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Transgastric repair of transfixing gastroesophageal junction gunshot wound: video case report.

ABSTRACT: Managing traumatic injuries of the gastroesophageal junction (GEJ) is infrequent due to associated lesions of adjacent highly vascularized organs. Its anatomical localization in the upper abdomen makes the repair challenging to perform. A stable 23-year-old male was presented at the emergency department with two thorax gunshot wounds. Computed tomography revealed air in the periesophageal space and right hemopneumothorax with no injury of the major vessels. A chest tube was placed and the patient was transferred hemodynamically stable to the operating. Abdominal exploration identified injuries to the left diaphragm; liver lateral segment; 1-cm transfixing perforation of the GEJ and right diaphragmatic pillar. Primary repair of the GEJ was performed and patched with a partial fundoplication. The diaphragm was repaired and the liver bleeding controlled. Finally, drains and a feeding jejunostomy were placed. The patient had an uneventful early postoperative course and was discharged home on the 12th postoperative day.

SUBMITTER: Vela J

PROVIDER: S-EPMC8140550 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BACKGROUND:Carcinomas composed predominantly or purely of malignant Paneth cells were rarely reported in gastrointestinal system. They have not been reported at gastroesophageal junction nor has the association with Barrett esophagus been explored. None of the previous studies has mentioned any peculiar histologic features other than typical adenocarcinoma containing neoplastic Paneth cells. The Her2/neu status and the expression of beta-catenin in Paneth cell carcinoma at gastroesophageal junction have not been studied although the activated beta-catenin pathway was recently demonstrated in neoplastic Paneth cells in colon. CASE PRESENTATION:A 70-year-old Caucasian male who initially presented in the emergency room due to upper gastrointestinal bleeding was subsequently found to have a submucosal nodule at gastroesophageal junction. A diagnosis of adenocarcinoma was rendered on biopsy. Histologic examination of the subsequent endoscopic mucosal resection revealed an adenocarcinoma with various levels of differentiation which are zonally distributed. The deeper portion of the tumor showed well-differentiated bland-appearing glands with extensive cystic and secretory changes. The cytoplasm of tumor cells and secretion demonstrated marked reactivity with lysozyme antibody on immunohistochemical stain. The tumor had a peculiar Her2/neu staining pattern with cytoplasmic and nuclear stain in poorly-differentiated area and no stain in well-differentiated area. Only membranous stain was detected with beta-catenin antibody. CONCLUSION:We reported the first case of Paneth cell carcinoma at gastroesophageal junction. The tumor had well-differentiated area which, when sampled in small biopsies, can mimic benign lesions including those related to proton pump inhibitor therapy. Lysozyme immunohistochemical stain may be helpful when difficulty in diagnosis arises. Her-2/neu was negative but showed a distinct staining pattern. In contrast to neoplastic Paneth cells in colon, beta-catenin pathway did not seem to be activated. More studies are needed for the etiology, pathogenesis, clinical course, prognosis and treatment of Paneth cell carcinoma.

Project description:ObjectiveEsophageal adenocarcinoma (EAC) continues to be a disease associated with high mortality. Among the factors leading to poor outcomes are innate resistance to currently available therapies, advanced stage at diagnosis, and complex biology. Platinum and ionizing radiation form the backbone of treatment for the majority of patients with EAC. Of the multiple processes involved in response to platinum chemotherapy or ionizing radiation, deoxyribonucleic acid (DNA) repair has been a major player in cancer sensitivity to these agents. DNA repair defects have been described in various malignancies. The purpose of this study was to determine whether alterations in DNA repair are present in EAC compared with normal gastroesophageal tissues.MethodsWe analyzed the expression of genes involved in homologous recombination (HR), nonhomologous end-joining, and nucleotide excision repair (NER) pathways in 12 EAC tumor samples with their matched normal counterparts. These pathways were chosen because they are the main pathways involved in the repair of platinum- or ionizing-radiation-induced damage. In addition, abnormalities in these pathways have not been well characterized in EAC.ResultsWe identified increased expression of at least one HR gene in eight of the EAC tumor samples. Alterations in the expression of EME1, a structure-specific endonuclease involved in HR, were the most prevalent, with messenger (m)RNA overexpression in six of the EAC samples. In addition, all EAC samples revealed decreased expression of at least one of numerous NER genes including XPC, XPA, DDB2, XPF, and XPG.ConclusionOur study identified DNA repair dysregulation in EAC involving two critical pathways, HR and NER, and is the first demonstration of EME1 upregulation in any cancer. These DNA repair abnormalities have the potential to affect a number of processes such as genomic instability and therapy response, and the consequences of these defects deserve further study in EAC.

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Transgastric repair of transfixing gastroesophageal junction gunshot wound: video case report.

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