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Pancreatic Neoplasms: HELP
Articles by Wei Jiang
Based on 15 articles published since 2009
(Why 15 articles?)
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Between 2009 and 2019, Wei Jiang wrote the following 15 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial Cytoplasmic HuR Status Predicts Disease-free Survival in Resected Pancreatic Cancer: A Post-hoc Analysis From the International Phase III ESPAC-3 Clinical Trial. 2018

Tatarian, Talar / Jiang, Wei / Leiby, Benjamin E / Grigoli, Amanda / Jimbo, Masaya / Dabbish, Nooreen / Neoptolemos, John P / Greenhalf, William / Costello, Eithne / Ghaneh, Paula / Halloran, Christopher / Palmer, Daniel / Buchler, Markus / Yeo, Charles J / Winter, Jordan M / Brody, Jonathan R. ·Jefferson Pancreas, Biliary, and Related Cancer Center, Department of Surgery, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA. · Department of Pathology, Anatomy, and Cell Biology, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA. · Division of Biostatistics, Department of Pharmacology and Experimental Therapeutics, Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, PA. · Institute of Translational Medicine, Cancer Research UK Liverpool Cancer Trials Unit, Liverpool, UK. · Department of Surgery, University of Heidelberg, Heidelberg, Germany. ·Ann Surg · Pubmed #27893535.

ABSTRACT: OBJECTIVES: We tested cytoplasmic HuR (cHuR) as a predictive marker for response to chemotherapy by examining tumor samples from the international European Study Group of Pancreatic Cancer-3 trial, in which patients with resected pancreatic ductal adenocarcinoma (PDA) received either gemcitabine (GEM) or 5-fluorouracil (5-FU) adjuvant monotherapy. BACKGROUND: Previous studies have implicated the mRNA-binding protein, HuR (ELAVL1), as a predictive marker for PDA treatment response in the adjuvant setting. These studies were, however, based on small cohorts of patients outside of a clinical trial, or a clinical trial in which patients received multimodality therapy with concomitant radiation. METHODS: Tissue samples from 379 patients with PDA enrolled in the European Study Group of Pancreatic Cancer-3 trial were immunolabeled with an anti-HuR antibody and scored for cHuR expression. Patients were dichotomized into groups of high versus low cHuR expression. RESULTS: There was no association between cHuR expression and prognosis in the overall cohort [disease-free survival (DFS), P = 0.44; overall survival, P = 0.41). Median DFS for patients with high cHuR was significantly greater for patients treated with 5-FU compared to GEM [20.1 months, confidence interval (CI): 8.3-36.4 vs 10.9 months, CI: 7.5-14.2; P = 0.04]. Median DFS was similar between the treatment arms in patients with low cHuR (5-FU, 12.8 months, CI: 10.6-14.6 vs GEM, 12.9 months, CI: 11.2-15.4). CONCLUSIONS: Patients with high cHuR-expressing tumors may benefit from 5-FU-based adjuvant therapy as compared to GEM, whereas those patients with low cHuR appear to have no survival advantage with GEM compared with 5-FU. Further studies are needed to validate HuR as a biomarker in both future monotherapy and multiagent regimens.

2 Article Stage III should be subclassified into Stage IIIA and IIIB in the American Joint Committee on Cancer (8 2018

Yu, Hai-Feng / Zhao, Bing-Qing / Li, Yong-Cheng / Fu, Jun / Jiang, Wei / Xu, Rong-Wei / Yang, Hao-Chang / Zhang, Xiao-Jun. ·Department of General Surgery, Tianjin First Central Hospital, Tianjin 300192, China. · Department of Surgery, Tianjin Second People's Hospital, Tianjin 300192, China. · Department of Medical Oncology, XuZhou Central Hospital, The Affiliated XuZhou Hospital of Medical College of Southeast University, Xuzhou 221009, Jiangsu Province, China. · Department of Hepatic-Biliary-Pancreatic-Splenic Surgery, XuZhou Central Hospital, The Affiliated XuZhou Hospital of Medical College of Southeast University, Xuzhou 221009, China. · Department of Vascular Surgery, Shandong Provincial Qianfoshan Hospital, Shandong University, Jinan 250014, China. · College of Clinical Medicine, Binzhou Medical University, Yantai 264003, China. · Department of Hepatic-Biliary-Pancreatic-Splenic Surgery, XuZhou Central Hospital, The Affiliated XuZhou Hospital of Medical College of Southeast University, Xuzhou 221009, China. exiaojun@163.com. ·World J Gastroenterol · Pubmed #29904247.

