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Pancreatic Neoplasms: HELP
Articles by Katrina S. Pedersen
Based on 6 articles published since 2010
(Why 6 articles?)
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Between 2010 and 2020, Katrina Pedersen wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Clinical Trial Phase II trial of gemcitabine and tanespimycin (17AAG) in metastatic pancreatic cancer: a Mayo Clinic Phase II Consortium study. 2015

Pedersen, Katrina S / Kim, George P / Foster, Nathan R / Wang-Gillam, Andrea / Erlichman, Charles / McWilliams, Robert R. ·Division of Medical Oncology, Mayo Clinic, Rochester, MN, USA, pedersen.katrina@mayo.edu. ·Invest New Drugs · Pubmed #25952464.

ABSTRACT: OBJECTIVES: Heat Shock Protein 90 (HSP90) is a molecular chaperone that stabilizes many oncogenic proteins. HSP90 inhibitors may sensitize tumors to cytotoxic agents by causing client protein degradation. Gemcitabine, which has modest activity in pancreas cancer, activates Chk1, a client protein of HSP90. This phase II trial was designed to determine whether 17AAG could enhance the clinical activity of gemcitabine through degradation of Chk1 in patients with stage IV pancreatic cancer. METHODS: A multicenter, prospective study combining gemcitabine and 17AAG enrolled patients with stage IV pancreatic adenocarcinoma, adequate liver and kidney function, ECOG performance status 0-2, and no prior chemotherapy for metastatic disease. The primary goal was to achieve a 60 % overall survival at 6 months. Sixty-six patients were planned for accrual, with an interim analysis after 25 patients enrolled. RESULTS: After a futility analysis to achieve the endpoint, accrual was halted with 21 patients enrolled. No complete or partial responses were seen. Forty percent of patients were alive at 6 months. Median overall survival was 5.4 months. Tolerability was moderate, with 65 % of patients having ≥ grade 3 adverse events (AE), and 15 % having grade 4 events. CONCLUSIONS: The lack of clinical activity suggests that targeting Chk1 by inhibiting HSP90 is not important in pancreatic cancer sensitivity to gemcitabine alone. Further studies of HSP90 targeted agents with gemcitabine alone are not warranted.

2 Article Phase Ib/II study combining tosedostat with capecitabine in patients with advanced pancreatic adenocarcinoma. 2020

Grierson, Patrick / Teague, Andrea / Suresh, Rama / Lim, Kian-Huat / Amin, Manik / Pedersen, Katrina / Tan, Benjamin / Huffman, Jesse / Boice, Nick / Du, Lingling / Liu, Jingxia / Lockhart, A Craig / Wang-Gillam, Andrea. ·Department of Internal Medicine, Division of Medical Oncology, Washington University in St. Louis, St. Louis, MO, USA. · New Mexico Cancer Care Associates, Santa Fe, NM, USA. · Ochsner Health System, New Orleans, LA, USA. · Department of Surgery, Division of Public Health Sciences, Section of Oncologic Biostatistics, Washington University in St. Louis, St. Louis, MO, USA. · University of Miami, Miller School of Medicine, Sylvester Comprehensive Cancer Center, Miami, FL, USA. ·J Gastrointest Oncol · Pubmed #32175106.

ABSTRACT: Background: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with limited therapeutic options. We evaluated the safety and efficacy of the aminopeptidase inhibitor tosedostat with capecitabine in advanced PDAC. Methods: We conducted a phase Ib/II trial of tosedostat with capecitabine as second-line therapy for advanced PDAC. Planned enrollment was 36 patients. Eligible patients were treated with capecitabine 1,000 mg/m Results: Sixteen patients were enrolled. Tosedostat 120 mg oral twice daily with capecitabine 1,000 mg/m Conclusions: Tosedostat with capecitabine displayed tolerable toxicity, and prolonged disease control in a subset of patients. These data encourage further exploration of aminopeptidase inhibitors in pancreatic cancer.

3 Article None 2018

McWilliams, Robert R / Wieben, Eric D / Chaffee, Kari G / Antwi, Samuel O / Raskin, Leon / Olopade, Olufunmilayo I / Li, Donghui / Highsmith, W Edward / Colon-Otero, Gerardo / Khanna, Lauren G / Permuth, Jennifer B / Olson, Janet E / Frucht, Harold / Genkinger, Jeanine / Zheng, Wei / Blot, William J / Wu, Lang / Almada, Luciana L / Fernandez-Zapico, Martin E / Sicotte, Hugues / Pedersen, Katrina S / Petersen, Gloria M. ·Department of Oncology, Mayo Clinic, Rochester, Minnesota. Mcwilliams.robert@mayo.edu. · Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota. · Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota. · Department of Health Sciences Research, Mayo Clinic, Rochester, Minnesota. · Department of Health Sciences Research, Mayo Clinic, Jacksonville, Florida. · Division of Epidemiology, Vanderbilt-Ingram Cancer Center, Nashville, Tennessee. · Departments of Medicine and Human Genetics, University of Chicago Medical Center, Chicago, Illinois. · Department of Gastrointestinal Medical Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas. · Department of Medicine, Division of Hematology/Oncology, Mayo Clinic, Jacksonville, Florida. · Department of Medicine, Columbia University Medical Center, New York, New York. · Departments of Cancer Epidemiology and Gastrointestinal Oncology, Moffitt Cancer Center, Tampa, Florida. · Department of Epidemiology, Columbia University Medical Center, New York, New York. · Herbert Irving Comprehensive Cancer Center, New York, New York. · Schulze Center for Novel Therapeutics, Division of Oncology Research, Mayo Clinic, Rochester, Minnesota. · Division of Oncology, Washington University, St. Louis, Missouri. ·Cancer Epidemiol Biomarkers Prev · Pubmed #30038052.

