Search PubMed⌕ Search

Biomedical subjects

Y Tatemoto

Publications and source records attributed to Y Tatemoto.

At least 37 records · Page 2Linked to original sources

Squamous odontogenic tumor: immunohistochemical identification of keratins.

Two cases of squamous odontogenic tumors are described in terms of histopathology and keratin immunohistochemistry. Histopathologically, the lesions were composed of squamous epithelial islands without peripheral columnar cells and well-differentiated stromal tissue. Immunohistochemical detection of keratin proteins was done with the use of polyclonal antikeratin antiserum (TK, detecting 41 to 65 kDa keratins) and monoclonal antibodies (KL1, 55 to 57 kDa; PKK1, 40, 45, and 52.5 kDa). Staining for PKK1-detectable keratin was absent in tumor epithelial cells and that with KL1 and TK immunoreagents was confined to squamous cells, being strong in the keratinized cells. In view of the results, the squamous odontogenic tumor appears to arise from the rests of Malassez in periodontal tissue rather than from oral squamous epithelium.

Adult↗

Immunohistochemical expression of keratin proteins in urinary bladder carcinoma.

Transitional carcinomas of the urinary bladder were examined immunohistochemically for keratin proteins with the use of polyclonal antiserum (TK, 41-65 kDa) and 3 monoclonal antibodies (KL 1, 55-57 kDa; PKK 1, nos. 19, 18, 8; and K 8.12, nos. 16, 13). Umbrella cells gave particularly strong staining for TK, KL 1 and PKK 1, whereas they were negative for K 8.12. Basal- and intermediate-layer cells in urothelial epithelium were moderately positive for all keratins. Brunn's nests cells showed comparatively slight or moderate keratin staining, and K 8.12 staining of Brunn's nests was higher than in urothelial epithelial cells. Transitional carcinoma (grades I and II) indicated uniform keratin distribution, and staining was strong with TK, while that of KL 1, PKK 1 and K 8.12 varied, and grade III tumors showed the lowest intensity of staining. K 8.12 staining in papillary transitional carcinomas was strongly positive in basal located tumor cells, as compared with apical tumor cells. Squamous cell carcinoma was varying positive to keratin reactions dependent on the degree of keratinization. Heterogenity of keratin distribution in papillary transitional carcinomas was given between basal tumor cells and well differentiated tumor cells including umbrella-like cells.

Antibodies, Monoclonal↗

Calcifying odontogenic cyst immunohistochemical detection of keratin and involucrin in cyst wall.

Calcifying odontogenic cysts (COC) were immunohistochemically described using different keratin proteins and involucrin as well as histopathology. The cystic lining epithelium was composed of calcifying, keratinizing, squamous, and columnar epithelial cells, and included calcified masses of irregular shape and various size as well as ghost cells. Calcifying epithelium gave negative or only trace staining for keratins detected with low molecular keratin (PKK1), but were regularly positive with high molecular keratin (KL1) and polyclonal antibody for keratin (TK). They were occasionally positive for involucrin. The cells located in the periphery of the calcified masses had a particular abundance of high molecular weight and total keratins (KL1 and TK). Calcified bodies and ghost cells were devoid of any immunoreactivity. Squamous epithelium was relatively similar to that of normal squamous cell epithelium in the oral mucosa. It were most commonly found in columnar cystic epithelial cells which displayed intense staining with all immunoreagents. It is postulated that such epithelial cells may have a strong potentiality to transform into ghost cells or to undergo metaplasia. They may develop altered synthesis of homogenous acellular materials and finally become transformed into calcifying epithelium containing dystrophic calcified masses.

Adolescent↗

Adenomatoid odontogenic tumour: co-expression of keratin and vimentin.

Immunohistochemical observations of intermediate sized proteins in five cases of adenomatoid odontogenic tumour (AOT) are described. The immunohistochemical detections of keratins were made with polyclonal antiserum (TK, 41-65 kDa) and three monoclonal keratin antibodies (KL1: 55-57 kDa; PKK1: 40, 45, and 52.5 kDa and nos. 19, 18, 8; K8.12: nos. 16, 13) and vimentin and desmin monoclonal antibodies. Histologically, the tumour epithelia could be divided into two types: type A cells were a spindle or columnar shape and formed solid, ductal, tubular or whorled structures. Type B cells were small and compact cells at the periphery of the A cell-containing focus. Immunohistochemically, the type A cells showed very slight reaction with all antibodies to keratins, whereas the type B cells indicated slight-to-moderate expression of keratin and vimentin, and showed coexpression. Both types of cell showed a negative reaction for desmin. Only one case was associated with cystic lesions, and the cyst-lining was composed of thin squamous epithelium. Keratin expression in this epithelium was strong. In the histogenesis of AOT it was postulated that the tumour cells may have originated from undifferentiated odontogenic epithelium or stratum intermedium cells.

