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Pancreatic Neoplasms: HELP
Articles by Sean F. Altekruse
Based on 6 articles published since 2010
(Why 6 articles?)
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Between 2010 and 2020, Sean Altekruse wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Association of Cigarette, Cigar, and Pipe Use With Mortality Risk in the US Population. 2018

Christensen, Carol H / Rostron, Brian / Cosgrove, Candace / Altekruse, Sean F / Hartman, Anne M / Gibson, James T / Apelberg, Benjamin / Inoue-Choi, Maki / Freedman, Neal D. ·Office of Science, Center for Tobacco Products, Food and Drug Administration, Silver Spring, Maryland. · United States Census Bureau, Suitland, Maryland. · National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland. · Tobacco Control Research Branch, Behavioral Research Program, Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health, Bethesda, Maryland. · Information Management Services, Inc. · Metabolic Epidemiology Branch, Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Rockville, Maryland. ·JAMA Intern Med · Pubmed #29459935.

ABSTRACT: Importance: Tobacco products have changed in recent years. Contemporary mortality risk estimates of combustible tobacco product use are needed. Objective: To investigate the mortality risks associated with current and former use of cigars, pipes, and cigarettes. Design, Setting, and Participants: The National Longitudinal Mortality Study is a longitudinal population-based, nationally representative health survey with mortality follow-up that includes demographic and other information from the Current Population Survey, tobacco product use information from the Tobacco Use Supplement, and mortality data from the National Death Index. In this study, participants provided tobacco use information at baseline in surveys starting from 1985 and were followed for mortality through the end of 2011. The study includes 357 420 participants who reported exclusively using cigar, pipes, or cigarettes or reported never using any type of tobacco product. Exposures: Current or former exclusive use of any cigar (little cigar, cigarillos, large cigar), traditional pipe, or cigarette and never tobacco use. Information on current daily and nondaily use was also collected. Estimates adjusted for age, sex, race/ethnicity, education, and survey year. Main Outcomes and Measures: All-cause and cause-specific mortality as identified as the primary cause of death from death certificate information. Results: Of the 357 420 persons included in the analysis, the majority of current and former cigar and pipe smokers were male (79.3%-98.0%), and smokers were more evenly divided by sex (46% of current daily smokers were male). There were 51 150 recorded deaths during follow-up. Exclusive current cigarette smokers (hazard ratio [HR], 1.98; 95% CI, 1.93-2.02) and exclusive current cigar smokers (HR, 1.20; 95% CI, 1.03-1.38) had higher all-cause mortality risks than never tobacco users. Exclusive current cigarette smokers (HR, 4.06; 95% CI, 3.84-4.29), exclusive current cigar smokers (HR, 1.61; 95% CI, 1.11-2.32), and exclusive current pipe smokers (HR, 1.58; 95% CI, 1.05-2.38) had an elevated risk of dying from a tobacco-related cancer (including bladder, esophagus, larynx, lung, oral cavity, and pancreas). Among current nondaily cigarette users, statistically significant associations were observed with deaths from lung cancer (HR, 6.24; 95% CI, 5.17-7.54), oral cancer (HR, 4.62; 95% CI, 1.84-11.58), circulatory death (HR, 1.43; 95% CI, 1.30-1.57), cardiovascular death (HR, 1.24; 95% CI, 1.11-1.39), cerebrovascular death (stroke) (HR, 1.39; 95% CI, 1.12-1.74), and chronic obstructive pulmonary disease (HR, 7.66; 95% CI, 6.09-9.64) as well as for daily smokers. Conclusions and Relevance: This study provides further evidence that exclusive use of cigar, pipes, and cigarettes each confers significant mortality risks.

