[Long-Term Survival with Distal Pancreatectomy and Postoperative Chemotherapy in a Patient of Pancreatic Invasive Ductal Adenocarcinoma of the Tail with Peritoneal Dissemination].

A 68-year-old man was referred to our hospital for detailed examination of the pancreatic tail tumor. The tumor was diagnosed as the pancreatic invasive ductal adenocarcinoma and the distal pancreatectomy was scheduled. During surgery, a 2 mm white nodule was observed on the posterior wall of the stomach. Intraoperative frozen section showed no obvious malignant findings, suggesting leiomyoma or gastrointestinal stromal tumor. Distal pancreatectomy with D2 lymphadenectomy was completed as planned. However, this nodule was later confirmed by permanent pathological specimen to be peritoneal dissemination of pancreatic cancer and final diagnosis was invasive ductal carcinoma of pancreatic tail, pT3, pN1a, M1 (PER), pStage Ⅳ. He received chemotherapy for 17 months. Although liver metastasis was appeared 26 months after surgery, the disease is still being controlled with chemotherapy at 33 months.

Simple quantitative analysis of asbestos body using the sediment of formalin injected into surgically resected lung cancers.

A simple screening method for quantitatively analyzing asbestos bodies that can be carried out even in community hospitals, is needed in order for laborers and neighborhoods in the vicinity of asbestos factories to apply for compensation for asbestos-related injury. Eighty-eight consecutive cases of surgically resected primary lung cancer were analyzed for asbestos bodies using two methods, and the correlation between them was statistically examined. The first was the conventional technique using lung tissue digestion and phase-contrast scanning, and the second was the authors' method using light microscopy to scan the sediment of formalin-injected lung specimens. The overall correlation coefficient of the concentration of asbestos bodies between the authors' method (C(AB/SED)) and the conventional method (C(AB/DLT)) was 0.4576, a weak statistically significant correlation; in patients with occupational asbestos exposure, however, the correlation coefficient was 0.7341. Despite the cost, it may be prudent to use the conventional method under the present law for patients with C(AB/SED)>or=3.5/mL. C(AB/DLT) >3000/g dry lung tissue when C(AB/SED) is >or=3.5/mL suggests the potential for the accumulation of asbestos absorption by lung tissue.

IgA-producing lymphoplasmacytic lymphoma carrying the chromosomal abnormality t(8;14).

IgA-producing lymphoplasmacytic lymphoma (LPL) is rare and IgH/c-myc translocation is rare in LPL. This is the first report of a case of IgA-producing LPL carrying t(8;14). An 86-year-old woman presented inguinal and intra-abdominal lymph node swelling, and lytic bone lesions in the lumbar vertebrae. A diagnosis of IgA-producing LPL was immunohistochemically made by inguinal lymph node biopsy. The serum IgA level was 1,180 mg/dL, which was revealed to be composed of IgA-λ monoclonal protein. Bone marrow chromosomal analysis demonstrated a complex abnormal karyotype, including t(8;14)(q24;q32), which was confirmed by FISH analysis. Abnormal lymphocytes positive for CD19, CD20, cyIgA, and cyλ were detected on flow cytometry analysis of marrow cells. Best supportive care was selected because of dementia and refractory urinary tract infection. Circulating lymphoplasmacytic cells with the same phenotype and karyotype were observed, and increased in number. The aggressive clinical course, including lytic bone lesions, may have been due to IgH/c-myc translocation or the nature of IgA-producing LPL.

Coconut atrium in long-standing rheumatic valvular heart disease.

BACKGROUND: Complete calcification of the left atrium (LA) is called "coconut atrium", which decreases the compliance of LA, leading to the elevation of LA pressure that is transmitted to the right-side of the heart. The pathogenesis of LA calcification in patients with rheumatic heart disease is unknown; however, possible mechanisms include chronic strain force in the atrial wall and inflammation. We report here a patient with long-standing rheumatic valvular heart disease with coconut atrium. CASE REPORT: A 76-year-old man presented with breathlessness and leg edema due to right-sided heart failure. He was diagnosed with rheumatic fever at 8 years of age. Mitral commissurotomy and the mitral and aortic valve replacement were previously performed to treat mitral and aortic valvular stenosis. The profile view of the chest X-ray indicated a diffuse calcified outline of the LA wall. A transthoracic echocardiogram revealed pulmonary hypertension and dilatation of both atria. Moreover, computed tomography showed nearly circumferential calcification of the LA wall. Despite intense medical treatment, he succumbed to heart failure. An autopsy demonstrated that the LA was markedly dilated, its wall was calcified, and its appearance was similar to the surface of an atherosclerotic aorta. Microscopic examination revealed intensive calcification in the endocardium. Minimal accumulation of inflammatory cells was noted. Although slight fibrosis was observed, the cardiac musculature was preserved. CONCLUSIONS: To the best of our knowledge, this is the first report that identifies the histological changes of LA calcification associated with long-standing rheumatic valvular heart disease.