Adolescent↗

Ameloblastic fibroma: growth potentiality of odontogenic epithelium and coexpression of intermediate filament proteins in fibromatous cells.

Four cases of ameloblastic fibroma are described immunohistochemically in terms of intermediate-sized proteins in both epithelial and mesodermal components. Keratin proteins were demonstrated by polyclonal anti-keratin antiserum (TK: detecting 41-65 kDa keratins) and 2 monoclonal antibodies to keratin (KL1: 55-57 kDa, PKK1: 44, 46, 52 and 54 kDa), and monoclonal antibodies to vimentin and desmin. Two types of odontogenic epithelial tumour cells were discriminated: undifferentiated odontogenic cells and common ameloblastoma cells. Keratin expression was found to be stronger in undifferentiated cells than in the ameloblastoma cells. Undifferentiated cells were PAS-positive, while ameloblastoma cells were negative. Fibroma cells were strongly positive for vimentin, and negative for desmin. Keratin proteins were also expressed slightly. Thus, coexpression of keratin and vimentin was seen in fibroma cells. Histogenesis is discussed from the standpoint of the distribution patterns of keratin and vimentin, as well as with respect to the histopathology.

Child↗

Immunohistochemical localization of intermediate filament proteins in calcifying epithelial odontogenic tumors.

Three calcifying epithelial odontogenic tumors (CEOT) were examined immunohistochemically. The localization of intermediate filaments was characterized through the use of polyclonal anti-keratin antiserum (TK which detects 41-65 kd keratins), 2 monoclonal keratin antibodies (PKK1 specific for the 44, 46, 52 & 53 kd keratins and KL1, specific for the 55-57 kd keratins) and monoclonal antibodies for vimentin and desmin. The tumor epithelial cells were slightly positive or negative for PKK1 detectable keratins, but slightly to strongly positive for KL1 and TK antibodies. Tumor epithelium was slightly positive for vimentin but negative for desmin. The tumor foci were composed of both dark-staining and pale-staining cells; the former had a more intense reaction with KL1 and TK antibodies than the latter. Homogeneous acellular material was either PAS-positive or negative, with or without calcification, and keratin-negative.

Adult↗

Immunohistochemical detection of human epidermal growth factor in submandibular glands and their tumors using a polyclonal antiserum and a monoclonal antibody.

We applied immunohistochemical procedures to detect hEGF in salivary glands and pleomorphic adenomas of salivary-gland origin using a polyclonal hEGF antiserum and a monoclonal antibody against hEGF synthesized by applying the synthetic gene technique using Escherichia coli. In normal salivary glands, hEGF was mainly localized in the ductal system (i.e., intercalated, striated, and excretory ducts). The staining intensity and intracellular localization exhibited some variation depending on the fixative used. When a polyclonal hEGF antiserum was used for immunostaining, slight background staining was observed in sections prepared using the fixatives tested. Therefore, precise localization of hEGF was obtainable only in formalin-fixed sections using the monoclonal antibody against hEGF. In pleomorphic adenomas, positive hEGF staining was seen on the luminal side of tumors and in cells of ductal origin; no reactivity was present on the outer side of tumors or in cells of myoepithelial origin. Occasionally, long, spindle-shaped tumor cells and chondroidally changed tumor cells also exhibited positive staining for hEGF.

Adenoma↗

Expression of keratins during experimentally induced carcinogenesis in hamster cheek pouch visualized polyclonal and monoclonal antibodies.

We obtained immunohistochemical profiles of several keratin proteins during experimentally induced carcinogenesis in hamster cheek-pouch mucosa using a polyclonal antibody (TK; detecting keratins with molecular masses of 41-65 kilodalton) and two monoclonal antibodies (KL1, 55- to 57-kilodalton keratins; PKK1; 40-, 45- and 52.5-kilodalton keratins). The squamous epithelium of normal pouch mucosa exhibited positive TK staining in all layers, KL1 staining in the spinous layer and PKK1 staining in the basal layer, thus indicating a regional or zonal distribution pattern. Epithelia undergoing basal hyperplasia showed irregular localization of PKK1 binding, while hyperkeratinized lesions exhibited the binding pattern found in normal epithelium. In case of epithelial dysplasia, there was reduced KL1 staining in spinous cells and decreased PKK1 staining in the basal and parabasal layers. Papillomas exhibited a rather zonal distribution of keratin staining. All squamous-cell carcinomas, irrespective of their degree of keratinization and infiltration pattern, showed slight or no PKK1 staining. Such lesions were only positive for KL1-detectable keratins in keratinizing tumour cells and exhibited an irregular distribution of TK binding. The expression of keratin proteins during carcinogenesis in hamster cheek-pouch mucosa may parallel that of keratins in human squamous-cell carcinomas originating in the oral mucosa.