2 Article Expression of the scaffold connector enhancer of kinase suppressor of Ras 1 (CNKSR1) is correlated with clinical outcome in pancreatic cancer. 2017

Quadri, Humair S / Aiken, Taylor J / Allgaeuer, Michael / Moravec, Radim / Altekruse, Sean / Hussain, S Perwez / Miettinen, Markku M / Hewitt, Stephen M / Rudloff, Udo. ·Thoracic and Gastrointestinal Oncology Branch, Gastrointestinal Oncology Section, Investigator Center for Cancer Research, National Cancer Institute, Building 10 - Hatfield CRC, Room 4-5950, Bethesda, MD, 20892, USA. · Laboratory of Pathology, National Cancer Institute, Bethesda, MD, USA. · Surveillance Informatics Branch, National Cancer Institute, Bethesda, MD, USA. · Laboratory of Human Carcinogenesis, National Cancer Institute, Bethesda, MD, USA. · Experimental Pathology Laboratory, Laboratory of Pathology, National Cancer Institute, Bethesda, MD, USA. · Thoracic and Gastrointestinal Oncology Branch, Gastrointestinal Oncology Section, Investigator Center for Cancer Research, National Cancer Institute, Building 10 - Hatfield CRC, Room 4-5950, Bethesda, MD, 20892, USA. rudloffu@mail.nih.gov. ·BMC Cancer · Pubmed #28732488.

ABSTRACT: BACKGROUND: Despite the near universal occurrence of activating codon 12 KRAS somatic variants in pancreatic cancer, there is considerable heterogeneity in the molecular make-up, MAPK/ERK pathway activation states, and clinical outcome in this disease. We analyzed the expression levels of CNKSR1, a scaffold that influences MAPK/ERK pathway activity, in clinical pancreas cancer specimens and their impact on survival of patients with pancreatic cancer. METHODS: Immunohistochemical staining for CNKSR1 expression was performed on 120 specimens from three independent pancreatic cancer tissue registries, phospho-ERK levels were measured in 86 samples. Expression was divided into CNKSR1 low and CNKSR1 high and correlated with clinicopathological variables including overall survival using multivariate Cox proportional hazard ratio models. RESULTS: CNKSR1 expression was increased in tumors compared to matched normal uninvolved resection specimens (p = 0.004). 28.3% (34/120) of patient specimens stained as CNKSR1 low compared to 71.7% (86/120) of specimens which stained as CNKSR1 high. High CNKSR1 expression was more prevalent in low grade tumors (p = 0.04). In multivariate analysis, low CNKSR1 expression status was independently correlated with decreased overall survival (HR = 2.146; 95% CI 1.34 to 3.43). When stratifying primary, non-metastatic tumor biopsies by CNKSR1 expression, resection was associated with improved survival in patients with high CNKSR1 expression (p < 0.0001) but not low CNKSR1 expression (p = 0.3666). Pancreatic tumors with nuclear in addition to cytoplasmic CNKSR1 staining (32/107) showed increased nuclear phospho-ERK expression compared to tumor with cytoplasmic CNKSR1 staining only (p = 0.017). CONCLUSION: CNKSR1 expression is increased in pancreatic tissue specimens and was found to be an independent prognostic marker of overall survival. CNKSR1 may help to identify patient subgroups with unfavorable tumor biology in order to improve risk stratification and treatment selection. Cellular distribution of CNKSR1 was correlated with nuclear pERK expression.

3 Article Loss of SOD3 (EcSOD) Expression Promotes an Aggressive Phenotype in Human Pancreatic Ductal Adenocarcinoma. 2015

O'Leary, Brianne R / Fath, Melissa A / Bellizzi, Andrew M / Hrabe, Jennifer E / Button, Anna M / Allen, Bryan G / Case, Adam J / Altekruse, Sean / Wagner, Brett A / Buettner, Garry R / Lynch, Charles F / Hernandez, Brenda Y / Cozen, Wendy / Beardsley, Robert A / Keene, Jeffery / Henry, Michael D / Domann, Frederick E / Spitz, Douglas R / Mezhir, James J. ·Department of Surgery, University of Iowa, Iowa City, Iowa. · Department of Radiation Oncology, University of Iowa, Iowa City, Iowa. · Department of Pathology, University of Iowa, Iowa City, Iowa. · Department of Biostatistics, University of Iowa, Iowa City, Iowa. · National Cancer Institute, Bethesda, Maryland. · Department of Epidemiology, University of Iowa, Iowa City, Iowa. · University of Hawaii Cancer Center, Honolulu, Hawaii. · University of Southern California, Los Angeles, California. · Galera Therapeutics, Malvern, Pennsylvania. · Department of Microbiology, University of Iowa, Iowa City, Iowa. · Department of Surgery, University of Iowa, Iowa City, Iowa. Department of Radiation Oncology, University of Iowa, Iowa City, Iowa. james-mezhir@uiowa.edu. ·Clin Cancer Res · Pubmed #25634994.