Adenosquamous cell carcinoma arising from the papilla major.

A 47-year-old man was admitted to hospital with complaint of general fatigue. Shortly before the admission a suspected obstructive jaundice was diagnosed at a local hospital. On admission, the physical examination was significant for jaundice; total bilirubin was 6.43 mg/dl. The tumor marker CA19-9 was 2056 U/ml. Endoscopic retrograde cholangiopancreatography (ERCP) was performed and showed dilatation of common bile duct and main pancreatic duct, accompanied with an endoscopic naso-biliary drainage (ENBD) in order to reduce the jaundice. The duodenoscopy showed enlarged and deformed papilla. Hypotonic duodenography showed a filling defect at the medial side of the second portion of the duodenum. Ultrasonography (US) showed a hyperechoic lesion, sized 15 mm in diameter, at the pancreas head with dilatation of biliary tract and main pancreatic duct. An abdominal enhanced CT scan showed a mass sized 15 mm at the lower edge of the common bile duct. A selective hepatic arteriography showed no special finding. We performed a pancreatoduodenectomy with dissection of the lymph nodes. The tumor, sized 22x15x20 mm, was white colored and solid on the papilla. Histopathological inspection of the specimen showed an adenosquamous cell carcinoma of the bile duct in the papilla. The tumor was found to infiltrate the neighboring pancreas and to contain metastasis in lymph nodes in the hepatoduodenal ligament, post pancreaticoduodenal and para-aortic lymph nodes. This is the first report on a case of adenosquamous carcinoma of the papilla major.

Telomerase activity and hTERT mRNA in development and progression of adenoma to colorectal cancer.

Telomerase activity and hTERT mRNA expression are upregulated in colorectal cancer. Whether they are inherent in colorectal adenomas, premalignant lesions to cancer, however, remains to be elucidated. We examined telomerase activity by the fluorescence-based telomeric repeat amplification protocol method and analyzed the level of hTERT mRNA by real-time polymerase chain reaction in 74 surgically obtained neoplasms from 29 patients. The specimens were divided into 6 categories according to the criteria of the Vienna Classification. The control comprising 29 non-pathological mucosa were classified into category 1, 6 adenomas indefinite for neoplasia into category 2, 21 non-invasive low grade adenomas into category 3, 23 high grade adenomas or non-invasive carcinomas into category 4, and 15 intramucosal or submucosal carcinomas into category 5. Carcinoma invading beyond the submucosa (9 samples) was referentially subdivided into category 6. Telomerase activity (mean +/- standard error) in 1 categories to 6 were 5.0+/-1.2, 1.8+/-1.7, 4.3+/-1.6, 20.2+/-2.1, 36.4+/-5.5, and 55.5+/-8.2 units/microg protein, respectively. There were no statistical differences between categories 1 and 2, 1 and 3, and 2 and 3. A significant statistical difference in the other two was observed by the multiple comparison test. The mean levels of hTERT mRNA was 103.1+/-102.4, 103.6+/-103.0, 103.6+/-102.9, 103.7+/-102.9, 104.0+/-103.4, and 104.4+/-104.0 copies/microg total RNA, respectively. There was a significant statistical difference only between category 6 and each of the other categories. These results suggest that telomerase activation occurs during the progression from low-grade to high-grade dysplasia in adenomas and increases steadily with the progression of the degree of dysplasia and invasion during colorectal carcinogenesis, and that hTERT mRNA expression is a feature of the late stage development of colorectal cancer.

Epigenetic Alteration by DNA Promoter Hypermethylation of Genes Related to Transforming Growth Factor-ß (TGF-ß) Signaling in Cancer.

Epigenetic alterations in cancer, especially DNA methylation and histone modification, exert a significant effect on the deregulated expression of cancer-related genes and lay an epigenetic pathway to carcinogenesis and tumor progression. Global hypomethylation and local hypermethylation of CpG islands in the promoter region, which result in silencing tumor suppressor genes, constitute general and major epigenetic modification, the hallmark of the neoplastic epigenome. Additionally, methylation-induced gene silencing commonly affects a number of genes and increases with cancer progression. Indeed, cancers with a high degree of methylation (CpG island methylator phenotype/CIMP) do exist and represent a distinct subset of certain cancers including colorectal, bladder and kidney. On the other hand, signals from the microenvironment, especially those from transforming growth factor-ß (TGF-ß), induce targeted de novo epigenetic alterations of cancer-related genes. While TGF-ß signaling has been implicated in two opposite roles in cancer, namely tumor suppression and tumor promotion, its deregulation is also partly induced by epigenetic alteration itself. Although the epigenetic pathway to carcinogenesis and cancer progression has such reciprocal complexity, the important issue is to identify genes or signaling pathways that are commonly silenced in various cancers in order to find early diagnostic and therapeutic targets. In this review, we focus on the epigenetic alteration by DNA methylation and its role in molecular modulations of the TGF-ß signaling pathway that cause or underlie altered cancer-related gene expression in both phases of early carcinogenesis and late cancer progression.