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H Enzan

Publications and source records attributed to H Enzan.

At least 37 records · Page 2Linked to original sources

Distribution and role of CD34-positive stromal cells and myofibroblasts in human normal testicular stroma.

CD34-positive stromal cells are distributed in various organs including breast, Fallopian tubes, thyroid gland, colon, pancreas, and uterine cervix. To elucidate the distribution of CD34-positive stromal cells, smooth muscle cells, and myofibroblasts in normal human testis, we examined 48 testes obtained by autopsy and operation, including five fetal, one neonatal, and 42 adult cases without evident testicular lesions, using a streptavidin-biotin immunoperoxidase technique. The expression of alpha-smooth muscle actin (ASMA), h-caldesmon, CD34, and CD31 were immunohistochemically examined in all cases. The tunica albuginea and the inner layer of seminiferous tubules in adult testis were predominantly composed of myofibroblasts. Smooth muscle cells were also scattered throughout these sites in some cases. CD34-positive stromal cells were abundant, and they formed a reticular network around the seminiferous tubules and Leydig cells as well as the outer layer of seminiferous tubules. Moreover, myofibroblasts and the CD34 reticular network were already present in the testicular stroma during fetal or neonatal development. Double immunostaining of fetal, neonatal and adult testes using ASMA and CD34 confirmed that myofibroblasts and CD34-positive stromal cells were present in the inner and outer layers of peritubular tissue, respectively. This distribution and cytological identification was also confirmed by an ultrastructural study of four cases. Finally, CD34-positive stromal cells and myofibroblasts are major components of human testicular stroma.

Actins↗

Fascin-positive dendritic cells and fibroblastic reticulum cells build a framework of T-cell areas in lymph nodes.

Fascin, a 55-kDa actin-bundling protein, and alpha-smooth muscle actin (ASMA) were immunohistochemically examined in murine normal and stimulated lymph nodes. In specific pathogen-free young female mice, a few fascin-positive cells (FPCs) were located in the sinus and surrounding tissues, but ASMA-positive cells were undetectable. Following a subcutaneous injection of sheep red blood cells, the numbers of FPCs and their dendrites increased in the paracortex, with the accumulation of activated lymphocytes. Fibroblastic reticulum cells (FRCs), endothelial cells, histiocytic cells and lymphocytes in various stages of maturation were all fascin negative. These results indicated that fascin could be a reliable marker of paracortical dendritic cells in murine lymph nodes. However, FRCs became ASMA positive. Immunoelectron microscopy showed that the FPCs were interdigitating cells and that they closely contacted with FRCs. These two types of cells and reticular fiber formed a network in the paracortex and contacted with each other. In active paracortical response, both FPCs and FRCs are also stimulated and might play a significant role in the maturation of the lymphocytes.

Actins↗

Review of chromophobe renal cell carcinoma with focus on clinical and pathobiological aspects.

In recent years, the concept of chromophobe renal cell carcinoma (RCC) has been established. Chromophobe RCCs account for about 4-6% of all renal tumors. Macroscopically, the cut surface of the tumor is generally grey-beige in color. Histologically, there are two variants (typical and eosinophilic). In the typical variant, large tumor cells with architecture of a compact tubulo-cystic pattern proliferate. The cytoplasm is abundant and shows a fine reticular translucent pattern. The cell border is thick, prominent and eosinophilic. In the eosinophilic variant, tumor cells are smaller and markedly eosinophilic, and a perinuclear halo is often seen. Histochemically, the tumor cells generally show a diffuse and strong reaction for Hale's colloidal iron staining. Ultrastructurally, tumor cells contain many cytoplasmic microvesicles (150-300 nm). In chromosomal analysis, a low chromosome number is characteristic of chromophobe RCCs, due to the frequent occurrence of a combined loss of chromosomes 1, 2, 6, 10, 13, 17, and 21. In differential diagnosis, histological distinction from oncocytomas, which share a common phenotype (intercalated cells of the collecting duct system), is most important. In this diagnostic setting, recent studies have given rise to several problems. Firstly, some cases of coexistent chromophobe RCC and oncocytoma (so-called renal oncocytosis) or cases of oncocytoma with metastasis have recently been reported. Secondly, the existence of chromophobe adenoma, which is the benign counterpart of chromophobe RCC, and an oncocytic variant of chromophobe RCC has recently been suggested. Therefore, further studies are needed to elucidate the relationship between chromophobe RCCs and oncocytomas, to confirm whether chromophobe adenoma actually exists or not, and to identify the key gene that causes chromophobe RCCs.