ABSTRACT: PURPOSE: Pancreatic ductal adenocarcinoma (PDA) cells are known to produce excessive amounts of reactive oxygen species (ROS), particularly superoxide, which may contribute to the aggressive and refractory nature of this disease. Extracellular superoxide dismutase (EcSOD) is an antioxidant enzyme that catalyzes the dismutation of superoxide in the extracellular environment. This study tests the hypothesis that EcSOD modulates PDA growth and invasion by modifying the redox balance in PDA. EXPERIMENTAL DESIGN: We evaluated the prognostic significance of EcSOD in a human tissue microarray (TMA) of patients with PDA. EcSOD overexpression was performed in PDA cell lines and animal models of disease. The impact of EcSOD on PDA cell lines was evaluated with Matrigel invasion in combination with a superoxide-specific SOD mimic and a nitric oxide synthase (NOS) inhibitor to determine the mechanism of action of EcSOD in PDA. RESULTS: Loss of EcSOD expression is a common event in PDA, which correlated with worse disease biology. Overexpression of EcSOD in PDA cell lines resulted in decreased invasiveness that appeared to be related to reactions of superoxide with nitric oxide. Pancreatic cancer xenografts overexpressing EcSOD also demonstrated slower growth and peritoneal metastasis. Overexpression of EcSOD or treatment with a superoxide-specific SOD mimic caused significant decreases in PDA cell invasive capacity. CONCLUSIONS: These results support the hypothesis that loss of EcSOD leads to increased reactions of superoxide with nitric oxide, which contributes to the invasive phenotype. These results allow for the speculation that superoxide dismutase mimetics might inhibit PDA progression in human clinical disease.

4 Article CLPTM1L promotes growth and enhances aneuploidy in pancreatic cancer cells. 2014

Jia, Jinping / Bosley, Allen D / Thompson, Abbey / Hoskins, Jason W / Cheuk, Adam / Collins, Irene / Parikh, Hemang / Xiao, Zhen / Ylaya, Kris / Dzyadyk, Marta / Cozen, Wendy / Hernandez, Brenda Y / Lynch, Charles F / Loncarek, Jadranka / Altekruse, Sean F / Zhang, Lizhi / Westlake, Christopher J / Factor, Valentina M / Thorgeirsson, Snorri / Bamlet, William R / Hewitt, Stephen M / Petersen, Gloria M / Andresson, Thorkell / Amundadottir, Laufey T. ·Authors' Affiliations: Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics; Pediatric Oncology Branch; Laboratory of Pathology; Division of Cancer Control and Population Sciences; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda; Laboratory of Proteomics and Analytical Technologies, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research; Laboratory of Protein Dynamics and Signaling and Laboratory of Cell & Developmental Signaling, NCI-Frederick, Frederick, Maryland; Keck School of Medicine, University of Southern California, Los Angeles, California; University of Hawaii Cancer Center, Honolulu, Hawaii; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota. · Authors' Affiliations: Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics; Pediatric Oncology Branch; Laboratory of Pathology; Division of Cancer Control and Population Sciences; Laboratory of Experimental Carcinogenesis, National Cancer Institute, NIH, Department of Health and Human Services, Bethesda; Laboratory of Proteomics and Analytical Technologies, Leidos Biomedical Research, Frederick National Laboratory for Cancer Research; Laboratory of Protein Dynamics and Signaling and Laboratory of Cell & Developmental Signaling, NCI-Frederick, Frederick, Maryland; Keck School of Medicine, University of Southern California, Los Angeles, California; University of Hawaii Cancer Center, Honolulu, Hawaii; Department of Epidemiology, College of Public Health, University of Iowa, Iowa City, Iowa; and Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota amundadottirl@mail.nih.gov. ·Cancer Res · Pubmed #24648346.