ABSTRACT: AIM: To ascertain the prognostic role of the T4 and N2 category in stage III pancreatic cancer according to the 8 METHODS: Patients were collected from the Surveillance Epidemiology and End Results (SEER) database (2004-2013) and were divided into three groups: T(1-3)N2, T4N(0-1), and T4N2. Overall survival (OS) and disease-specific survival (DSS) of patients were evaluated by the Kaplan-Meier method. RESULTS: For the first time, we found a significant difference in OS and DSS between T(1-3)N2/T4N(0-1) and T4N2 but not between T(1-3)N2 and T4N(0-1). A higher grading correlated with a worse prognosis in the T(1-3)N2 and T4N2 groups. CONCLUSION: Patients with stage T4N2 had a worse prognosis than those with stage T(1-3)N2/T4N(0-1) in the 8

3 Article Elevated HuR in Pancreas Promotes a Pancreatitis-Like Inflammatory Microenvironment That Facilitates Tumor Development. 2018

Peng, Weidan / Furuuchi, Narumi / Aslanukova, Ludmila / Huang, Yu-Hung / Brown, Samantha Z / Jiang, Wei / Addya, Sankar / Vishwakarma, Vikalp / Peters, Erika / Brody, Jonathan R / Dixon, Dan A / Sawicki, Janet A. ·Lankenau Institute for Medical Research, Wynnewood, Pennsylvania, USA. · Sidney Kimmel Cancer Center at the Jefferson Pancreatic, Biliary, and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania, USA. · University of Kansas Medical Center, Kansas City, Kansas, USA. · Lankenau Institute for Medical Research, Wynnewood, Pennsylvania, USA sawickij@mlhs.org. ·Mol Cell Biol · Pubmed #29133460.

ABSTRACT: Human antigen R (ELAVL1; HuR) is perhaps the best-characterized RNA-binding protein. Through its overexpression in various tumor types, HuR promotes posttranscriptional regulation of target genes in multiple core signaling pathways associated with tumor progression. The role of HuR overexpression in pancreatic tumorigenesis is unknown and led us to explore the consequences of HuR overexpression using a novel transgenic mouse model that has a >2-fold elevation of pancreatic HuR expression. Histologically, HuR-overexpressing pancreas displays a fibroinflammatory response and other pathological features characteristic of chronic pancreatitis. This pathology is reflected in changes in the pancreatic gene expression profile due, in part, to genes whose expression changes as a consequence of direct binding of their respective mRNAs to HuR. Older mice develop pancreatic steatosis and severe glucose intolerance. Elevated HuR cooperated with mutant K-ras

4 Article Identification of a novel metabolic-related mutation (IDH1) in metastatic pancreatic cancer. 2018

Brody, Jonathan R / Yabar, Cinthya S / Zarei, Mahsa / Bender, Joseph / Matrisian, Lynn M / Rahib, Lola / Heartwell, Craig / Mason, Kimberly / Yeo, Charles J / Peiper, Stephen C / Jiang, Wei / Varieur, Katelyn / Madhavan, Subha / Petricoin, Emanuel / Fortuna, Danielle / Curtis, Mark / Wang, Zi-Xuan / Pishvaian, Michael J / Winter, Jordan M. ·a Department of Surgery , Jefferson Pancreas, Biliary and Related Cancer Center, Sidney Kimmel Medical College, Thomas Jefferson University , Philadelphia , PA , USA. · b Perthera, Inc. , McLean , VA , USA. · c The Pancreatic Cancer Action Network , Manhattan Beach , CA , USA. · d Department of Pathology , Thomas Jefferson University , Philadelphia , PA , USA. · e Lombardi Comprehensive Cancer Center, Georgetown University Medical Center , Washington , DC , USA. ·Cancer Biol Ther · Pubmed #27466707.