Carcinoma, Renal Cell↗

Review of metanephric adenoma of the kidney with focus on clinical and pathobiological aspects.

The concept of metanephric adenoma has become established in recent years. Metanephric adenoma is a rare neoplasm. Macroscopically, the cut surface of the tumor displays a tan to gray or yellow color, and tumors generally form well-circumscribed masses. Histologically, tumors are composed of small epithelial cells that form small acini. Glomeruloid bodies, which are composed of lobulated papillary projections, are occasionally seen. Although there have been few studies using chromosomal analysis, two recent studies have shown partial monosomy or LOH of 2p. On the other hand, the concept of metanephric tumors has recently become broadened. These tumors include metanephric adenomas, adenofibromas and stromal tumors, and they compose a continuous histological spectrum. Therefore, further studies on various aspects are needed to identify the gene responsible for the occurrence of metanephric tumors and, furthermore, to clarify the association among the three types of metanephric tumors.

Adenoma↗

Review of papillary renal cell carcinoma with focus on clinical and pathobiological aspects.

Recent studies have shown that papillary renal cell carcinoma (RCC) is clinically and genotypically a distinct entity. Papillary RCCs account for about 10-15% of renal parenchymal neoplasms. Macroscopically, the cut surface is yellow or brown in color and large tumors frequently show cystic change. Hemorrhage and necrosis are common. Histologically, Delahunt and Eble have classified papillary RCCs into type 1 (small cells, single layer) and type 2 (large cells, pseudostratification) according to the cytoplasmic volume and thickness of the lining cells. In chromosomal analysis, gain of chromosomes 7 and 17, loss of Y chromosome and additional gains (chromosome 3q, 8p, 12q, 16q and 20q) are frequently found in type 1 papillary RCCs, but the chromosomal aberration of type 2 papillary RCCs seems to be more heterogenous than that of type 1 papillary RCCs. Mutations of MET proto-oncogenes in some cases of both hereditary and sporadic papillary RCCs have recently been detected. Furthermore, all hereditary and sporadic papillary RCCs with MET proto-oncogene show type 1 histological features. Type 1 papillary RCCs generally seem to have a favorable prognosis, but type 2 tumors have a worse prognosis than do type 1 tumors. Papillary RCCs with involvement of the X chromosome and cancer syndrome with predisposition to cutaneous/uterine leiomyomas and papillary RCCs, the histological features of which are basically different from those of usual papillary RCCs, have also been recently reported. Since papillary RCCs seem to constitute clinically, histologically, and even genetically more heterogenous groups than previously thought, further investigations are needed to characterize the subtype of papillary RCC.

Carcinoma, Papillary↗

Review of sarcomatoid renal cell carcinoma with focus on clinical and pathobiological aspects.

In sarcomatoid renal cell carcinoma (RCC), it is generally accepted that the sarcomatoid portion is derived from metaplastic transformation of carcinoma. Sarcomatoid RCCs account for about 1-8% of all renal tumors. Macroscopically, tumors generally form encapsulated masses and show invasive growth. Sarcomatoid RCCs originate from all subtypes of RCCs, including conventional, papillary, chromophobe, and collecting duct carcinomas. With regard to the growth pattern of the sarcomatoid component, malignant fibrous histiocytomatous, fibrosarcomatous and unclassified sarcomatous patterns are frequently seen. Immunohistochemically, sarcomatoid RCCs are generally positive for AE1/AE3, epithelial membrane antigen (EMA) and vimentin and negative for desmin, actin and S-100. Little is know about genetic alterations in sarcomatoid RCCs. Further studies are therefore needed to identify the key gene involved in sarcomatoid transformation of RCCs.

Animals↗

Review of renal oncocytoma with focus on clinical and pathobiological aspects.

