Publications by authors named "J Mendelin"

Distinguishing Barrett esophagus with high-grade dysplasia (BE-HGD) from intramucosal and submucosal adenocarcinomas on biopsies is challenging, yet important, in the choice of therapy. The current study evaluates preresection biopsies from patients who underwent esophagectomy for at least BE-HGD, to compare the recently published histologic categories by the University of Michigan (UM) and Cleveland Clinic (CC), correlate preresection and final resection diagnosis, and identify histologic features in biopsies that might be predictive of adenocarcinoma on esophagectomy. A total of 112 cases with a consensus biopsy diagnosis (agreement by ≥4 of 7 gastrointestinal pathologists) were statistically analyzed to identify histologic features that predicted adenocarcinoma on resection.

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Objective: Grading Barrett's dysplasia at the lower end of the metaplasia-dysplasia spectrum (negative, indefinite, and low-grade dysplasia) suffers from poor interobserver agreement, even among gastrointestinal pathologists. Data evaluating interobserver agreement in Barrett's mucosal biopsies with changes at the upper end of the dysplasia spectrum (high-grade dysplasia, intramucosal, and submucosal adenocarcinoma) have not been published. The accurate categorization of pretreatment biopsies drives therapeutic decision making, but if the diagnostic distinction between cancer and high-grade dysplasia in Barrett's biopsies is inconsistent, then the use of these diagnoses to make management decisions is suspect.

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Barrett's esophagus (BE) is a complication of chronic reflux that results in the replacement of esophageal squamous epithelium with columnar epithelium. BE is endoscopically recognized and pathologically confirmed. The presence of goblet cells is diagnostic.

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Identification of inheritable mutations associated with the development of malignancy has led to prophylactic surgeries to remove tissues at risk. We report seven unrelated patients with family histories of breast and/or ovarian cancer, five of whom underwent prophylactic salpingo-oophorectomy with hysterectomy. Four had proven BRCA-1 or -2 mutations.

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Formalin-fixed, paraffin-embedded sections from 28 cases of ductal carcinoma in situ (DCIS; 12 with coexisting invasive neoplasm) were analyzed for numerical alterations of chromosomes 7, 8, 16, and 17 by performing fluorescence in situ hybridization (FISH) using centromeric (alpha-satellite) probes. Based on signal counts in 200 to 300 nuclei, each hybridization was classified as disomic (copy loss in <40%, copy gain in < 10%), monosomic (copy loss in at least 50% of nuclei, partial if 40% to 49%) or trisomic/polysomic (copy gain in at least 20% of nuclei, partial if 10% to 19%). Grade I lesions were characterized by complete lack of significant chromosome gain, but 29% showed partial (focal) monosomy.

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