ABSTRACT: Isocitrate dehydrogenase 1 (IDH1) is a metabolic enzyme implicated in cancer cell metabolic reprogramming. This is underscored by the detection of functional, somatic IDH1 mutations frequently found in secondary glioblastoma. To our knowledge, there has never been a reported, validated case of an IDH1 mutation in a pancreatic ductal adenocarcinoma (PDA). Herein, we present a case of a patient with metastatic PDA that harbored a potentially actionable, albeit rare, IDH1 mutation. As part of the Know Your Tumor project (Pancreatic Cancer Action Network), a 48-year-old female was diagnosed with metastatic PDA and subsequently started on standard of care chemotherapy, during which her hepatic lesions progressed. Detailed molecular profiling was performed on a biopsy from a liver lesion that demonstrated an IDH1 mutation, R132H. This mutation was confirmed by an independent sequencing reaction from the tumor sample, and by immunohistochemistry using an antibody specific for the IDH1 R132H mutation. The patient subsequently received a mutant IDH1 inhibitor (AG-120, Agios Pharmaceuticals, Cambridge, MA), but with no response. IDH1 mutations are common in certain cancer types, but have not been reported in PDA. We report the first case of an IDH1 mutation in this tumor type, perhaps providing a rare opportunity for a targeted therapy as a treatment option for PDA.

5 Article Posttranscriptional Regulation of 2017

Chand, Saswati N / Zarei, Mahsa / Schiewer, Matthew J / Kamath, Akshay R / Romeo, Carmella / Lal, Shruti / Cozzitorto, Joseph A / Nevler, Avinoam / Scolaro, Laura / Londin, Eric / Jiang, Wei / Meisner-Kober, Nicole / Pishvaian, Michael J / Knudsen, Karen E / Yeo, Charles J / Pascal, John M / Winter, Jordan M / Brody, Jonathan R. ·Department of Surgery, The Jefferson Pancreas, Biliary and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania. · Department of Cancer Biology, Thomas Jefferson University, Philadelphia, Pennsylvania. · Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania. · Computational Medicine Center, Thomas Jefferson University, Philadelphia, Pennsylvania. · Department of Pathology, Thomas Jefferson University, Philadelphia, Pennsylvania. · Novartis Institute for Biomedical Research, Basel, Switzerland. · Division of Hematology and Oncology, Lombardi Comprehensive Cancer Center, Georgetown University, Washington, DC. · Department of Biochemistry and Molecular Medicine, Université de Montréal, Montréal, Québec, Canada. · Department of Surgery, The Jefferson Pancreas, Biliary and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania. jonathan.brody@jefferson.edu. ·Cancer Res · Pubmed #28687616.

ABSTRACT: The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRNA stability factor HuR (ELAV-L1) to drive cancer growth and progression. Here, we show that CRISPR-Cas9-mediated silencing of the HuR locus increases the relative sensitivity of PDAC cells to PARP inhibitors (PARPi). PDAC cells treated with PARPi stimulated translocation of HuR from the nucleus to the cytoplasm, specifically promoting stabilization of a new target, poly (ADP-ribose) glycohydrolase (

6 Article Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells. 2017

Zarei, Mahsa / Lal, Shruti / Parker, Seth J / Nevler, Avinoam / Vaziri-Gohar, Ali / Dukleska, Katerina / Mambelli-Lisboa, Nicole C / Moffat, Cynthia / Blanco, Fernando F / Chand, Saswati N / Jimbo, Masaya / Cozzitorto, Joseph A / Jiang, Wei / Yeo, Charles J / Londin, Eric R / Seifert, Erin L / Metallo, Christian M / Brody, Jonathan R / Winter, Jordan M. ·Department of Surgery, Division of Surgical Research, Jefferson Pancreas, Biliary and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania. · Department of Bioengineering, University of California, San Diego, La Jolla, California. · MitoCare Center, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania. · Department of Pathology, Thomas Jefferson University, Philadelphia, Pennsylvania. · Computational Medicine Center, Thomas Jefferson University, Philadelphia, Pennsylvania. · Moores Cancer Center, University of California, San Diego, La Jolla, California. · Department of Surgery, Division of Surgical Research, Jefferson Pancreas, Biliary and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania. jordan.winter@jefferson.edu. ·Cancer Res · Pubmed #28652247.