Renal oncocytomas account for about 3-7% of all renal tumors. Macroscopically, the cut surface of the tumor is generally mahogany brown or dark red in color. A central scar is occasionally observed. Histologically, tumor cells with finely granular cytoplasm proliferate in an edematous, myxomatous or hyalinized stroma with a nested, tubulocystic, solid or trabecular pattern. Ultrastructurally, tumor cells contain many mitochondria with lamellar cristae. Mitochondrial DNA alterations are consistently observed in renal oncocytomas. In chromosomal analysis, renal oncocytomas comprise a heterogenous group. Combined loss of chromosomes Y and 1, rearrangements affecting band 11q12-13, involvement of 12q12-13, loss of 14q, and the lack of combination of LOH at specific chromosomal sites have been reported. In differential diagnosis, the histological separation from chromophobe RCCs is of great importance. In such a setting, ultrastructural or chromosomal analysis is very useful. However, there are several findings suggesting a close relationship between chromophobe RCC and oncocytoma. First, both tumors share a phenotype of intercalated cells of the collecting duct system and mitochondrial DNA alterations. Second, some cases of coexistent oncocytoma and chromophobe RCC, designated as "renal oncocytosis", have recently been reported. Third, oncocytic variants of chromophobe RCCs that have similar ultrastructural features to those of oncocytomas have been reported. Fourth, the existence of chromophobe adenoma, which is the benign counterpart of chromophobe RCC and shows loss of chromosomes Y and 1, has recently been suggested. Finally, although almost all oncocytomas behave in a benign fashion, some cases of oncocytoma that caused metastasis or resulted in death have also been reported. Therefore, further studies are needed to resolve these problems and also to elucidate the genetic mechanisms responsible for the occurrence of oncocytomas.

Adenoma, Oxyphilic↗

The number of CD10-positive glomerular epithelial cells reflects renal prognosis in IgA nephropathy patients.

BACKGROUND: The glomerular epithelial cells play an important role in glomerular filtration of the kidney. The disruption of these cells contributes to the development of glomerulosclerosis. The present study was performed to elucidate whether loss of the glomerular epithelial cells is associated with renal injury in patients with IgA nephropathy. PATIENTS AND METHODS: Thirty renal biopsy specimens from IgA nephropathy, 12 from minor glomerular abnormalities and 5 from normal controls were observed. The specimens from IgA nephropathy were divided into 2 groups: Group IgA-1, including 11 patients who had received a follow-up renal biopsy because of deterioration of renal function, and Group IgA-2, consisting of the remaining 19 patients without follow-up biopsy. Immunohistochemistry was performed using a monoclonal antibody against CD10 antigen that appears on mature epithelial cells of glomeruli. RESULTS: The average number of CD10-positive glomerular epithelial cells (GECs) was significantly lower in IgA nephropathy than in either minor glomerular abnormalities or the normal controls. In IgA nephropathy, there were significant correlations of the GECs with renal functions. The GECs were reduced along with the progression of histopathological damage. In group IgA-1, the GECs were significantly reduced at the second biopsy compared with the first biopsy, and significantly fewer in group IgA-1 than in group IgA-2 at the first biopsy. The GECs showed a significant correlation with renal prognosis during the follow-up period. CONCLUSIONS: The reduction of GECs was associated with renal dysfunction, histopathological damage and renal prognosis. The GECs may be a useful predictor of renal prognosis in IgA nephropathy.

Adult↗

Exertion of the suppressive effects of IFN-gamma on experimental immune mediated blepharoconjunctivitis in Brown Norway rats during the induction phase but not the effector phase.

