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Results: 1 to 10 of 230

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Surveillance of Gastric Intestinal Metaplasia.
Shah SC, Gawron AJ, Li D
(2020) Am J Gastroenterol 115: 641-644
MeSH Terms: Cause of Death, Gastric Mucosa, Global Health, Humans, Morbidity, Patient Selection, Population Surveillance, Precancerous Conditions, Risk Assessment, Stomach Neoplasms, Survival Rate
Added March 3, 2020
0 Communities
1 Members
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11 MeSH Terms
Spotlight: Gastric Intestinal Metaplasia.
Shah SC, Gupta S, Li D, Morgan D, Mustafa RA, Gawron AJ
(2020) Gastroenterology 158: 704
MeSH Terms: Algorithms, Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Population Surveillance, Practice Guidelines as Topic, Precancerous Conditions, Risk Factors, Stomach Neoplasms
Added March 3, 2020
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13 MeSH Terms
Histologic Subtyping of Gastric Intestinal Metaplasia: Overview and Considerations for Clinical Practice.
Shah SC, Gawron AJ, Mustafa RA, Piazuelo MB
(2020) Gastroenterology 158: 745-750
MeSH Terms: Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Health Knowledge, Attitudes, Practice, Humans, Metaplasia, Population Surveillance, Precancerous Conditions, Stomach Neoplasms
Added March 3, 2020
0 Communities
1 Members
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9 MeSH Terms
Advancing the Science in Gastric Pre-Neoplasia: Study Design Considerations.
Davitkov P, Altayar O, Shah SC, Gawron AJ, Mustafa RA, Sultan S, Morgan DR
(2020) Gastroenterology 158: 751-759
MeSH Terms: Biomedical Research, Biopsy, Endoscopy, Gastrointestinal, Gastric Mucosa, Humans, Incidence, Metaplasia, Population Surveillance, Precancerous Conditions, Prevalence, Research Design, Risk Factors, Stomach Neoplasms
Added March 3, 2020
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1 Members
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13 MeSH Terms
AGA Technical Review on Gastric Intestinal Metaplasia-Epidemiology and Risk Factors.
Altayar O, Davitkov P, Shah SC, Gawron AJ, Morgan DR, Turner K, Mustafa RA
(2020) Gastroenterology 158: 732-744.e16
MeSH Terms: Ethnic Groups, European Continental Ancestry Group, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Precancerous Conditions, Risk Factors, Stomach Neoplasms, United States
Added March 3, 2020
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1 Members
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11 MeSH Terms
AGA Technical Review on Gastric Intestinal Metaplasia-Natural History and Clinical Outcomes.
Gawron AJ, Shah SC, Altayar O, Davitkov P, Morgan D, Turner K, Mustafa RA
(2020) Gastroenterology 158: 705-731.e5
MeSH Terms: Biopsy, Disease Progression, Endoscopy, Gastrointestinal, Gastric Mucosa, Helicobacter Infections, Helicobacter pylori, Humans, Metaplasia, Population Surveillance, Precancerous Conditions, Prevalence, Risk Factors, Stomach Neoplasms, United States
Added March 3, 2020
0 Communities
1 Members
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14 MeSH Terms
Targeted mobilization of Lrig1 gastric epithelial stem cell populations by a carcinogenic type IV secretion system.
Wroblewski LE, Choi E, Petersen C, Delgado AG, Piazuelo MB, Romero-Gallo J, Lantz TL, Zavros Y, Coffey RJ, Goldenring JR, Zemper AE, Peek RM
(2019) Proc Natl Acad Sci U S A 116: 19652-19658
MeSH Terms: Adenocarcinoma, Animals, Carcinogenesis, Disease Models, Animal, Epithelial Cells, Female, Gastric Mucosa, Gastritis, Helicobacter Infections, Helicobacter pylori, Humans, Male, Membrane Glycoproteins, Mice, Mice, Knockout, Nerve Tissue Proteins, Precancerous Conditions, Primary Cell Culture, Risk Factors, Stem Cells, Stomach, Stomach Neoplasms, Type IV Secretion Systems
Show Abstract · Added September 27, 2019
-induced gastritis is the strongest risk factor for gastric adenocarcinoma, a malignancy preceded by a series of well-defined histological stages, including metaplasia. One microbial constituent that augments cancer risk is the type 4 secretion system (T4SS), which translocates the oncoprotein CagA into host cells. Aberrant stem cell activation is linked to carcinogenesis, and Lrig1 (leucine-rich repeats and Ig-like domains 1) marks a distinct population of progenitor cells. We investigated whether microbial effectors with carcinogenic potential influence Lrig1 progenitor cells ex vivo and via lineage expansion within -infected gastric mucosa. Lineage tracing was induced in (Lrig1/YFP) mice that were uninfected or subsequently infected with or an isogenic mutant (nonfunctional T4SS). In contrast to infection with wild-type (WT) for 2 wk, infection for 8 wk resulted in significantly increased inflammation and proliferation in the corpus and antrum compared with uninfected or mice infected with the mutant. WT -infected mice harbored significantly higher numbers of Lrig1/YFP epithelial cells that coexpressed UEA1 (surface cell marker). The number of cells coexpressing intrinsic factor (chief cell marker), YFP (lineage marker), and GSII lectin (spasmolytic polypeptide-expressing metaplasia marker) were increased only by WT In human samples, Lrig1 expression was significantly increased in lesions with premalignant potential compared with normal mucosa or nonatrophic gastritis. In conclusion, chronic infection stimulates Lrig1-expressing progenitor cells in a -dependent manner, and these reprogrammed cells give rise to a full spectrum of differentiated cells.
