• 한국간담췌외과학회지
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• 제26권1호
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• pp.91-97
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• 2022

Backgrounds/Aims: Metastatic lesions of the pancreas (PMET) account for 1%-5% of all malignant solid pancreatic lesions (SPL). In this study we evaluated the utility of endoscopic ultrasonography with fine needle aspiration (EUS-FNA) in diagnosing PMET. Methods: Patients who underwent EUS-FNA at a community referral center between 2011-2017 for SPL were identified. Clinical, radiologic, and EUS-FNA features of those with PMET were compared to those with primary solid tumors of the pancreas: pancreatic adenocarcinoma (PDAC) and neuroendocrine tumors (PNET). Results: A total of 191 patients were diagnosed with solid pancreatic malignancy using EUS-FNA: 156 PDAC, 27 PNET, and eight (4.2%) had PMET. Patients with PMET were less likely to have abdominal pain (25.0% vs. 76.3% vs. 48.2%; p < 0.01) or obstructive jaundice (37.5% vs. 58.3% vs. 0%; p < 0.01) compared to PDAC and PNET. Those with PMET were more likely to have mass lesions with/without biliary or pancreatic ductal dilatations (100% vs. 86.5% vs. 85.2%; p < 0.01) and lower CA19-9 (82.5 ± 43.21 U/mL vs. 4,639.30 ± 11,489.68 U/mL vs. 10.50 ± 10.89 U/mL; p < 0.01) compared to PDAC and PNET. Endosonographic features were similar among all groups. Seven (87.5%) patients with PMET had a personal history of malignancy prior to PMET diagnosis. The primary malignancy was renal cell carcinoma in five PMET. Conclusions: PMET are exceedingly rare, comprising less than 5% of SLP. Patients with PMET are less likely to present with symptoms and mostly identified by surveillance imaging for the primary malignancy.

• Asian Pacific Journal of Cancer Prevention
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• 제16권1호
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• pp.373-376
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• 2015

Background: EVA1A (eva-1 homolog A) is a novel gene that regulates programmed cell death through autophagy and apoptosis. Our objective was to investigate the expression profiles and potential role of EVA1A in normal and neoplastic human pancreatic tissues. Materials and Methods: The expression pattern of EVA1A in normal pancreatic tissue was examined by indirect immunofluorescence and confocal microscopy. Protein levels in paraffin-embedded specimens from normal and diseased pancreatic and matched non-tumor tissues were evaluated by immunohistochemistry. Results: EVA1A colocalized with glucagon but not with insulin, demonstrating production in islet alpha cells. Itwas strongly expressed in chronic pancreatitis, moderately or weakly expressed in the plasma membrane and cytoplasm in pancreatic acinar cell carcinoma, and absent in normal pancreatic acinar cells. Although the tissue architecture was deformed, EVA1A was absent in the alpha cells of pancreatic ductal adenocarcinomas, intraductal papillary mucinous neoplasms, mucinous cystadenomas, solid papillary tumors and pancreatic neuroendocrine tumors. Conclusions: EVA1A protein is specifically expressed in islet alpha cells, suggesting it may play an important role in regulating alpha-cell function. The ectopic expression of EVA1A in pancreatic neoplasms may contribute to their pathogenesis and warrants further investigation.

• Journal of Gynecologic Oncology
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• 제29권6호
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• pp.90.1-90.12
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• 2018

Objective: We performed small-scale mutation and large genomic rearrangement (LGR) analysis of BRCA1/2 in ovarian cancer patients to determine the prevalence and the characteristics of the mutations. Methods: All ovarian cancer patients who visited a single institution between September 2015 and April 2017 were included. Sanger sequencing, multiplex ligation-dependent probe amplification (MLPA), and long-range polymerase chain reaction (PCR) were performed to comprehensively study BRCA1/2. The genetic risk models BRCAPRO, Myriad, and BOADICEA were used to evaluate the mutation analysis. Results: In total, 131 patients were enrolled. Of the 131 patients, Sanger sequencing identified 16 different BRCA1/2 small-scale mutations in 20 patients (15.3%). Two novel nonsense mutations were detected in 2 patients with a serous borderline tumor and a large-cell neuroendocrine carcinoma. MLPA analysis of BRCA1/2 in Sanger-negative patients revealed 2 LGRs. The LGRs accounted for 14.3% of all identified BRCA1 mutations, and the prevalence of LGRs identified in this study was 1.8% in 111 Sanger-negative patients. The genetic risk models showed statistically significant differences between mutation carriers and non-carriers. The 2 patients with LGRs had at least one blood relative with breast or ovarian cancer. Conclusion: Twenty-two (16.8%) of the unselected ovarian cancer patients had BRCA1/2 mutations that were detected through comprehensive BRCA1/2 genetic testing. Ovarian cancer patients with Sanger-negative results should be considered for LGR detection if they have one blood relative with breast or ovarian cancer. The detection of more BRCA1/2 mutations in patients is important for efforts to provide targeted therapy to ovarian cancer patients.