A5090099699- Genetic factors in colorectal cancer
- Glioma Diagnosis and Treatment
- Cancer Genomics and Diagnostics
- Pancreatic and Hepatic Oncology Research
- Esophageal Cancer Research and Treatment
- Inflammatory Bowel Disease
- Gastric Cancer Management and Outcomes
- Colorectal Cancer Screening and Detection
- Esophageal and GI Pathology
- Colorectal Cancer Treatments and Studies
- Pancreatitis Pathology and Treatment
- Helicobacter pylori-related gastroenterology studies
- Gastroesophageal reflux and treatments
- Microscopic Colitis
- Gastrointestinal disorders and treatments
- Gastrointestinal Tumor Research and Treatment
- Gut microbiota and health
- Eosinophilic Esophagitis
- Liver Disease Diagnosis and Treatment
- Cancer-related molecular mechanisms research
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Telomeres, Telomerase, and Senescence
- Hepatitis C virus research
- Molecular Biology Techniques and Applications
- Diverticular Disease and Complications
University of Utah
2015-2024
Huntsman Cancer Institute
2015-2024
ARUP Laboratories (United States)
2012-2023
ARUP Institute for Clinical and Experimental Pathology
2013-2020
Cleveland Clinic
2004-2017
London Health Sciences Centre
2015
Molecular Oncology (United States)
2014
University of Washington
1997-2011
University College London
2011
Royal London Hospital
2011
Barrett's esophagus, a condition of intestinal metaplasia the is associated with an increased risk esophageal adenocarcinoma. We assessed whether endoscopic radiofrequency ablation could eradicate dysplastic esophagus and decrease rate neoplastic progression.
Malignant tumors shed DNA into the circulation. The transient half-life of circulating tumor (ctDNA) may afford opportunity to diagnose, monitor recurrence, and evaluate response therapy solely through a non-invasive blood draw. However, detecting ctDNA against normally occurring background cell-free derived from healthy cells has proven challenging, particularly in non-metastatic solid tumors. In this study, distinct differences fragment length size between ctDNAs normal are defined. Human...
Background: Patients with ulcerative colitis and primary sclerosing cholangitis are at high risk for colonic dysplasia cancer. This approaches 50% after 25 years of colitis. Ursodiol has been shown to protect against development colorectal neoplasia in animal models. Objective: To assess the relationship between ursodiol use dysplasia, precursor colon cancer, patients cholangitis. Design: Cross-sectional study. Setting: University medical center. Patients: 59 who were undergoing colonoscopic...
Background: Pancreatic cancer, the fourth most common cause of cancer death in United States, is hereditary an estimated 10% cases. Surveillance patients with a familial predisposition for pancreatic has not been systematically evaluated. Objective: To develop surveillance program that can identify and treat who have precancerous conditions pancreas family history cancer. Design: Prospective cohort study. Setting: University medical center. Patients: 14 from three kindreds Interventions:...
Background Pancreatic cancer is a deadly disease. Discovery of the mutated genes that cause inherited form(s) disease may shed light on mechanism(s) oncogenesis. Previously we isolated susceptibility locus for familial pancreatic to chromosome location 4q32–34. In this study, our goal was discover identity gene 4q32 and determine function gene. Methods Findings A customized microarray candidate chromosomal region affecting revealed greatest expression change in palladin (PALLD), encodes...
The effective treatment of pancreatic cancer relies on the diagnosis disease at an early stage, a difficult challenge. One major obstacle in development diagnostic biomarkers has been dual expression potential both chronic pancreatitis and cancer. To better understand limitations protein biomarkers, we used ICAT technology tandem mass spectrometry-based proteomics to systematically study pancreatitis. Among 116 differentially expressed proteins identified pancreatitis, most biological...
Understanding the initiation and progression of pancreatic ductal adenocarcinoma (PDAC) may provide therapeutic strategies for this deadly disease. Recently, we others made surprising finding that PDAC its preinvasive precursors, intraepithelial neoplasia (PanIN), arise via reprogramming mature acinar cells. We therefore hypothesized master regulator differentiation, PTF1A, could play a central role in suppressing initiation. In study, demonstrate PTF1A expression is lost both mouse human...
Endoscopic ultrasound (EUS) and hormone-stimulated pancreatic function tests are considered useful, possibly complementary, in the diagnosis of early chronic pancreatitis (CP). Few past studies have compared either methods with a histological gold standard. The aims were to assess correlations EUS score endoscopic test (ePFT) results degree fibrosis, as well sensitivity each method for detecting fibrosis.This was retrospective study patients who underwent EUS, ePFT, or both within 12 months...
Abstract Inflammation plays a role in the progression to cancer and it is linked presence of senescent cells. Ulcerative colitis (UC) chronic inflammatory disease that predisposes colorectal cancer. Tumorigenesis this setting associated with telomere shortening can be observed nondysplastic epithelium UC patients high-grade dysplasia (HGD) or (UC progressors). We hypothesized preneoplastic field inflammation, shortening, senescence underlies tumor progressors. Multiple biopsies varying...
Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal cancers largely due to disseminated disease at time presentation. Here, we investigated role and mechanism action metastasis-associated protein anterior gradient 2 (AGR2) in pathogenesis pancreatic cancer. AGR2 was induced all sporadic familial intraepithelial precursor lesions (PanIN), PDACs, circulating tumor cells, metastases studied. Confocal microscopy flow cytometric analyses indicated that localized endoplasmic...
Abstract Background When interpreting sequencing data from multiple spatial or longitudinal biopsies, detecting sample mix-ups is essential, yet more difficult than in studies of germline variation. In most genomic tumors, genetic variation detected through pairwise comparisons the tumor and a matched normal tissue donor. many cases, only somatic variants are reported, which hinders use existing tools that detect swaps solely based on genotypes inherited variants. To address this problem, we...