Animals↗

Immunohistochemical observations of keratins, involucrin, and epithelial membrane antigen in urinary bladder carcinomas from patients infected with Schistosoma haematobium.

Squamous cell carcinomas of the urinary bladder and the epithelial lesions associated with infection by Schistosoma haematobium were histopathologically and immunohistochemically described for keratin proteins (TK, 41-65 kDa; KL1, 55-57 kDa; PKK1, 40, 45 and 52.5 kDa), involucrin, and epithelial membrane antigen (EMA). Normal urothelial epithelium was positive for all keratins, and showed absent or slight reactions for involucrin and EMA in superficial umbrella cells. The intestinal type of epithelium was composed of columnar cells and small basal cells; TK was positive in the basal cells, KL1 staining was positive in the columnar cells, whereas PKK1 was negative or slight in the columnar cells. Involucrin was confined to columnar cells. Squamous metaplastic epithelium showed a rather regional keratin distribution: TK was distributed in all layers, KL1 decorated upper spinous and granular layers, but PKK1 did not bind, and involucrin staining existed only in upper spinous and granular cells. Keratin expression in squamous cell carcinomas indicated heterogeneity and its stainability was dependent on the degree of keratinization: The G 1 type revealed strong reaction, the G 2 type showed a similar distribution pattern, but the staining intensity was less, and the G3 type showed irregular staining with decreased intensity. Involucrin staining was limited to keratinized cells of carcinoma as was that for EMA.

Adult↗

Immunohistochemical observations on binding of monoclonal antibody to epithelial membrane antigen in epithelial tumors of the oral cavity and skin.

A total of 211 cases of benign and malignant tumors of epithelial origin were studied by the immunoperoxidase method to determine the distribution profile of epithelial membrane antigen (EMA) with the use of monoclonal antibody. Normal epithelial cells in the oral mucosa and skin were usually negative for EMA staining, as were epithelial cells in hyperplastic lesions and papillomas. Paget cells and tumor cells of Bowen's disease (carcinoma in situ) demonstrated a high incidence of EMA positivity, whereas the frequency in basal cell carcinoma was unexpectedly low. Squamous cell carcinomas revealed positive EMA staining of cytoplasmic membranes, and the antigen was also present in keratinized areas. EMA expression in squamous cell carcinoma generally showed a high incidence (85%) and was higher in keratinized lesions than in unkeratinized or less well-differentiated neoplasms. EMA distribution could be classified into two forms: one in which the cytoplasmic membranes demonstrate positivity and in which a positive cytoplasmic pattern is found in parakeratinized cells in malignant foci.

Antibodies, Monoclonal↗

Epithelial membrane antigen as a marker of human salivary gland acinar and ductal cell function.

Monoclonal antibody to epithelial membrane antigen (EMA) from human milk fat globule membrane was used with the immunoperoxidase method to examine the distribution of EMA in normal human salivary glands and in their obstructive lesions. EMA staining in the normal salivary gland was limited to luminal and lateral borders of acinar cells. The antigen was also present in high concentration on the luminal side of ductal cells. In obstructive lesions or sialoadenitis, lateral border and luminal positive staining in atrophic acinar cells was reduced or absent, and the EMA staining in duct-like structures was also markedly decreased on even absent in chronic stage. The degree of reduction in EMA staining was dependent on the extent of degeneration. Expression of immunohistochemically detectable EMA in paraffin sections suggests the antigen to be useful as a new marker of salivary gland function, of either acinar compartments or ductal segments.

Antibodies, Monoclonal↗

Distribution profiles of keratin proteins during rat amelogenesis.

We examined rat cells undergoing amelogenesis for the presence of three types of keratin proteins using a polyclonal antibody to keratin (against total keratins (TK) with molecular masses ranging from 41 to 65 kilodaltons (kd) and monoclonal antibodies keratins to KL1 and PKK1 (reactive with keratins with molecular masses of 55-57 and 41-56 kd, respectively). In normal oral epithelia from young rats, the TK, KL1, and PKK1 antibodies bound to all of the epithelial strata. The epithelial cap on the top of incisors and the dental lamina of molar teeth exhibited strong TK staining, moderate staining KL1, and little or no PKK1 staining. In developing molar enamel organs, both the outer and inner enamel epithelia, the stratum intermedium, and stellate reticulum cells were all positively stained by the TK immunoreagent. In developing incisors, TK only bound strongly to stratum-intermedium cells, and no KL1 and PKK1 staining antibodies was observed in ameloblasts or the stratum intermedium.

Amelogenesis↗

Immunohistochemical localization of amylase in sialoadenitis and salivary gland tumors.