ABSTRACT: Cancer aggressiveness may result from the selective pressure of a harsh nutrient-deprived microenvironment. Here we illustrate how such conditions promote chemotherapy resistance in pancreatic ductal adenocarcinoma (PDAC). Glucose or glutamine withdrawal resulted in a 5- to 10-fold protective effect with chemotherapy treatment. PDAC xenografts were less sensitive to gemcitabine in hypoglycemic mice compared with hyperglycemic mice. Consistent with this observation, patients receiving adjuvant gemcitabine (

7 Article Microscopic lymphovascular invasion is an independent predictor of survival in resected pancreatic ductal adenocarcinoma. 2017

Epstein, Jeffrey D / Kozak, Geoffrey / Fong, Zhi Ven / He, Jin / Javed, Ammar A / Joneja, Upasana / Jiang, Wei / Ferrone, Cristina R / Lillemoe, Keith D / Cameron, John L / Weiss, Matthew J / Lavu, Harish / Yeo, Charles J / Fernandez-Del Castillo, Carlos / Wolfgang, Christopher L / Winter, Jordan M. ·Sidney Kimmel Medical College at Thomas Jefferson University, Philadelphia, Pennsylvania. · Department of Surgery, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania. · Department of Surgery, Massachusetts General Hospital, Boston, Massachusetts. · Department of Surgical Oncology, Johns Hopkins Hospital, Baltimore, Maryland. · Department of Pathology, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania. ·J Surg Oncol · Pubmed #28628722.

ABSTRACT: Background and Objectives Despite routine inclusion of lymphovascular invasion (LVI) status in pathologic reports of resected pancreatic ductal adenocarcinomas (PDA), the clinical implications of LVI have not been well characterized. Methods This study is a retrospective review of 2640 patients who underwent a pancreatectomy for PDA at Thomas Jefferson University Hospital, Massachusetts General Hospital, or Johns Hopkins Hospital (2003-2014). Clinical and pathologic records were extracted from institutional databases. Results The median post-resection survival for the total cohort was 19.2 months with a 5-year survival rate of 15.2%. In a multivariate Cox proportional hazards model including conventional pathologic features, LVI was an independent predictor of survival (HR = 1.14, P = 0.017). In a stratified Kaplan-Meier survival analysis, patients with N0, LVI- PDA had a significantly improved overall survival compared to those with N0, LVI+ PDA (median 31 vs 24 mo, P = 0.020). Similarly, patients with N1, LVI- PDA had superior survival to patients with N1, LVI+ disease (18.6 vs 16.5 mo, P = 0.001). Conclusions As the first large scale study focused on the clinical impact of LVI status in PDA, these data indicate that this routinely reported pathologic feature is a bona fide and independent adverse prognostic factor.

8 Article Vitamin C Intake and Pancreatic Cancer Risk: A Meta-Analysis of Published Case-Control and Cohort Studies. 2016

Hua, Yong-Fei / Wang, Gao-Qing / Jiang, Wei / Huang, Jing / Chen, Guo-Chong / Lu, Cai-De. ·Department of Hepatobiliary and Pancreatic Surgery, Ningbo Medical Treatment Center Lihuili Hospital, Ningbo, 315000, China. · Department of Nutrition and Food Hygiene, School of Public Health, Soochow University, Suzhou, 215123, China. ·PLoS One · Pubmed #26859881.

ABSTRACT: BACKGROUND: Observational studies inconsistently reported the relationship between vitamin C intake and risk of pancreatic cancer. We conducted a meta-analysis of published case-control and cohort studies to quantify the association. METHODS: Potentially eligible studies were found on PubMed and EMBASE databases through May 31, 2015. A random-effects model was assigned to compute summary point estimates with corresponding 95% confidence intervals (CIs). Subgroup and meta-regression analyses were also performed to explore sources of heterogeneity. RESULTS: Our final analyses included 20 observational studies comprising nearly 5 thousand cases of pancreatic cancer. When comparing the highest with the lowest categories of vitamin C intake, the summary odds ratio/relative risk for case-control studies (14 studies), cohort studies (6 studies) and all studies combined was 0.58 (95% CI: 0.52-0.66), 0.93 (95% CI: 0.78-1.11) and 0.66 (95% CI: 0.58-0.75), respectively. The difference in the findings between case-control and cohort studies was statistically significant (P < .001). Possible publication bias was shown in the meta-analysis of case-control studies. CONCLUSION: There is insufficient evidence to conclude any relationship between vitamin C intake and risk of pancreatic cancer. The strong inverse association observed in case-control studies may be affected by biases (eg, recall and selection biases) that particularly affect case-control studies and/or potential publication bias. Future prospective studies of vitamin C intake and pancreatic cancer are needed.

