Biomedical subjects
Publications and source records attributed to F Tezuka.
Carcinoma ex pleomorphic adenoma presenting in the nasopharynx is extremely rare. We present a case of carcinoma ex pleomorphic adenoma occupying the nasopharynx and the soft palate in a 51-year-old woman. To the best of our knowledge, this is the first reported case of carcinoma ex pleomorphic adenoma in the nasopharynx.
A 71-year-old man was first diagnosed with primary transitional cell carcinoma of the prostate with a skip lesion on the distal urethra. The patient received three courses of intra-arterial chemotherapy of cisplatin (CDDP) and pirarubicin (THP-ADM) followed by a radical prostatectomy. Histopathologic examination of the prostatectomy specimen revealed adenocarcinoma invasion along the prostatic duct extending to the peripheral acini, which was diagnosed as ductal adenocarcinoma. The clinical and histopathologic features of this case are entirely different from usual adenocarcinomas of the prostate. This rare histopathologic feature should be recognized as 'ductal carcinoma of the prostate', to distinguish it from papillary adenocarcinoma or adenocarcinoma with endometrioid features. The patient has had no sign of recurrence 14 months after the operation. CDDP-based chemotherapy followed by radical prostatectomy may be one of the promising therapeutic modalities for this rare entity.
The number of pathologists in hospitals has been increasing and they are responsible for both surgical pathology and clinical laboratory medicine. In the future they will also play important roles in the modernized reform of the central laboratory as it establishes its own importance in improving the quality and safety of medical activities. As a pathologist, the author reports on challenges faced since assuming the present directorship of the department of laboratory medicine in 1995 including (a) establishing a decision-making system in collaboration with technologists, (b) improving expertise in the department through joining a variety of seminars, conferences and research activities, (c) publishing an annual department report, and (d) introducing both internal and external quality assessment. In the future, for young pathologists training in both pathology and laboratory medicine will be essential.
Three-dimensional (3D) reconstruction and morphometry of resected colonic adenomas were undertaken to extend current knowledge of clinically significant features such as the frequency of occurrence of cancer, and the size and spatial distribution of dysplastic zones in these tumours. Fifty endoscopically resected colonic adenomas were serially sectioned at intervals of 0.2 mm and the sectional images were loaded into a computer system in order to visualize the spatial distribution of dysplastic zones. These were graded into five groups according to the criteria of Morson and Dawson: normal mucosa, mild dysplasia, moderate dysplasia, severe dysplasia, and cancer. The way in which zones of different grades are distributed in a polyp was visualized in a computer display and the volume of each dysplastic zone was estimated by the Cavalieri principle. In five polyps, adenocarcinoma was found growing in an adenoma. In all of these, the cancer was surrounded by less dysplastic zones, in the form of 'cancer in adenoma'. In pedunculated polyps, submucosal invasion could occur even if the volume percent of severe dysplasia was less than 10%. In such a case, multiple biopsy specimens are advisable. Semipedunculated polyps smaller than 200 mm(3) can also harbour submucosal invasion. In this study it was found that if the adenomas had been examined by only a single section, as many as one in five of the cases in which submucosal invasion had already developed would have escaped microscopic confirmation. To prevent such diagnostic failure, it is advisable to add a few deeper sections. Thus, 3D reconstruction and morphometry have been helpful in establishing a better standard for the diagnostic histopathology of colonic tumours.
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A case of clear-cell odontogenic tumor with unusual histological features is presented. A 61-year-old Japanese man was admitted because of swelling of the left premolar-molar region of the mandible. Radiological examination revealed a multilocular radiolucency with irregular margins. Histological examination of the resected specimen showed infiltrative proliferation of both clear and eosinophilic cells into the adjacent soft tissue without encapsulation, suggesting the malignant potential of the tumor. The tumor cells sporadically formed cystic lesions. In addition, several tumor cell nests showed duct-like characteristics, and many eosinophilic dentin-like structures were attached to the tumor cell nests, suggesting the potential for epithelial-mesenchymal induction. Histochemically, the clear tumor cells possessed cytoplasmic glycogen granules. Both clear and eosinophilic tumor cells showed positive immunoreactivities for cytokeratin 19, epithelial membrane antigen and filaggrin, indicating an odontogenic epithelial origin.