BACKGROUND/AIMS: Interferon gamma (IFN-gamma) knockout mice exhibit severe allergic conjunctivitis (AC), indicating that IFN-gamma regulates the development of AC. The authors examined whether this inhibitory effect of IFN-gamma is exerted during the induction or effector phase of experimental AC. METHODS: Experimental immune mediated blepharoconjunctivitis (EC) was induced in Brown Norway (BN) rats, using ovalbumin (OVA) as the antigen. To investigate the role of IFN-gamma in the induction phase, EC was induced by active immunisation and IFN-gamma (10 micro g/time, total 70 micro g), or phosphate buffered saline (PBS) as a control, was injected intraperitoneally every other day from the day of immunisation. The rats were challenged with OVA eye drops 13 days after immunisation, and 24 hours later, the eyes were harvested for histology. To examine the effects of IFN-gamma in the effector phase, OVA specific T cells were transferred into syngeneic rats and IFN-gamma (10 micro g/time, total 50 micro g) or PBS was injected each day after the transfer until induction of EC 4 days later with an OVA challenge. To investigate the role of endogenous IFN-gamma during the effector phase, an anti-IFN-gamma monoclonal antibody (3 mg/time) was injected on days 3 and 4. RESULTS: Injection of IFN-gamma into actively immunised rats suppressed eosinophilic infiltration but not infiltration of mononuclear cells. In contrast, neither IFN-gamma nor anti-IFN-gamma affected EC in passively immunised rats. CONCLUSION: IFN-gamma is a suppressive cytokine for the development of EC and exerts this suppressive effect during the induction phase.

Adoptive Transfer↗

Microinvasive lobular carcinoma associated with intraductal spread arising in a mammary hamartoma.

A 53 year old woman presented with a lump in the inner lower quadrant of the left breast. Histological examination of the breast tumour confirmed that the lesion was a mammary hamartoma. Carcinoma with foci of microinvasion was observed in the lobules of the hamartoma concomitant with the intraductal spread of lobular carcinoma. Immunohistochemically, the cancer cells were negative for beta-catenin, which generally stained normal breast ducts and ductal carcinomas. This is only the sixth case of breast carcinoma arising in a mammary hamartoma to be reported and, moreover, the fourth case of lobular carcinoma occurring within a hamartoma. Despite the apparent rarity of this case, pathologists should be aware of the possibility of carcinomas arising within mammary hamartomas.

Breast Diseases↗

Alpha smooth muscle actin positive stromal cells in gastric carcinoma.

AIMS: To investigate the distribution and roles of alpha smooth muscle actin (ASMA) positive stromal cells (ASMA+ cells), which belong to the myofibroblast group, within gastric carcinomas, with reference to three histological types (diffuse type, intestinal type, and solid type). METHODS: In total, 74 surgically resected gastric carcinomas (24 diffuse type, 43 intestinal type, and seven solid type) were examined. ASMA positive and high molecular weight caldesmon (HCD) negative stromal cells were regarded as ASMA+ cells. The distribution of CD34 positive stromal cells (CD34+ cells) was also analysed immunohistochemically. RESULTS: In the 24 diffuse-type gastric carcinomas, six of the 13 carcinomas invading the subserosa had ASMA+ cells in the tumour stroma, whereas all six diffuse-type gastric carcinomas confined to the submucosa and all five invading the muscularis propria had no ASMA+ cells in the tumour stroma. In the 43 intestinal-type gastric carcinomas, only five of the 21 carcinomas confined to the submucosa had ASMA+ cells in the tumour stroma, whereas 21 of the 22 intestinal-type gastric carcinomas invading the muscularis propria and the subserosa had ASMA+ cell bundles in the tumour stroma. The distribution of CD34+ cells in diffuse-type and intestinal-type gastric carcinomas was similar to that seen in a previously published series. All seven solid-type gastric carcinomas examined had ASMA+ cells but not CD34+ cells in the tumour stroma. No stromal cells double positive for ASMA and CD34 were detected within the diffuse-type tumours examined. CONCLUSIONS: These results suggest that ASMA expression in stromal cells is associated with tumour stroma formation of diffuse-type gastric carcinomas invading the subserosa, intestinal-type gastric carcinomas invading the muscularis propria and subserosa, and solid-type gastric carcinomas.

Actins↗

High molecular weight caldesmon positive stromal cells in the capsule of thyroid follicular tumours and tumour-like lesions.