Immunohistochemical demonstration of alpha-amylase has been made in sialoadenitis-involved tissue and salivary gland tumors, as well as in normal salivary glands. Immunoreactive alpha-amylase with trypsin pretreatment was confined to irregularly staining serous acinar cells in the parotid and submandibular glands, and to demilunes in sublingual glands. In obstructive adenitis, staining was irregular from high to negative in acini in early or intermediate stages. Dilated ductal segments contained cells positive for alpha-amylase in the early stage following obstruction. Pleomorphic adenomas were usually negative for alpha-amylase but in rare cases tumor epithelia stained variably positive; i.e., staining occurred throughout the cytoplasm or at the periphery or apical part of the tumor cells. Luminal cavities of tubular and duct-like structures contained alpha-amylase-positive material. Epithelia in Warthin's tumor were also negative in general; however, scattered single or grouped tumor cells containing alpha-amylase were found. Mucoepidermoid tumors were also negative, though slightly positive cells were found intermingled among the negative squamous and mucous tumor cells. Cystic lesions in mucoepidermoid tumor were sometimes positive in the wall cells together with material secreted into the lumen.

Adenoma, Pleomorphic↗

Lectin-binding patterns in the developing tooth.

The lectin-binding patterns of the cells involved in amelogenesis and dentinogenesis in developing teeth of rats were studied. Undifferentiated odontogenic epithelia exhibited very slight staining with almost all of the lectins examined. The lectin-staining affinities of secretory ameloblasts could be divided into two categories: Concanavalin-A (Con-A), Wheat germ agglutinin (WGA) and Soybean agglutinin (SBA) binding occurred from the middle to apical cytoplasm, whereas Ricinus communis agglutinin-I (RCA-I) and Ulex europeus I (UEA-I) binding predominated in the basal regions. The cells of the stratum intermedium exhibited relatively strange lectin staining, which appeared to be dependent on ameloblastic maturation. The basement membranes in undifferentiated epithelia were markedly positive for lectin binding. Odontoblasts showed moderate Con-A staining on the apical side of the cells, as well as slight-to-moderate reactions with WGA and SBA. Pulp cells and dental papillae showed slight-to-moderate lectin staining, and predentin and dentin were also moderately positive for Con-A and RCA-I binding and slightly so for WGA and SBA. The lectin-binding affinities were enhanced during the formation of enamel and dentin, and appeared to be dependent on the degree of cellular differentiation in ameloblasts and odontoblasts.

Ameloblasts↗

False positive reaction for carcinoembryonic antigen in Paget cells. Immunohistochemical observation.

Paget cells from cases of mammary and extramammary Paget's disease were examined for carcinoembryonic antigen (CEA) and CEA-related antigens by the immunoperoxidase method. Paget cells showed a conspicuous positive reaction with antiserum to CEA, but were negative when nonspecific cross-reacting-antigen (NCA)-absorbed antiserum to CEA, or a monoclonal antibody to CEA was used as the detecting agents. Paget cells may contain large amounts of NCA antigen or CEA-related substances.

Antibodies, Monoclonal↗

Immunohistochemical detection of epidermal growth factor in submandibular gland tumours of mice administered testosterone.

Immunohistochemical identification of epidermal growth factor (EGF) is described in experimental carcinoma of the submandibular gland of mice given testosterone before sacrifice. EGF in the submandibular gland was confined to the granular convoluted tubule (GCT) cells, and its level was enhanced following testosterone injection. In the initial phase of carcinogenesis of the gland, degranulation of the GCT cells occurred as well as decreased EGF staining in the degranulated cells. In the testosterone-treated animals, changed GCT cells showed intense EGF deposition. Histological aspects during carcinogenesis in submandibular glands indicated duct-like structures, squamous metaplasia, and squamous cell types of carcinoma with different keratinization. Immunohistochemically detectable EGF was characterized by positive staining in pre-neoplastic or early neoplastic epithelial structures in testosterone-treated mice. However, tumour epithelia did not show any EGF reaction.

Animals↗

Histochemical studies of obstructive adenitis in human submandibular salivary glands. I. Immunohistochemical demonstration of lactoferrin, lysozyme and carcinoembryonic antigen.

Immunohistochemical detection of lactoferrin (LF), lysozyme (LZ) and carcinoembryonic antigen (CEA) was made in obstructive adenitis of the submandibular glands. Atrophic and altered acinar cells in the early stage of the lesion stained strongly for LF, whereas they were unreactive or stained slightly for LZ. Ductal cells usually stained for LZ. Staining for CEA was strong and irregularly distributed in altered acinar cells. Duct-like structures and dilated ductal segments in the chronic stage were generally negative for LF, LZ and CEA. Secretory components in luminal cavities gave abundant staining for LF, LZ and CEA. Histocytes which infiltrated into the connective tissue in the later stage showed a positive LZ reaction.

Acute Disease↗