Phosphoinositide turnover and protein kinase C (PKC) mediate the signaling of angiotensin II, which plays a pivotal role in ventricular remodeling after myocardial infarction (MI). To determine whether PKC is activated after MI, rat hearts after MI were subjected to in vitro quantitative autoradiography with [3H]phorbol 12,13-dibutyrate (PDBu), which is highly selective for PKC. [3H]PDBu binding in the infarcted area increased significantly compared with the non-infarcted region 7 and 21 days after MI, but not 1 and 3 days and 10 months after MI. [3H]PDBu binding in the noninfarcted area was similar to that in the sham-operated rats. Immunohistochemical analysis revealed that abundant macrophages (7 days after MI), fibroblasts, and myofibroblasts (7 and 21 days after MI) occupied the infarcted region. To investigate whether myocardial [3H]PDBu binding is affected by captopril, hearts were subjected to in vitro autoradiography with [3H]PDBu after 1- or 3-week captopril treatment or no treatment. Captopril treatment significantly suppressed [3H]PDBu binding in the infarcted area 3 weeks after MI, but not 1 week after MI nor in the noninfarcted areas. These results suggest that PKC is upregulated during the healing and fibrogenic process after MI and that captopril treatment suppresses the upregulation in the infarcted area.
A questionnaire-based investigation was performed on 325 Japanese school children with Down syndrome ages 6 to 18. Data on height and body weight, eating habits, physical activity for these children were obtained through their parents. Proportion of obese children was higher among these subjects than the average for Japanese children (34.3% and 7.47% respectively, for the ages from 6 to 14). We examined characteristics of eating habits and physical activities between the obese group (obesity index greater than 20% above the average of Japanese school children) and the non-obese group. Obesity started to increase in the obese group around age 7. The obese group tended to have had a greater intake of sweets, juice and total foods in their preschool days, but unexpectedly had been physically more active in their primary school days.
UNLABELLED: Phosphoinositide turnover mediates the signaling of angiotensin II, which plays a pivotal role in ventricular remodeling after myocardial infarction (MI). We tested the hypothesis that phosphoinositide turnover can be visualized by 1-[1 -(11)C]butyryl-2-palmitoyl-rac-glycerol (11C-DAG) in both infarcted and noninfarcted myocardium after MI in rats. METHODS: Rats received an injection of 11C-DAG 7 d after left coronary artery ligation, and myocardial lipids were extracted from both infarcted and noninfarcted areas of myocardium (n = 3). Metabolites of 11C-DAG were determined by thin-layer chromatography. Quantitative autoradiography of hearts was performed to visualize myocardial phosphoinositide turnover in rats that received an injection of 11C-DAG 1 d (n = 3) and 7 d (n = 5) after MI and 7 d after a sham operation (n = 3). Quantitative autoradiography with 201TlCl was also performed to evaluate myocardial blood flow in rats 7 d after MI (n = 3). Cells occupying the infarcted myocardium were identified by immunohistochemistry. RESULTS: The radioactivity incorporated into the intermediates of phosphoinositide turnover was predominant in both the infarcted (67.1% +/- 5.2% of the total activity) and the noninfarcted (57.4% +/- 3.2%) myocardium. 11C-DAG radioactivity in the infarcted region normalized to that in the noninfarcted region was 1.09 +/- 0.04 in rats 7 d after MI, which was significantly higher than that in rats 1 d after MI (0.38 +/- 0.03, P < 0.001). 201Tl radioactivity in the infarcted region normalized to that in the noninfarcted region was only 0.19 +/- 0.01 7 d after MI. 11C-DAG radioactivity in the noninfarcted region normalized to that in the right ventricular free wall tended to be increased in rats 1 and 7 d after MI compared with the sham-operated rats; the differences, however, were not statistically significant (1.30 +/- 0.15, 1.20 +/- 0.07, and 1.13 +/- 0.02, respectively). Immunohistochemistry revealed that abundant fibroblasts, myofibroblasts, and macrophages occupied the infarcted myocardium 7 d after MI, but the cellularity was low during the first day after MI. CONCLUSION: These data suggest that 11C-DAG may be useful for visualizing regions with activated phosphoinositide turnover after MI. Because wound healing and fibrogenic processes are important factors of ventricular remodeling, 11C-DAG and PET may offer new information benefiting patient management after MI.
Expression of the 37-kDa laminin binding protein (37LBP/p40), a precursor of the 67-kDa laminin receptor, is well-correlated with the biological aggressiveness of cancer cells. To elucidate the direct role played by 37LBP/p40 in cancer cells, a murine lung cancer cell line T11, the 37LBP/p40 expression of which was remarkably diminished, was established by the introduction of the antisense 37LBP/p40-RNA using a retroviral vector. As a result, the population doubling time of T11 was prolonged (60 h) compared with that of P29, the non-transfected parental cell line (42 h), and TN2, a transfectant with vehicle only (40 h). In-vitro studies also showed that T11 cells adhered to immobilized laminin less firmly than P29 cells did. When 5 x 10(5) cells were subcutaneously inoculated into syngenic mice, the mean survival time of T11-recipients (77.0+/-14.8 days) was also significantly prolonged compared with that for P29 (34.8+/-5.5 days) and TN2 (36.7+/-6.1 days) recipients (P < 0.001). The electron-microscopic view of the tumour tissue revealed that T11 cells were loosely apposed and their intercellular space was markedly widened. Some of the T11 cells sporadically degenerated with the infiltration of lymphocytes and neutrophils. These results suggest that the suppressed expression of 37LBP/p40 reduces the capability of lung cancer cell proliferation in vitro and tumour formation in vivo.
