1.A Case of Large Cell Neuroendocrine Carcinoma of the Colon.
Hi Gu KIM ; Jung Il LEE ; Seok JEONG ; Jin Woo LEE ; Kye Sook KWON ; Hyung Gil KIM ; Yong Woon SHIN ; Lucia KIM
The Korean Journal of Gastroenterology 2009;54(1):46-49
Neuroendocrine carcinoma of the colon can be classified into small cell carcinoma and large cell neuroendocrine carcinoma. The incidence of neuroendocrine carcinoma is so low that the guideline for the treatment of large cell neuroendocrine carcinoma of the colon are not established. The prognosis of large cell neuroendocrine carcinoma of the colon is worse than that of conventional adenocarcinoma of the colon. We report a case of large cell neuroendocrine carcinoma of the colon that treated with right hemicolectomy and 6th sequential combination chemotherapy of 5-fluorouracil and cisplatin. There has been no evidence of the recurrence or metastasis of tumor for 6 months.
Adult
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Carcinoma, Large Cell/*diagnosis/pathology/radiography
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Carcinoma, Neuroendocrine/*diagnosis/pathology/radiography
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Colonic Neoplasms/*diagnosis/pathology/radiography
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Colonoscopy
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Humans
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Male
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Tomography, X-Ray Computed
2.Primary Large Cell Neuroendocrine Carcinoma of the Breast: Radiologic and Pathologic Findings.
Jin Woo KIM ; Ok Hee WOO ; Kyu Ran CHO ; Bo Kyung SEO ; Hwan Seok YONG ; Aeree KIM ; Eun Young KANG
Journal of Korean Medical Science 2008;23(6):1118-1120
Some breast neoplasms are classified as primary neuroendocrine carcinomas because they are positive for neuroendocrine markers. Although neuroendocrine carcinomas can originate from various organs of the body, primary neuroendocrine carcinomas of the breast are extremely rare. The diagnosis of primary neuroendocrine carcinoma of the breast can only be made if nonmammary sites are confidently excluded or if an in situ component can be found. Here we report a primary large-cell neuroendocrine carcinoma (LCNL) involving the left breast. Breast ultrasonography revealed a lobulated, heterogeneous, low-echoic mass in the left breast, and the lesion ap-peared as a well-defined, highly-enhancing mass on a chest computed tomography scan. Ultrasound-guided core needle biopsy was performed on the mass, and primary LCNC was confirmed by histopathologic examination.
Adult
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Breast Neoplasms/*diagnosis/pathology/ultrasonography
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Carcinoma, Large Cell/*diagnosis/pathology/radiography
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Carcinoma, Neuroendocrine/*diagnosis/pathology/radiography
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Diagnosis, Differential
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Female
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Humans
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Tomography, X-Ray Computed
3.The Expression of p53, p16, Cyclin D1 in Esophageal Squamous Cell Carcinoma and Esophageal Dysplasia.
Sang Gyune KIM ; Su Jin HONG ; Kye Won KWON ; Sung Won JUNG ; Whan Yeol KIM ; In Seop JUNG ; Bong Min KO ; Chang Beom RYU ; Young Seok KIM ; Jong Ho MOON ; Jin Oh KIM ; Joo Young CHO ; Joon Seong LEE ; Moon Sung LEE ; Chan Sup SHIM ; Boo Sung KIM
The Korean Journal of Gastroenterology 2006;48(4):269-276
BACKGROUND/AIMS: p53 is known to play a central role in sensing and signaling for the growth arrest and apoptosis in cells with DNA damage. Mutation of p53 is a frequent event in esophageal squamous cell carcinoma (ESCC). p16 protein binds to cyclin dependent kinase 4 (CDK4) inhibiting the ability of CDK4 to interact with cyclin D1, and stimulates the passage through the G1 phase of cell cycle. We observed the expression patterns and frequencies of p53, p16, and cyclin D1 in esophageal dysplasia and in esophageal squamous cell carcinomas. METHODS: In 15 patients of ESCC, 5 patients of esophageal dysplasia and 5 volunteers with normal esophagus, tissue specimens were taken from esophageal lesions during the operation or endoscopic examination. We used specific monoclonal antibodies for p53 protein, p16INK4 protein and cyclin D1. Immunoreactivity was scored. RESULTS: Mean age of all groups was 66 years old (range 47-93) and men to women ratio was 19:1. p53 mutation was observed in 87% (13/15) of ESCC, in 80% (4/5) of esophageal dysplasia, in 0% (0/5) of normal mucosa (p=0.001). p16 expression was seen in 40% (2/5) of esophageal dysplasia, 27% (4/15) of ESCC and 100% (5/5) of normal mucosa (p=0.016). Cyclin D1 expression was not significantly different among 20% (1/5) of esophageal dysplasia, 53% (8/15) of ESCC and 20% (1/5) of normal mucosa. Either the expression of p53 mutation or the loss of p16 occurred in 80% (4/5) of esophageal dysplasia and in 93% (14/15) of ESCC. CONCLUSIONS: The expression of p53 mutation and the loss of p16 might play a central role in the pathogenesis of esophageal squamous cell carcinoma (ESCC), and contribute to the development of precancerous lesion such as dysplasia. In addition, there is a possibility that the mutations of p53 and p16 silencing would be the early events in ESCC development.
Aged
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Carcinoma, Neuroendocrine/*diagnosis/pathology
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Chromogranin A/analysis/immunology
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Drainage
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Female
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Humans
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Immunohistochemistry
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Liver Abscess/*radiography/surgery
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Liver Neoplasms/*diagnosis/pathology
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Radiography, Abdominal
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Synaptophysin/analysis/immunology
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Tomography, X-Ray Computed