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1.  Adenocarcinoma with adenoma in the jejunum suggesting an adenoma-carcinoma sequence in the small bowel: A case report 
Oncology Letters  2014;8(2):633-636.
Other than that in the duodenum, adenocarcinoma in the small bowel is rare. The present study describes a case of adenocarcinoma with adenoma in the jejunum. A 70-year-old male was admitted to hospital due to dehydration induced by abdominal discomfort and difficulty with oral intake. Computed tomography revealed a tumor in the upper side of the jejunum, which was subsequently resected. The tumor contained adenocarcinoma and adenoma. The protein expression of p53 and Ki-67 was analyzed in the normal mucosa, adenoma and adenocarcinoma. The number of epithelial cells expressing p53 and Ki-67 was found to increase in the adenoma tissue compared with that in the normal mucosa. In the adenocarcinoma tissue, the number of cells expressing p53 and Ki-67 further increased, suggesting that an adenoma-adenocarcinoma sequence may occur in the small bowel, similar to that observed in the large bowel.
PMCID: PMC4081429  PMID: 25009647
adenocarcinoma; adenoma; jejunum; small bowel; p53; Ki-67
2.  Solitary fibrous tumor of the kidney with focus on clinical and pathobiological aspects 
Renal solitary fibrous tumor (SFT) is a rare, and a large scale study on this topic is lacking to date. In this article, we summarize the previously reported cases. The symptoms and signs resemble those of renal cell carcinoma, including hematuria, flank/abdominal/lumbar pain and palpable abdominal mass. Grossly, the tumor demonstrates a well-circumscribed solid mass. Microscopically, the tumor consists of fusiform or ovoid spindle cells and a various amounts of collagen bundles with patternless, storiform, or fascicular arrangements with an occasional hemangiopericytomatous pattern. Immunohistochemically, CD34, CD99 and bcl-2 are often detected. Ultrastructurally, tumor cells contain irregular nuclei, prominent Golgi apparatus, branching rough endoplasmic reticulum, variable numbers of mitochondria. Surgical resection is considered to be the gold standard therapy. Most of renal SFT are benign, but cases of approximately 10 to 15% behave in an aggressive fashion. All patients need to be on long-term follow-up because clinical behavior is rather unpredictable. As the molecular genetic study of renal SFTs is lacking, a large scale study will be desirable in the future.
PMCID: PMC4097243  PMID: 25031693
Solitary fibrous tumor; kidney; CD34; STAT6
3.  Renal carcinoid tumor: An immunohistochemical and molecular genetic study of four cases 
Oncology Letters  2010;1(1):87-90.
Few genetic studies of renal carcinoid tumor have been conducted thus far. We performed immunohistochemical and genetic examinations on four renal carcinoid tumors. Histologically, the tumors consisted of neoplastic cells with round to oval nuclei. Various growth patterns such as tightly packed cords and trabeculae, ribbon-like, trabecular, sheet-like or solid growth were observed. Nuclear chromatin showed a coarse and granular pattern. Immunohistochemically, tumors were positive for chromogranin A and synaptophysin. In the fluorescence in situ hybridization study, three of four tumors revealed monosomy of chromosome 3 (D3Z1), but one tumor showed monosomy of chromosome 13 (D13S319/13q34). Using PCR amplification and fragment analysis of three microsatellite markers (D3S1300, D3S666 and D3S1768) of chromosome arm 3p, one tumor showed loss of heterozygosity at D3S1300 and D3S1768, one tumor was not informative and the analysis of two tumors failed due to low DNA quality. In three cases, the VHL gene status was tested. Two tumors showed wild-type, but the analysis of one tumor failed to provide adequate results. In conclusion, we suggest that the abnormality of chromosome 3 is involved in the pathogenesis of renal carcinoid tumor.
PMCID: PMC3436420  PMID: 22966261
renal carcinoid tumor; fluorescence in situ hybridization; chromosome 3; VHL gene; 3p LOH
4.  Pigmented villonodular synovitis originating from the lumbar facet joint: a case report 
European Spine Journal  2007;16(Suppl 3):301-305.
The authors successfully treated a rare case of pigmented villonodular synovitis (PVNS) that originated from the lumbar facet joint (L4-5). A 43-year-old man presented with a complaint of left severe sciatica causing difficulty in walking. Magnetic resonance imaging (MRI) demonstrated an extradural mass on the left side at L4 and the mass compressed the dural tube and was continuous with the left L4-5 facet joint. A computed tomography myelogram revealed an extradural defect of contrast medium at the L4 level and an erosion of the L4 lamina. A total synovectomy with unilateral osteoplastic laminectomy was performed. The histological findings were a diagnosis of PVNS. The patient’s symptoms resolved completely and the MRI at postoperative 3 years demonstrated no recurrence of PVNS. It is important to totally remove the synovium, which is the origin of PVNS in order to prevent the recurrence. We think that our procedure is reasonable and adequate for lumbar PVNS.
PMCID: PMC2148097  PMID: 17566795
Pigmented villonodular synovitis; Lumbar spine; Synovectomy; Juxtafacet cyst; Laminoplasty

Results 1-4 (4)