1 Communities
1 Members
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23 MeSH Terms
Nicotinic treatment of post-chemotherapy subjective cognitive impairment: a pilot study.
Vega JN, Albert KM, Mayer IA, Taylor WD, Newhouse PA
(2019) J Cancer Surviv 13: 673-686
MeSH Terms: Adult, Aged, Aged, 80 and over, Antineoplastic Combined Chemotherapy Protocols, Cancer Survivors, Cognition, Cognitive Dysfunction, Female, Humans, Male, Middle Aged, Neoplasms, Nicotine, Pilot Projects, Quality of Life, Self Report, Survivors, Transdermal Patch
Show Abstract · Added March 3, 2020
PURPOSE - Persistent chemotherapy-related cognitive impairment (pCRCI) is commonly reported following cancer treatment and negatively affects quality of life; however, there is currently no pharmacological treatment indicated for pCRCI. This pilot study obtained preliminary data regarding the use of transdermal nicotine patches as a therapeutic strategy for women with pCRCI to (1) reduce subjective cognitive complaints and (2) enhance objective cognitive performance in breast, colon, lymphoma, or ovarian cancer survivors with pCRCI.
METHODS - Participants were randomized to either placebo (n = 11) or transdermal nicotine (n = 11) for 6 weeks, followed by 2 weeks of treatment withdrawal for a total of 8 weeks. Participants were assessed using both subjective and objective measures of cognitive functioning at five visits before, during, and after treatment.
RESULTS - Over the course of the study, women in both groups improved substantially in severity of self-reported cognitive complaints measured by Functional Assessment of Cancer Therapy-Cognitive Function Perceived Cognitive Impairments regardless of treatment arm. Additionally, objective cognitive performance measures improved in both groups; however, there was no significant difference in improvement between groups.
CONCLUSIONS - Due to a large placebo response, we were unable to determine if a drug effect was present. However, we did observe substantial improvement in self-reported cognitive symptoms, likely resulting from factors related to participation in the trial rather than specific drug treatment effects.
TRIAL REGISTRATION - The study was registered with clinicaltrials.gov (trial registration: NCT02312943).
IMPLICATIONS FOR CANCER SURVIVORS - These results suggest that women with pCRCI can exhibit improvement in subjective cognition, with attention paid to symptoms and close follow-up over a short period of time.
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18 MeSH Terms
Differential Cell Susceptibilities to Kras in the Setting of Obstructive Chronic Pancreatitis.
Shi C, Pan FC, Kim JN, Washington MK, Padmanabhan C, Meyer CT, Kopp JL, Sander M, Gannon M, Beauchamp RD, Wright CV, Means AL
(2019) Cell Mol Gastroenterol Hepatol 8: 579-594
MeSH Terms: Acinar Cells, Animals, Carcinogenesis, Carcinoma, Pancreatic Ductal, Cell Transformation, Neoplastic, Disease Models, Animal, Genes, ras, Metaplasia, Mice, Mutation, Pancreatic Neoplasms, Pancreatitis, Chronic, Precancerous Conditions, Proto-Oncogene Proteins p21(ras), Signal Transduction
Show Abstract · Added August 6, 2019
BACKGROUND & AIMS - Activating mutation of the KRAS gene is common in some cancers, such as pancreatic cancer, but rare in other cancers. Chronic pancreatitis is a predisposing condition for pancreatic ductal adenocarcinoma (PDAC), but how it synergizes with KRAS mutation is not known.
METHODS - We used a mouse model to express an activating mutation of Kras in conjunction with obstruction of the main pancreatic duct to recapitulate a common etiology of human chronic pancreatitis. Because the cell of origin of PDAC is not clear, Kras mutation was introduced into either duct cells or acinar cells.
RESULTS - Although Kras expression in both cell types was protective against damage-associated cell death, chronic pancreatitis induced p53, p21, and growth arrest only in acinar-derived cells. Mutant duct cells did not elevate p53 or p21 expression and exhibited increased proliferation driving the appearance of PDAC over time.
CONCLUSIONS - One mechanism by which tissues may be susceptible or resistant to KRAS-initiated tumorigenesis is whether they undergo a p53-mediated damage response. In summary, we have uncovered a mechanism by which inflammation and intrinsic cellular programming synergize for the development of PDAC.
Copyright © 2019 The Authors. Published by Elsevier Inc. All rights reserved.
2 Communities
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15 MeSH Terms
Management of Inflammatory Bowel Disease-Associated Dysplasia in the Modern Era.
Shah SC, Itzkowitz SH
(2019) Gastrointest Endosc Clin N Am 29: 531-548
MeSH Terms: Colorectal Neoplasms, Disease Management, Humans, Hyperplasia, Inflammatory Bowel Diseases, Intestines, Precancerous Conditions, Quality of Life, Risk Factors
Show Abstract · Added March 3, 2020
This article begins with a brief overview of risk factors for colorectal neoplasia in inflammatory bowel disease to concretize the approach to risk stratification. It then provides an up-to-date review of diagnosis and management of dysplasia in inflammatory bowel disease, which integrates new and emerging data in the field. This is particularly relevant in an era of increased attention to cost- and resource-containment from the health systems vantage point, coupled with a heightened prioritization of patient quality of life and shared decision-making. Also provided is a brief discussion of the status of newer therapeutic techniques, such as endoscopic submucosal dissection.
Copyright © 2019 Elsevier Inc. All rights reserved.
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MeSH Terms