OBJECTIVE AND STUDY DESIGN: Urocortin is a recently identified neuropeptide of the corticotrophin-releasing factor (CRF) family in the mammalian brain and has been demonstrated to stimulate ACTH secretion from pituitary cells, but its expression in human brain tissue including the hypothalamus has not been examined. In this study, we first examined urocortin expression in the hypothalamus (20 cases) and pituitary stalks (17 cases) of human brain obtained from autopsy using immunohistochemistry and mRNA in situ hybridization. RESULTS: Neither urocortin immunoreactivity nor mRNA hybridization signals were detected in the hypothalami and pituitary stalks while CRF immunoreactivity was detected in the paraventricular nuclei of the hypothalami in 10/20 cases and in nerve fibres of the stalks in 17/17 cases. These results indicate that urocortin does not act on the hypothalamo-pituitary-adrenal axis, at least not in the same manner as CRF in humans. We then examined urocortin expression in various portions of the brain in 7 cases. Both urocortin immunoreactivity and mRNA hybridization were detected in Purkinje cells of the cerebellum and anterior horn cells of the spinal cord in specimens examined. Urocortin expression was, however, variably seen in superior olivary nuclei (two out of six cases examined) and in the Edingar-Westphal nuclei (one out of three cases examined). CONCLUSIONS: The distribution of urocortin in the human central nervous system suggests that urocortin may work as a neurotransmitter like other neuropeptides in the human.
Emergency surgery for bowel perforation caused by metastases from lung cancer is rare. Two cases of small bowel perforation due to metastasizing lung cancer are reported. Both patients were admitted as a surgical emergency case. One of the two patients presented herein survived and was discharged from the hospital. Perforated small bowel due to metastatic lung cancer is a highly fatal event that occurs in the late phases of the disease. Despite the poor prognosis, early and appropriate therapy will occasionally yield successful surgical palliation. Patients with known lung cancer who develop abdominal complaints should be examined thoroughly and treated quickly.
A case of Pemphigus vulgaris concurrent with hepres simplex virus (HSV) infection in a 53-yr-old female is described, in which the diagnosis was based on oral scraping cytology. Two populations of abnormal cells were identified in the oral smear. One abnormal cell population was characterized by the presence of numerous single cells and sheets and smaller aggregates of loosely cohesive epithelial cells that appeared to have only a few points of intercellular attachment. A second population of abnormal cells showed characteristic signs of HSV infections such as ground-glass nuclear appearance and multinucleation. Subsequently, diagnosis of HSV infections based on polymerase chain reaction was applied to identify the specific DNA for HSV type 1 in the Papanicolaou specimens. To our knowledge, this is the first case in which the coexistence of Pemphigus vulgaris and HSV infection in the oral mucosa was established by cytologic diagnosis. This is discussed in view of our recent experience with this unusual oral lesion.
A case of metastatic dermatofibrosarcoma protuberans (DFSP) in a 47-year-old woman is presented. Dermatofibrosarcoma protuberans occasionally recurs, but rarely metastasizes. The patient underwent local removal of the nuchal tumor by a general practitioner, followed by a rapid recurrence. She underwent total removal of the tumor and a diagnosis of spindle cell sarcoma was made after an incisional biopsy was performed. This lesion had both a typical DFSP-like area and a fibrosarcoma (FS)-like area. After 7 years, an abnormal lung shadow was observed and a segmental lung resection was performed. Histologically, the lung tumor was similar to the FS-like area in the nuchal tumor. Confirming CD34 expression in the tumor cells, this lung tumor was diagnosed as metastatic DFSP. Usually CD34 expression is unique to DFSP but almost negative in FS-like areas. In the present case, the FS-like area in the nuchal tumor showed decreased CD34 reactivity, as previously reported, but the FS-like area in the metastatic tumor still widely preserved CD34 expression. The presented case suggests that the FS-like area in DFSP is histogenetically different from typical FS or malignant fibrous histiocytoma.