ABSTRACT:

4 Article Pancreatic cancer risk is modulated by inflammatory potential of diet and ABO genotype: a consortia-based evaluation and replication study. 2018

Antwi, Samuel O / Bamlet, William R / Pedersen, Katrina S / Chaffee, Kari G / Risch, Harvey A / Shivappa, Nitin / Steck, Susan E / Anderson, Kristin E / Bracci, Paige M / Polesel, Jerry / Serraino, Diego / La Vecchia, Carlo / Bosetti, Cristina / Li, Donghui / Oberg, Ann L / Arslan, Alan A / Albanes, Demetrius / Duell, Eric J / Huybrechts, Inge / Amundadottir, Laufey T / Hoover, Robert / Mannisto, Satu / Chanock, Stephen J / Zheng, Wei / Shu, Xiao-Ou / Stepien, Magdalena / Canzian, Federico / Bueno-de-Mesquita, Bas / Quirós, José Ramon / Zeleniuch-Jacquotte, Anne / Bruinsma, Fiona / Milne, Roger L / Giles, Graham G / Hébert, James R / Stolzenberg-Solomon, Rachael Z / Petersen, Gloria M. ·Division of Epidemiology, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. · Division of Biomedical Statistics and Informatics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA. · Division of Oncology, Washington University, St. Louis, MO, USA. · Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, CT, USA. · Cancer Prevention and Control Program, USA. · Department of Epidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, SC, USA. · Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN, USA. · Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA, USA. · Unit of Epidemiology and Biostatistics, Centro di Riferimento Oncologico, Aviano (PN), Italy. · Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy. · Department of Oncology, IRCCS-Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy. · Department of Gastrointestinal Medical Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA. · Department of Environmental Medicine, New York University School of Medicine, New York, NY, USA. · Department of Population Health, New York University School of Medicine, New York, NY, USA. · Department of Obstetrics and Gynecology, New York University School of Medicine, New York, NY, USA. · Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health, Department of Health and Human Services, Bethesda, MD, USA. · Unit of Nutrition and Cancer, Bellvitge Biomedical Research Institute-IDIBELL, Catalan Institute of Oncology-ICO. L'Hospitalet de Llobregat, Barcelona, Spain. · International Agency for Research on Cancer, World Health Organization, France. · Department of Public Health Solutions, National Institute for Health and Welfare Helsinki, Finland. · Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, and Vanderbilt-Ingram Cancer Center, Vanderbilt University, Nashville, TN, USA. · Genomic Epidemiology Group, German Cancer Research Center (DKFZ), Heidelberg, Germany. · Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, St Mary's Campus, Norfolk Place, London, UK. · Department of Social and Preventive Medicine, Faculty of Medicine, University of Malaya, Pantai Valley, Kuala Lumpur, Malaysia. · Public Health Directorate, Asturias, Spain. · Perlmutter Cancer Center, New York University School of Medicine, New York, NY, USA. · Cancer Epidemiology and Intelligence Division, Cancer Council Victoria, and Centre for Epidemiology and Biostatistics, Melbourne School of Global and Population Health, The University of Melbourne, Melbourne, Australia. ·Carcinogenesis · Pubmed #29800239.

ABSTRACT: Diets with high inflammatory potential are suspected to increase risk for pancreatic cancer (PC). Using pooled analyses, we examined whether this association applies to populations from different geographic regions and population subgroups with varying risks for PC, including variation in ABO blood type. Data from six case-control studies (cases, n = 2414; controls, n = 4528) in the Pancreatic Cancer Case-Control Consortium (PanC4) were analyzed, followed by replication in five nested case-control studies (cases, n = 1268; controls, n = 4215) from the Pancreatic Cancer Cohort Consortium (PanScan). Two polymorphisms in the ABO locus (rs505922 and rs8176746) were used to infer participants' blood types. Dietary questionnaire-derived nutrient/food intake was used to compute energy-adjusted dietary inflammatory index (E-DII®) scores to assess inflammatory potential of diet. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using multivariable-adjusted logistic regression. Higher E-DII scores, reflecting greater inflammatory potential of diet, were associated with increased PC risk in PanC4 [ORQ5 versus Q1=2.20, 95% confidence interval (CI) = 1.85-2.61, Ptrend < 0.0001; ORcontinuous = 1.20, 95% CI = 1.17-1.24], and PanScan (ORQ5 versus Q1 = 1.23, 95% CI = 0.92-1.66, Ptrend = 0.008; ORcontinuous = 1.09, 95% CI = 1.02-1.15). As expected, genotype-derived non-O blood type was associated with increased PC risk in both the PanC4 and PanScan studies. Stratified analyses of associations between E-DII quintiles and PC by genotype-derived ABO blood type did not show interaction by blood type (Pinteraction = 0.10 in PanC4 and Pinteraction=0.13 in PanScan). The results show that consuming a pro-inflammatory diet and carrying non-O blood type are each individually, but not interactively, associated with increased PC risk.

