Publications by authors named "Eric M Montminy"

Introduction: Iatrogenic esophageal perforation (IEP) is a severe adverse event (AE) of upper endoscopy procedures (UEPs) associated with morbidity. Management has shifted from surgery to endotherapy with clip closure (CC), self-expanding metal stent (SEMS), and vacuum therapy (VT). Limited analyses measure outcomes during contemporary interventional endoscopy periods.

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Background: Carcinoids, frequently classified as "colorectal cancer" contribute to rising early-onset colorectal cancer (EOCRC) incidence rates (IR) and have distinct staging distributions compared to often advanced stage adenocarcinomas (screening target). Thus, assessing temporal shifts in early-onset distant stage adenocarcinoma can impact public health.

Methods: 2000-2016 Surveillance Epidemiology and End Results (SEER) 18 yearly adenocarcinoma IRs were stratified by stage (, localized, regional, distant), age (20-29, 30-39, 40-49, 50-54-year-olds), subsite (colorectal, rectal-only, colon-only), and race [non-Hispanic whites, non-Hispanic Blacks (NHB), Hispanics] in 103,975 patients.

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Importance: Early-onset colorectal cancer incidence rates are rising faster in White individuals than Black individuals. However, prior National Cancer Institute Surveillance, Epidemiology, and End Results (SEER) racial stratification analyses used smaller SEER 13 databases, combined patients under age 50 years, did not stratify by sex, and did not focus on adenocarcinoma histologic subtypes (screening target).

Objective: To perform a race- and sex-stratified adenocarcinoma incidence rate analysis in individuals aged 40 to 49 years using larger SEER 18 databases with expanded race data to better understand the colorectal cancer burden in those at or approaching screening age.

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Background: Early-onset colorectal cancer (EOCRC) incidence rates (IRs) are rising, according to previous cancer registry analyses. However, analysis of histologic subtypes, including adenocarcinoma (the focus of CRC screening and diagnostic testing) and carcinoid tumors (which are classified as "colorectal cancer" in SEER [Surveillance, Epidemiology, and End Results] databases but have a distinct pathogenesis and are managed differently from adenocarcinoma), has not been reported.

Objective: To assess EOCRC IRs and changes in IRs over time, stratified by histology.

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Colorectal cancer screening is essential to detect and remove premalignant lesions to prevent the development of colorectal cancer. Multiple screening modalities are available, including colonoscopy and stool-based testing. Colonoscopy remains the gold standard for detection and removal of premalignant colorectal lesions.

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The United States has seen progress with colorectal cancer with both falling incidence and mortality rates. Factoring into this decline, the significance of early detection and removal of precancerous lesions through screening must be underscored. With the advancement of screening modalities, attention has been directed towards optimizing the quality of screening and detecting adenomas.

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Here we report a patient diagnosed with small cell lung cancer after first presenting with parathyroid hormone-related peptide-induced hypercalcemic pancreatitis and developed walled-off necrosis that resulted in disruption of the main pancreatic duct. Disconnected duct syndrome (DDS) is a rare syndrome that occurs when the main pancreatic duct exocrine flow is disrupted resulting in leakage of pancreatic enzymes and further inflammatory sequela. To date, no prior reports have described DDS occurring with paraneoplastic reactions.

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Background: Dilated cardiomoypathies (DCM) are a heterogeneous group of inherited and acquired diseases characterized by decreased contractility and enlargement of cardiac chambers and a major cause of morbidity and mortality. Mice with Glu54Lys mutation in α-tropomyosin (Tm54) demonstrate typical DCM phenotype with reduced myofilament Ca2+ sensitivity. We tested the hypothesis that early sensitization of the myofilaments to Ca2+ in DCM can prevent the DCM phenotype.

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Background: Hypertrophic cardiomyopathy (HCM) is a common genetic disorder caused mainly by mutations in sarcomeric proteins and is characterized by maladaptive myocardial hypertrophy, diastolic heart failure, increased myofilament Ca(2+) sensitivity, and high susceptibility to sudden death. We tested the following hypothesis: correction of the increased myofilament sensitivity can delay or prevent the development of the HCM phenotype.

Methods And Results: We used an HCM mouse model with an E180G mutation in α-tropomyosin (Tm180) that demonstrates increased myofilament Ca(2+) sensitivity, severe hypertrophy, and diastolic dysfunction.

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