BACKGROUND: In a previous study, morphometry and multivariate cluster analysis was performed on 97 lesions. These consisted of atypical adenomatous hyperplasia (AAH), considered to be an important lesion corresponding to a step of carcinogenesis for adenocarcinoma of the human lung, Clara cell type, and type 2 pneumocyte type adenocarcinomas. Although AAH and the two types of adenocarcinoma were re-classified into three clusters and AAH was defined in clear morphologic terms, the biologic nature of AAH has yet to be clarified. In the present study, immunohistochemical analysis was performed to gain a deeper understanding of the relationship between AAH and the two types of adenocarcinoma, and to compare the results with those obtained by morphometry. METHODS: The 97 lesions analyzed by morphometry were submitted to immunohistochemical analyses using antibodies against surfactant apoprotein A, urine protein 1, carcinoembryonic antigen and cytochrome P-450s (1A1-2, 2B1-2, 2E1). Also examined, as controls, were 17 lesions with adenomatous hyperplasia (AH), a non-neoplastic reactive change of bronchiolo-alveolar cells, 30 areas of normal Clara cells, and 36 areas of normal type 2 pneumocytes. The immunoreactivity was graded by introducing a semi-quantitative scoring system. RESULTS: Immunohistochemically, AAHs behaved quite similarly to the lesions classified as Clara cell type or type 2 pneumocyte type adenocarcinomas. For any of the antibodies employed, no significant difference in immunoreactivity was demonstrated among these lesions. CONCLUSIONS: The results suggest, in accordance with our previous morphometry, that AAH is a lesion closely related with Clara cell type and type 2 pneumocyte type adenocarcinomas, probably as their common precursor. However, the two types of adenocarcinomas, despite their characteristic morphologic features, are indistinguishable using the biological indicators applied in this study.
Papillary adenoma of type II pneumocytes is a rare tumour. It is considered to be a benign neoplasm and is derived from immature cells in the bronchioloalveolar epithelium, however, its biological nature has not been elucidated. We report a case of an adenomatous tumour; a papillary adenoma of type II pneumocytes, which we regard as possessing malignant potential. Light microscopically, as well circumscribed, papillary tumour of predominantly cuboidal cells resembling type II pneumocytes was found, but Clara type and ciliated cells were also present. Immunohistochemically, the tumour cells reacted positively with antibodies to surfactant apoproteins (A, B), carcinoembryonic antigen, cytochrome P-450 1A1-2 and 2B1-2. Ultrastructurally, many osmiophilic lamellar bodies and electron-dense granules were demonstrated. Semi-serial sections revealed signs of transbronchial dissemination and vascular invasion. Morphometry using 12-dimensional cluster analysis disclosed features of the tumour cells which resembled those of pneumocyte type II adenocarcinoma. These findings suggest that the present case has some malignant characteristics and originates from immature bronchiolar or alveolar cells, with a potential to develop into both type II pneumocyte and Clara cell type adenocarcinomas.
The B-cell leukemia/lymphoma-2 (bcl-2) proto-oncogene is peculiar, as its product appears to provide survival advantage to B cells by blocking apoptosis. Expression of bcl-2 protein was analyzed in 54 cases of primary non-Hodgkin's malignant lymphomas of the oral cavity by immunohistologic staining of paraffin-embedded tissue. The immunophenotype of each tumor was established with the use of a panel of monoclonal and polyclonal antibodies to lymphoid cell differentiation antigens. The cases in the present study were 42 B-cell lymphomas, 7 T-cell lymphomas and 5-lymphomas revealing histiocytic markers. Sixteen of the 42 B-cell lymphomas were positive for bcl-2 protein, and were composed of 7 low-grade B-cell lymphomas and 9 high-grade B-cell lymphomas. Seven low-grade B-cell lymphomas were composed of one mucosa-associated lymphoid tissue type, three centrocytic types and three centroblastic-centrocytic types. Nine high-grade B-cell lymphomas comprised four centroblastic types, one immunoblastic type and four lymphoblastic types. Enhanced expression of the bcl-2 oncogenic protein was detectable in lymphoma cells in 2 cases for the T-cell lymphoma, and one case for the true histiocytic lymphoma. In contrast to the previous reports of American node-based lymphomas, Japanese primary oral lymphomas in our series expressed a lower frequency of bcl-2 protein. Furthermore, the present study indicated that bcl-2 protein was expressed on a wide variety of B-cell lymphomas, T-cell lymphomas and true histiocytic lymphoma, and that differences in bcl-2 protein expression may be useful in the diagnostic separation of lymphoblastic lymphoma with B-cell marker from Burkitt's lymphoma.
To understand genetic events which play a role in the development and/or progression of human endometrial cancer, we studied allelotypes on all autosomal chromosomes, as well as chromosome X, with 42 microsatellite markers and 56 endometrial cancers. The most frequent loss of heterozygosity (LOH) was observed on the long arm of chromosome 10 (14 of 30, 47%), which was commonly detected in grade 1 cancer. We constructed a detailed deletion map and defined two commonly deleted regions in 10q25-q26; one was the 8 cM region between D10S209 and D10S216, the other was the 12 cM region between D10S217 and D10S590. Replication errors at two or more loci were observed in 24 of 56 tumours (43%), suggesting that disruption of the DNA mismatch repair system also plays an important role in the course of endometrial carcinogenesis.