9 Article Recurrence and Survival After Resection of Small Intraductal Papillary Mucinous Neoplasm-associated Carcinomas (≤20-mm Invasive Component): A Multi-institutional Analysis. 2016

Winter, Jordan M / Jiang, Wei / Basturk, Olca / Mino-Kenudson, Mari / Fong, Zhi Ven / Tan, Wei Phin / Lavu, Harish / Vollmer, Charles M / Furth, Emma E / Haviland, Dana / Klimstra, David S / Jarnagin, William R / Lillemoe, Keith D / Yeo, Charles J / Fernandez-Del Castillo, Carlos / Allen, Peter J. ·*Department of Surgery and the Jefferson Pancreas, Biliary, and Related Cancer Center, Thomas Jefferson University, Philadelphia, PA †Department of Pathology, Thomas Jefferson University, Philadelphia, PA ‡Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, NY §Department of Pathology, Massachusetts General Hospital, Boston, MA ¶Department of Surgery, Massachusetts General Hospital, Boston, MA ||Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia, PA **Department of Pathology, Hospital of the University of Pennsylvania, Philadelphia, PA ††Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, NY. ·Ann Surg · Pubmed #26135696.

ABSTRACT: BACKGROUND: Early invasive carcinoma may be encountered in association with intraductal papillary mucinous neoplasms (IPMNs) of the pancreas. The natural history of these early invasive lesions is unknown. METHODS: Pancreatic surgical databases from 4 high-volume centers were queried for IPMNs, with invasive components measuring 20 mm or less. All cases were reviewed by GI gastrointestinal pathologists, and pathologic features were analyzed to identify predictors of recurrence and survival. RESULTS: A total of 70 small IPMN-associated invasive carcinomas (≤20-mm invasion) were identified, comprising 25% of resected IPMN-associated carcinomas (n = 280). Most of these small invasive cancers were multifocal (66%), less than 10 mm in size (73%), and arose in the setting of a main duct IPMN (96%). The most common adenocarcinoma subtypes were tubular (57%) and colloid (29%). Lymph node metastases were present in 19% of cases and 23% were T3 lesions. The overall recurrence rate was 24% (n = 17), and the median time to recurrence was 16 months (range: 4-132 months). Median and 5-year survival rates were 99 months and 59%. Recurrence patterns of invasive disease were local in 35%, distant in 47%, and both in 18%. Lymphatic spread and T3 stage were predictive of recurrence (univariate, P = 0.006), whereas tubular carcinoma type was the most predictive of poor overall survival (multivariate hazard ratio = 3.7, P = 0.04). CONCLUSIONS: This study represents the largest multi-institutional experience of resected small IPMN-associated carcinoma. Although these malignancies may frequently be cured with resection, recurrence risk is significant. Lymphatic spread, increased T stage, and tubular type carcinoma were associated with the poorest outcome.

10 Article CD44 regulates pancreatic cancer invasion through MT1-MMP. 2015

Jiang, Wei / Zhang, Yaqing / Kane, Kevin T / Collins, Meredith A / Simeone, Diane M / di Magliano, Marina Pasca / Nguyen, Kevin Tri. ·Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan. · Program in Cell and Molecular Biology, University of Michigan Medical School, Ann Arbor, Michigan. · Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan. Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan. · Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan. Program in Cell and Molecular Biology, University of Michigan Medical School, Ann Arbor, Michigan. Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, Michigan. marinapa@umich.edu ktnguyen74@yahoo.com. · Department of Surgery, University of Michigan Medical School, Ann Arbor, Michigan. marinapa@umich.edu ktnguyen74@yahoo.com. ·Mol Cancer Res · Pubmed #25566991.

ABSTRACT: IMPLICATIONS: This study sets the stage for CD44 and MT1-MMP as therapeutic targets in pancreatic cancer, for which small molecule or biologic inhibitors are available. Visual Overview: http://mcr.aacrjournals.org/content/early/2014/09/10/1541-7786.MCR-14-0076/F1.large.jpg.

11 Article MUC1 Promoter-Driven DTA as a Targeted Therapeutic Strategy against Pancreatic Cancer. 2015

Tholey, Renee M / Lal, Shruti / Jimbo, Masaya / Burkhart, Richard A / Blanco, Fernando F / Cozzitorto, Joseph A / Eisenberg, Josh D / Jiang, Wei / Iacobuzio-Donahue, Christine A / Witkiewicz, Agnieszka K / Glbert, Melissa / Yeo, Charles J / Brody, Jonathan R / Sawicki, Janet A / Winter, Jordan M. ·Department of Surgery and the Jefferson Pancreas, Biliary, and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania. · Department of Pathology, Thomas Jefferson University, Philadelphia, Pennsylvania. · Department of Pathology and the David Rubenstein Pancreatic Cancer Research Center, Memorial Sloan Kettering Cancer Center, New York, New York. · Department of Pathology, UT Southwestern Medical Center; Dallas, Texas. · Lankenau Institute for Medical Research, Wynnewood, Pennsylvania. jordan.winter@jefferson.edu SawickiJ@MLHS.org. · Department of Surgery and the Jefferson Pancreas, Biliary, and Related Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania. jordan.winter@jefferson.edu SawickiJ@MLHS.org. ·Mol Cancer Res · Pubmed #25336517.