ABSTRACT: Genome-wide association studies (GWAS) of 10 different cancers have identified pleiotropic cancer predisposition loci across a region of chromosome 5p15.33 that includes the TERT and CLPTM1L genes. Of these, susceptibility alleles for pancreatic cancer have mapped to the CLPTM1L gene, thus prompting an investigation of the function of CLPTM1L in the pancreas. Immunofluorescence analysis indicated that CLPTM1L localized to the endoplasmic reticulum where it is likely embedded in the membrane, in accord with multiple predicted transmembrane domains. Overexpression of CLPTM1L enhanced growth of pancreatic cancer cells in vitro (1.3-1.5-fold; PDAY7 < 0.003) and in vivo (3.46-fold; PDAY68 = 0.039), suggesting a role in tumor growth; this effect was abrogated by deletion of two hydrophilic domains. Affinity purification followed by mass spectrometry identified an interaction between CLPTM1L and non-muscle myosin II (NMM-II), a protein involved in maintaining cell shape, migration, and cytokinesis. The two proteins colocalized in the cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes. Overexpression of CLPTM1L and depletion of NMM-II induced aneuploidy, indicating that CLPTM1L may interfere with normal NMM-II function in regulating cytokinesis. Immunohistochemical analysis revealed enhanced staining of CLPTM1L in human pancreatic ductal adenocarcinoma (n = 378) as compared with normal pancreatic tissue samples (n = 17; P = 1.7 × 10(-4)). Our results suggest that CLPTM1L functions as a growth-promoting gene in the pancreas and that overexpression may lead to an abrogation of normal cytokinesis, indicating that it should be considered as a plausible candidate gene that could explain the effect of pancreatic cancer susceptibility alleles on chr5p15.33.

5 Article Association of prion protein expression with pancreatic adenocarcinoma survival in the SEER residual tissue repository. 2011

Sy, Man-Sun / Altekruse, Sean F / Li, Chaoyang / Lynch, Charles F / Goodman, Marc T / Hernandez, Brenda Y / Zhou, Lan / Saber, Maria Sibug / Hewitt, Stephen M / Xin, Wei. ·Department of Pathology, Case Western Reserve University, School of Medicine, Cleveland, OH 44106, USA. ·Cancer Biomark · Pubmed #22820080.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is an important cause of cancer death with no clear prognostic biomarker. Expression of prion (PrP) has been reported to be a marker of poor prognosis in a series of Caucasian PDAC cases. We determined the prognostic value of PrP in a racially and geographically diverse population-based series of PDAC cases. PrP expression was examined in 142 PDAC cases from three cancer registries. Cases included 71 Caucasian, 54 Asian/Pacific Islanders and 17 Blacks diagnosed from 1983-2000, and followed through 2008. Hazard ratios (HR) and 95% confidence intervals (CIs) for the association of PrP expression with survival were computed after adjustment for case attributes. The risk of death was about four times higher (HR=3.8; 95% PDAC cases with PrP(+) tumors (median survival 5 months) compared to the 34 cases with PrP(-) tumors (median survival 20 months). Of 51 cases with resected, localized PDAC median survival was 74 months for 17 cases with PrP(-) tumors versus 14 months for 34 cases with PrP(+) tumors (HR=6.7; 95% CI: 2.6, 17.4). All 6 surviving cases had PrP(-) negative tumors (median survival, > 10 years). PrP may have potential as a prognostic biomarker in PDAC patient management.

6 Minor The sole presence of CDK4 is not a solid criterion for discriminating between tumor and healthy pancreatic tissues. 2012

Altirriba, Jordi / García, Ainhoa / Sánchez, Begoña / Haba, Laura / Altekruse, Sean / Stratmann, Thomas / Bombí, Josep Antoni / Mezquita, Cristóbal / Gomis, Ramon / Mora, Conchi. · ·Int J Cancer · Pubmed #21792898.

ABSTRACT: -- No abstract --