AIMS: To investigate the smooth muscle nature of the spindle stromal cells in the capsule of thyroid tumours and tumour-like lesions. METHODS: Immunostaining for high molecular weight caldesmon (HCD), a highly specific marker for smooth muscle differentiation, was performed in 70 primary thyroid tumours and tumour-like lesions (21 hyperplastic nodules, 29 follicular adenomas, five minimally invasive follicular carcinomas, six widely invasive follicular carcinomas, and nine encapsulated papillary carcinomas). RESULTS: HCD positive stromal cells (HCD+ cells) were detected in the capsule of 20 of the 21 hyperplastic nodules, and all of the 29 follicular adenomas and five minimally invasive follicular carcinomas, whereas HCD+ cells were seen in the capsule of only four of the six widely invasive follicular carcinomas and no HCD+ cells were seen in the capsule of the nine encapsulated papillary carcinomas examined. CONCLUSIONS: The presence of HCD+ cells in the capsule is characteristic of thyroid follicular tumours and tumour-like lesions. The stromal cells in the capsule of thyroid follicular tumours and tumour-like lesions are different from those of encapsulated papillary carcinoma.

Adenocarcinoma, Follicular↗

Lack of CD34 positive stromal cells within angiomyomas (vascular leiomyomas).

AIMS: To investigate the role of CD34 positive stromal cells in the morphogenesis and tumour growth regulation of angiomyomas (vascular leiomyomas). METHODS: Histochemical analysis using monoclonal antibodies to CD34 and CD31 was performed in 10 angiomyomas and their adjacent soft tissue. RESULTS: CD34 positive stromal cells were not seen within the tumour tissue; the thick walled vessels within the tumours lacked CD34 positive stromal cells. In contrast, bundles of CD34 positive stromal cells were detected at the tumour border of all of the angiomyomas and in the adventitial tissue of the surrounding normal vessels. CONCLUSIONS: The lack of CD34 positive stromal cells within an angiomyoma is associated with the characteristic morphology of an angiomyoma.

Angiomyoma↗

Review of collecting duct carcinoma with focus on clinical and pathobiological aspects.

In recent years, the concept of collecting duct carcinoma (CDC) has been established. CDCs constitute about 0.4 to 2% of RCCs. Macroscopically, CDCs occur in the renal medulla. On the cut surface, they are generally firm, white or grey and poorly circumscribed. Histologically, CDCs are characterized by various cytological and histological appearances. Furthermore, desmoplastic stromal reaction around the tumor and atypical hyperplastic changes or carcinoma in situ in the adjacent medullary collecting duct are frequently observed. Histological distinction from papillary RCCs is most important, because both tumors share some structural and histochemical features, and it seems that some investigators have confused diagnostic criteria for CDCs. On the other hand, the concept of medullary carcinoma, which preferentially occurs in a black race and shows histological features similar to those of CDC, has also recently been established. Although there have been few studies on chromosomal abnormalities of CDCs and consistent abnormalities have not been identified, a recent study using microsatellite analysis has shown a high frequency (60%) of LOH in 1q32.1-32.2. Further studies are needed to elucidate the genetic characteristics of CDCs and to determine the relationship or difference between CDCs and medullary carcinomas.

Animals↗

Eosinophil-induced liver injury: an experimental model using IL-5 transgenic mice.

BACKGROUND/AIMS: In certain liver diseases, activated eosinophils are considered to be important effector cells in addition to T-cell-mediated cytotoxicity. No experimental model, however, has been developed for in vivo analysis of the cytotoxic mechanisms. METHODS: Interleukin-5 (IL-5) transgenic mice (C3H/HeN-TgN(IL-5)Imeg), which exhibit marked eosinophilia without liver injury, were injected once with 25 microg of lipopolysaccharide (LPS) intraperitoneally. The mice were sacrificed weekly and eosinophilic injuries were assessed microscopically. To clarify the role of Kupffer cells and tumor necrosis factor-alpha (TNF-alpha) in the liver injury, gadolinium chloride (GdCl3) and anti-TNF-alpha neutralizing antibody were administrated before the LPS injection. RESULTS: Two weeks after injection, transgenic mice exhibited marked infiltration of eosinophils and extensive lobular necrosis. Transmigration of eosinophils through vascular endothelium and degranulation of eosinophil cytotoxic granules in inflamed areas were observed. These eosinophilic injuries were transient, but liver-specific. Pre-administration of GdCl3 and anti-TNF-alpha markedly reduced the hepatic inflammation, suggesting that LPS-activated Kupffer cells play a key role in producing the cytotoxicity of eosinophils by releasing TNF-alpha. CONCLUSIONS: We have established an experimental model of eosinophil-induced liver injury using IL-5 transgenic mice. Since this model is simple and highly reproducible, it will be useful for analysis of in vivo cytotoxic mechanisms of eosinophils.