ABSTRACT: IMPLICATIONS: MUC1 expression in primary and metastatic lesions provides a rationale for the development of a systemic MUC1 promoter-driven DTA therapy that may be further enhanced by combination with other promoter-driven DTA constructs.

12 Article High expression of survivin is prognostic of shorter survival but not predictive of adjuvant gemcitabine benefit in patients with resected pancreatic adenocarcinoma. 2013

Xie, Hao / Jiang, Wei / Xiao, Shu-Yuan / Liu, Xiuli. ·Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, USA. ·J Histochem Cytochem · Pubmed #23124118.

ABSTRACT: Overexpression of survivin has been associated with gemcitabine resistance in pancreatic adenocarcinoma, but previous studies have shown conflicting results. This study aims to determine its prognostic value in resected pancreatic adenocarcinoma with or without adjuvant therapy and its predictive value in adjuvant gemcitabine benefit in patients with resected pancreatic adenocarcinoma. This study included 118 patients who underwent pancreaticoduodectomy from 1999 to 2007, with no neoadjuvant chemoradiation. Forty-five patients received adjuvant gemcitabine. Survivin expression was assessed immunohistochemically and was graded as low (≤10% positive cells) and high (>10% positive cells) by recursive partitioning analysis. Prognostic factors, including tumor size, number of positive lymph nodes, perineural invasion, and stage, were identified for overall survival (OS) and progression-free survival (PFS) using Cox proportional hazards models. Multivariable analysis of the entire cohort revealed that both high survivin expression and perineural invasion predict significantly shorter OS (hazard ratio [HR] 2.0, p=0.01; HR 1.9, p=0.01, respectively) and shorter PFS (HR 1.9, p=0.04; HR 3.1, p=0.0006, respectively). Expression of survivin predicts neither OS nor PFS in patients treated with adjuvant gemcitabine. In summary, high expression of survivin is associated with shorter OS and PFS in patients with resected pancreatic adenocarcinoma after adjusting for other histopathological factors. However, survivin has no predictive value of adjuvant gemcitabine benefit.

13 Article Predictive and prognostic roles of ribonucleotide reductase M1 in resectable pancreatic adenocarcinoma. 2013

Xie, Hao / Jiang, Wei / Jiang, John / Wang, Yixin / Kim, Richard / Liu, Xiaobo / Liu, Xiuli. ·Department of Anatomic Pathology, The Cleveland Clinic, Ohio, USA. ·Cancer · Pubmed #22736490.

ABSTRACT: BACKGROUND: Ribonucleotide reductase M1 (RRM1) is an important molecule in different types of cancer. The objective of this study was to evaluate the predictive roles of RRM1 in the survival of patients with resectable pancreatic adenocarcinoma who received treatment with gemcitabine or nongemcitabine adjuvant therapy. METHODS: In total, 122 patients underwent tumor resection for pancreatic adenocarcinoma at the authors' institution from October 1999 to December 2007. Total RNA was isolated from microdissected, paraffin-embedded tumors. RRM1 expression levels were measured using quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) and were dichotomized using recursive partitioning analysis. The Kaplan-Meier method was used to estimate overall survival and progression-free survival, and the predictive value of RRM1 expression on survival was examined using Cox proportional hazards regression. RESULTS: RRM1 expression did not have significant prognostic value in the entire cohort regarding overall survival (P = .2) or progression-free survival (P = .7). In the subgroup of 44 patients who received adjuvant gemcitabine, patients who had low RRM1 expression had longer overall survival (median, 47.8 months vs 14.1 months; P = .005) and a trend toward longer progression-free survival (median not reached vs 12.9 months; P = .06). In contrast, in the subgroup of 35 patients who received nongemcitabine adjuvant therapy, patients who had high RRM1 expression had significantly longer overall survival (median, 41.9 months vs 19.8 months; P = .01) and progression-free survival (median, 70.0 months vs 11.8 months; P = .04). These results were confirmed in Cox proportional hazards multivariable analysis. CONCLUSIONS: In patients with resectable pancreatic adenocarcinoma, low RRM1 expression in the tumor predicted an overall survival benefit of adjuvant gemcitabine; and high RRM1 expression predicted the survival benefit of nongemcitabine adjuvant therapy.