5 Article Leukocyte DNA methylation signature differentiates pancreatic cancer patients from healthy controls. 2011

Pedersen, Katrina S / Bamlet, William R / Oberg, Ann L / de Andrade, Mariza / Matsumoto, Martha E / Tang, Hui / Thibodeau, Stephen N / Petersen, Gloria M / Wang, Liang. ·Department of Internal Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota, United States of America. ·PLoS One · Pubmed #21455317.

ABSTRACT: Pancreatic adenocarcinoma (PaC) is one of most difficult tumors to treat. Much of this is attributed to the late diagnosis. To identify biomarkers for early detection, we examined DNA methylation differences in leukocyte DNA between PaC cases and controls in a two-phase study. In phase I, we measured methylation levels at 1,505 CpG sites in treatment-naïve leukocyte DNA from 132 never-smoker PaC patients and 60 never-smoker healthy controls. We found significant differences in 110 CpG sites (false discovery rate <0.05). In phase II, we tested and validated 88 of 96 phase I selected CpG sites in 240 PaC cases and 240 matched controls (p≤0.05). Using penalized logistic regression, we built a prediction model consisting of five CpG sites (IL10_P348, LCN2_P86, ZAP70_P220, AIM2_P624, TAL1_P817) that discriminated PaC patients from controls (C-statistic = 0.85 in phase I; 0.76 in phase II). Interestingly, one CpG site (LCN2_P86) alone could discriminate resectable patients from controls (C-statistic= 0.78 in phase I; 0.74 in phase II). We also performed methylation quantitative trait loci (methQTL) analysis and identified three CpG sites (AGXT_P180_F, ALOX12_E85_R, JAK3_P1075_R) where the methylation levels were significantly associated with single nucleotide polymorphisms (SNPs) (false discovery rate <0.05). Our results demonstrate that epigenetic variation in easily obtainable leukocyte DNA, manifested by reproducible methylation differences, may be used to detect PaC patients. The methylation differences at certain CpG sites are partially attributable to genetic variation. This study strongly supports future epigenome-wide association study using leukocyte DNA for biomarker discovery in human diseases.

6 Article Prevalence of CDKN2A mutations in pancreatic cancer patients: implications for genetic counseling. 2011

McWilliams, Robert R / Wieben, Eric D / Rabe, Kari G / Pedersen, Katrina S / Wu, Yanhong / Sicotte, Hugues / Petersen, Gloria M. ·Department of Oncology, Mayo Clinic, Rochester, MN, USA. mcwilliams.robert@mayo.edu ·Eur J Hum Genet · Pubmed #21150883.

ABSTRACT: Germline mutations in CDKN2A have been reported in pancreatic cancer families, but genetic counseling for pancreatic cancer risk has been limited by lack of information on CDKN2A mutation carriers outside of selected pancreatic or melanoma kindreds. Lymphocyte DNA from consecutive, unselected white non-Hispanic patients with pancreatic adenocarcinoma was used to sequence CDKN2A. Frequencies of mutations that alter the coding of p16INK4 or p14ARF were quantified overall and in subgroups. Penetrance and likelihood of carrying mutations by family history were estimated. Among 1537 cases, 9 (0.6%) carried germline mutations in CDKN2A, including three previously unreported mutations. CDKN2A mutation carriers were more likely to have a family history of pancreatic cancer (P=0.003) or melanoma (P=0.03), and a personal history of melanoma (P=0.01). Among cases who reported having a first-degree relative with pancreatic cancer or melanoma, the carrier proportions were 3.3 and 5.3%, respectively. Penetrance for mutation carriers by age 80 was calculated to be 58% for pancreatic cancer (95% confidence interval (CI) 8-86%), and 39% for melanoma (95% CI 0-80). Among cases who ever smoked cigarettes, the risk for pancreatic cancer was higher for carriers compared with non-carriers (HR 25.8, P=2.1 × 10⁻¹³), but among nonsmokers, this comparison did not reach statistical significance. Germline mutations in CDKN2A among unselected pancreatic cancer patients are uncommon, although notably penetrant, especially among smokers. Carriers of germline mutations of CDKN2A should be counseled to avoid tobacco use to decrease risk of pancreatic cancer in addition to taking measures to decrease melanoma risk.