reduced the anticancer effects mediated by immunochemotherapy. Furthermore, the doxorubicin+IFN-a treatment increased the expression of major histocompatibility complex class I (MHC I) and NKG2D ligands on Panc02 cells, suggesting that the combined therapy may be a potential strategy for enhancing immunogenicity of tumors. All these data indicate that the combination therapy using doxorubicin and interferon-α (IFN-α) may be a potential strategy for treating pancreatic adenocarcinoma.

10 Article Pancreatic ductal adenocarcinoma with autoimmune pancreatitis-like histologic and immunohistochemical features. 2014

Zhang, Xuefeng / Liu, Xiuli / Joseph, Loren / Zhao, Lei / Hart, John / Xiao, Shu-Yuan. ·Department of Pathology, University of Chicago Medical Center, 5841S Maryland Ave, Chicago, IL 60605, USA. · Department of Pathology, Cleveland Clinics, Cleveland, OH 55195, USA. · Department of Pathology, University of Chicago Medical Center, 5841S Maryland Ave, Chicago, IL 60605, USA. Electronic address: sxiao@bsd.uchicago.edu. ·Hum Pathol · Pubmed #24457081.

ABSTRACT: Autoimmune pancreatitis (AIP) often manifests as a mass lesion causing obstructive jaundice, clinically mimicking pancreatic carcinoma. A diagnosis of AIP may obviate the need for surgical resection, as most patients respond to steroid treatment. However, it is not clear whether these 2 conditions can coexist. In this study, 105 specimens resected for pancreatic ductal adenocarcinoma (PDAC) that also have changes of chronic pancreatitis were examined for features considered to be characteristic of AIP. Of 105 cases of PDAC with changes of chronic pancreatitis, 10 (9.5%) exhibited histologic features of AIP, including exuberant fibrosis, lymphoplasmacytic infiltration, obliterative phlebitis, or granulocytic epithelial lesions. Of these 10 cases, 7 had more than 20 immunoglobulin G4+ plasma cells per high-power field. Of these 7 cases, 5 were analyzed for Kirsten rat sarcoma viral oncogene mutation and SMAD4 expression. Three cases showed K-ras mutation and/or loss of SMAD4 expression in benign AIP-like areas. These findings suggest 2 possibilities: first, AIP-like lesions may occur in a small but significant portion of PDAC cases; second, some PDACs may arise in a background of AIP. Therefore, caution is necessary when making a diagnosis of AIP by needle biopsy of a mass lesion, and patients with a tentative AIP diagnosis should be closely followed up clinically.

11 Article Radical distal gastrectomy in laparoscopic and open surgery: is it necessary for pancreatic capsule resection? 2012

Zhao, Lei / Wang, Zhifei / Xu, Jun / Ding, Mingfeng. ·General Surgery Department, Harbin Medical University, Harbin City, China. ·Hepatogastroenterology · Pubmed #22353530.

ABSTRACT: BACKGROUND/AIMS: To explore the involvement of the pancreatic capsule during radical gastrectomy in gastric cancer. METHODOLOGY: Pancreatic capsule samples were collected from the 83 cases (56 men and 27 women) during open radical gastrectomy and laparoscopic resection between January 2007 and July 2008. RT-PCR and immunohistochemistry were applied for tumor detection. There was a 2-year follow-up; the relationship of the pancreatic capsule involvement, tumor stage and survival rate were evaluated. Results from radical distal gastrectomy were combined with those of gastric cancer pancreatic capsule cleaning; clinical data, pathology, immunohistochemistry and RT-PCR were used to confirm the necessity of pancreatic capsule resection in laparoscopic radical gastrectomy. RESULTS: H&E staining of the pancreatic capsule showed no tumor existence in any of the 83 patients but immunohistochemistry showed CK20 positive cells in 20 patients (33.7%), while RT-PCR detected CK20 mRNA positive cells in 42 patients (50.6%). Cases with stage T1 and T2 were negative for CK20 in both RT-PCR and immunohistochemistry and the few cases with T3 and T4 were also negative in both RT-PCR and immunohistochemistry. The metastasis in the pancreatic capsule correlated mainly with the invasive serous membrane, lymph node metastasis and tumor stage (p<0.05) but not with gender and age (p>0.05). CONCLUSIONS: For T1 and T2 stage, there was no evidence of pancreatic capsule metastasis, which may facilitate the decision making of the pancreatic capsule resection during radical distal gastrectomy.

12 Minor Cytological features of pancreatic intraductal tubulopapillary neoplasm and an unexpected immunohistochemical profile. 2014

Zhao, Lei / Hart, John / Xiao, Shu-Yuan / Antic, Tatjana. ·Department of Pathology, The University of Chicago, Chicago, IL, USA. ·Pathology · Pubmed #25393265.

ABSTRACT: -- No abstract --