14 Article MTHFR polymorphisms and pancreatic cancer risk: lack of evidence from a meta-analysis. 2012

Li, Lei / Wu, Sheng-Di / Wang, Ji-Yao / Shen, Xi-Zhong / Jiang, Wei. ·Department of Gastroenterology, Zhongshan Hospital, Fudan University, Shanghai, China. ·Asian Pac J Cancer Prev · Pubmed #22901202.

ABSTRACT: OBJECTIVE: Methylenetetrahydrofolate reductase (MTHFR) gene polymorphisms have been reported to be associated with pancreatic cancer, but the published studies had yielded inconsistent results.We therefore performed the present meta-analysis. METHODS: A search of Google scholar, PubMed, Cochrane Library and CNKI databases before April 2012 was conducted to summarize associations of MTHFR polymorphisms with pancreatic cancer risk. Assessment was with odds ratios (ORs) and 95% confidence intervals (CIs). Publication bias were also calculated. RESULTS: Four relative studies on MTHFR gene polymorphisms (C667T and A1298C) were involved in this meta-analysis. Overall, C667T(TT vs. CC:OR=1.61, 95%CI=0.78-3.34; TT vs. CT:OR=1.41, 95%CI=0.88-2.25; dominant model: OR=0.68, 95%CI=0.40-1.17; recessive model: OR=0.82, 95%CI=0.52-1.30) and A1298C(CC vs. AA:OR=1.01, 95%CI=0.47-2.17; CC vs. AC:OR=0.99,95%CI=0.46-2.14; dominant model: OR=1.01, 95%CI=0.47-2.20; recessive model: OR=1.01, 95%CI=0.80-1.26) did not increase pancreatic cancer risk. CONCLUSION: This meta-analysis indicated that MTHFR polymorphisms (C667T and A1298C) were not associated with pancreatic cancer risk.

15 Article Ribonucleotide reductase M2 does not predict survival in patients with resectable pancreatic adenocarcinoma. 2012

Xie, Hao / Lin, Jingmei / Thomas, Dafydd G / Jiang, Wei / Liu, Xiuli. ·Anatomic Pathology, Cleveland Clinic, Cleveland, OH 44195, USA. ·Int J Clin Exp Pathol · Pubmed #22670179.

ABSTRACT: BACKGROUND: Ribonucleotide reductase M2 (RRM2) was associated with pancreatic tumor progression and resistance to gemcitabine. This study aimed to determine if RRM2 protein expression was prognostic in patients with resectable pancreatic adenocarcinoma and predictive of adjuvant gemcitabine benefit. METHODS: 117 patients underwent tumor resection for pancreatic adenocarcinoma from 10/1999 to 12/2007. We constructed tissue microarrays from paraffin-embedded tumors and determined RRM2 protein expression using immunohistochemistry and grouped as negative or positive. We estimated overall survival (OS) and progression-free survival (PFS) using the Kaplan-Meier method and examined the prognostic and predictive value of RRM2 expression using Cox proportional hazards model. RESULTS: RRM2 expression showed no prognostic value in the entire group regarding OS (median OS 30.9 months in RRM2-positive versus 13.7 months in RRM2-negative, P = 0.26) and PFS (median OS 20.6 months in RRM2-positive versus 11.8 months in RRM2-negative, P = 0.46). RRM2 expression did not predict adjuvant gemcitabine benefit in the subgroup of 44 patients who received gemcitabine therapy (median OS 31.2 versus 15.2 months, P = 0.62; median PFS 11.3 versus 14.0 months, P = 0.35). Cox proportional hazards regression showed no prognostic effect of RRM2 expression on OS and PFS in the subgroup of 44 patients. However, the number of positive lymph nodes and perineural invasion were prognostic factors for OS (HR 1.2, P = 0.005) and for PFS (HR 5.5, P = 0.007), respectively. CONCLUSION: RRM2 protein expression in pancreatic adenocarcinoma is neither prognostic nor predictive of adjuvant gemcitabine benefit in patients with resectable pancreatic adenocarcinoma.