Animals↗

Goblet cell carcinoid of the appendix: Investigation of the expression of beta-catenin and E-cadherin.

Goblet cell carcinoids are rare neoplasms that predominantly occur in the appendix. In this report we present a case of goblet cell carcinoid of the appendix. A 58-year-old male patient complaining of pain in the right lower quadrant was diagnosed with acute appendicitis and underwent an appendectomy. Histological examination of the resected appendix revealed goblet cell carcinoid. Infiltration of tumor cells beyond the appendix was observed and the surgically resected margin was positive for tumor cells. Carcinoembryonic antigen (CEA) was diffusely detected by immunohistochemistry, and cytokeratin 20, neuron-specific enolase (NSE), chromogranin A and serotonin were focally observed in the tumor cells. The expression of beta-catenin and E-cadherin was investigated to compare with that of typical rectal carcinoids (n = 3) and colon adenocarcinomas (n = 3). In normal colonic and rectal mucosae, beta-catenin and E-cadherin stained positive on the plasma membrane. In the case reported here, beta-catenin showed a preserved expression on the plasma membrane of goblet cell carcinoid; a pattern similar to typical carcinoids rather than to adenocarcinomas. However, E-cadherin demonstrated a reduced expression on the plasma membrane of the tumor cells. This staining pattern was identical to those both of carcinoids and of adenocarcinomas. These findings suggest the possibility that, in some cases, the adherens junctions of goblet cell carcinoids are similar to those of typical carcinoids rather than to those of adenocarcinomas.

Appendix↗

Adult-onset herpes simplex virus hepatitis with diffuse myofibroblastic transformation of hepatic stellate cells (Ito cells) in non-necrotic areas.

The myofibroblastic transformation of hepatic stellate cells (HSC; also known as Ito cells) usually occurs following necrosis of adjacent liver cells. No report has previously found that such a transformation occurs in herpes simplex virus (HSV) hepatitis. We present an autopsy case of HSV hepatitis with myofibroblastic transformation of HSC that is different from the usual transformation of HSC. The patient was a 66-year-old woman who had received various therapies for cutaneous T-cell lymphoma. An autopsy revealed submassive hepatic necrosis with hemorrhage due to HSV hepatitis. HSV infection was confirmed by DNA in situ hybridization in liver tissue. Immunohistochemical staining for alpha-smooth muscle actin (ASMA) showed a strong positive reaction in almost all of the HSC in non-necrotic areas. However, in necrotic areas, the HSC were completely negative for ASMA. These findings indicate that not only liver cells but also HSC can become necrotic in HSV hepatitis. In contrast, in non-necrotic areas, almost all of the HSC showed active transformation to myofibroblasts.

Actins↗

Malignant phyllodes tumor of the breast with expression of osteonectin and vinculin.

Phyllodes tumor is a very rare neoplasm which accounts for 2.5% of all fibroepithelial lesions of the breast. The mesenchymal component of a malignant phyllodes tumor frequently contains heterologous components. We report a case of malignant phyllodes tumor. The patient was a 40-year-old woman with a lump on the left breast. Histological examination revealed the lump to be a malignant phyllodes tumor with foci of liposarcomatous differentiation. The mesenchymal tumor cells, including those in the liposarcomatous components, were found to express vimentin, osteonectin and vinculin. However, they showed no immunoreaction to CAM 5.2, desmin, alpha-smooth muscle actin (ASMA), neuron-specific enolase (NSE) nor S-100. Ultrastructurally, the mesenchymal tumor cells were found to have abundant cytoplasmic organelles, but there was no evidence showing their differentiation to myofibroblasts. Further studies will be necessary to elucidate the significance of vinculin and osteonectin expression in malignant phyllodes tumor.

Adult↗