muramidase and Adenoma

Topics: Adenoma; alpha 1-Antitrypsin; alpha-Fetoproteins; Animals; Antigens; Carcinoembryonic Antigen; Fluorescent Antibody Technique; Humans; Immunoenzyme Techniques; Immunoglobulins; Lymphoma; Muramidase; Neoplasms; Pituitary Hormones; Pituitary Neoplasms

In the normal duodenal mucosa, differentiated cells (enterocytes, goblet cells and endocrine cells) migrate from stem cells to the tip of the villi, but the lysozyme-producing Paneth cells migrate to the bottom of the crypts. The position of the Paneth cells within duodenal adenomas was investigated.. Sections from 83 duodenal adenomas were stained with hematoxylin-eosin (H&E) and with anti-lysozyme. Mature Paneth cells were those showing coarse brightly red cytoplasmic granules in H&E stain whereas their precursors were the lysozyme-positive cells that were undetected by H&E.. The number of mature Paneth cells/high power field (x 40) varied in adenomas from 4 to 12 (mean 65) in H&E stain, while 32 to 62 cells/field (mean 46.5) were positive in anti-lysozyme immunostain (p < 0.05). The lysozyme-expressing cells were randomly distributed within the adenoma including the superficial cell layers.. Since mature Paneth cells and their precursors are positioned underneath stem cells, the presence of mature Paneth cells and their lysozyme-positive precursors in the surface epithelium of duodenal adenomas would imply that stem cells might have already exfoliated. An alternative explanation would mean that mutated stem cells, anchored in the bottom of the crypts of the adenoma would redirect, in an unparalleled fashion, the ontogenetic logistics of migration for Paneth cells. This stochastic molecular behaviour would require a reversal from the pre-determined migratory flow for Paneth cells to a paradoxical migration mode for these cells (from stem cells vertically along the villus, before exfoliation). Consequently, it is not inconceivable that stem cells might participate, together with other mature cells, in the cellular turnover of duodenal adenomas. If that is the case, the duodenal adenoma emerges as a suitable model to monitor the actual fate of mutated stem cells.

Topics: Adenoma; Adenomatous Polyposis Coli; Duodenal Neoplasms; Eosine Yellowish-(YS); Hematoxylin; Humans; Intestinal Mucosa; Muramidase; Neoplastic Stem Cells; Paneth Cells; Staining and Labeling

Intercalated duct lesions (IDLs) are rare, poorly understood and not well-studied lesions that have been associated with a small number of epithelial-myoepithelial carcinomas (EMC) and basal cell adenomas. To examine the nature of IDLs and their association with salivary gland tumors, we reviewed 34 lesions in 32 patients. The IDLs were stained with CK7, estrogen receptors (ER), progesterone receptors, lysozyme, S100, calponin, and CK14. The patients ranged in age from 19 to 80 years (mean 53.8) with a 1.7:1 female predominance. The majorities of IDLs were parotid lesions (82%), were small and nodular (average size 3.1 mm) and showed 3 architectural patterns: hyperplasia (20), adenoma (9), and hybrid forms (5). In 59% of cases, IDLs were seen in conjunction with another salivary gland tumor, most commonly basal cell adenoma (8 cases), followed by EMC (3 cases). One case showed a combination of intercalated duct hyperplasia and basal cell adenoma. The IDLs stained diffusely with CK7 (100%) and S100 (73%) and focally for ER (91%) and lysozyme (100%). Calponin and CK14 highlighted a thin myoepithelial cell layer around all ducts (100%). Normal intercalated ducts were also consistently positive for CK7 and lysozyme, and focally for ER, but were S100 negative. In summary, IDLs have a variety of patterns ranging from hyperplasia to adenoma with hybrid lesions and share morphologic and immunophenotypic features with normal intercalated ducts. There is an association with basal cell adenomas and EMC, which lends credence to their role as a putative precursor lesion.

Topics: Adenoma; Adult; Aged; Aged, 80 and over; Biomarkers, Tumor; Calcium-Binding Proteins; Calponins; Female; Humans; Hyperplasia; Keratins; Male; Microfilament Proteins; Middle Aged; Muramidase; Neoplasms, Multiple Primary; Parotid Gland; Receptors, Steroid; S100 Proteins; Salivary Ducts; Salivary Gland Neoplasms; Submandibular Gland; Young Adult

The expression profile of adenoma induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) in A/J mice was compared with that of normal lung tissue by suppression subtractive hybridization (SSH). The mRNAs of surfactant-associated protein A (SP-A) and lysozyme showed characteristically higher transcription in the adenoma tissue than in normal lung. High expression of both SP-A and lysozyme in tumor cells was confirmed by in situ hybridization (ISH). In normal lung, alveolar type II pneumocytes were positive for both SP-A and lysozyme, indicating that tumor cells retained the phenotypic characteristics of the murine alveolar type II pneumocytes. Previous studies of human adenocarcinomas have shown that the two proteins are expressed reciprocally; SP-A and lysozyme are differential markers of atypical adenomatous hyperplasia (AAH) and non-goblet cell type adenocarcinoma, and of goblet cell type adenocarcinoma, respectively. Thus, the present results indicate that the phenotype of NNK-induced A/J mouse adenoma differs from that of AAH, which is thought to be a preinvasive lesion of human adenocarcinoma.

Topics: Adenoma; Animals; Apoproteins; Carcinogens; DNA-Directed RNA Polymerases; DNA, Complementary; Female; In Situ Hybridization; Lasers; Lung; Mice; Microscopy, Electron, Transmission; Muramidase; Nitrosamines; Phenotype; Promoter Regions, Genetic; Pulmonary Surfactant-Associated Protein A; RNA; RNA, Messenger; Surface-Active Agents; Time Factors; Viral Proteins

It has been suggested that the behavior and function of Paneth cells in metaplasia are different from those found in normal intestinal mucosa. In this study, we investigated whether calnexin, a protein involved in secretory pathways, might be associated with differentiation and function of Paneth cells in normal small intestine, in complete intestinal metaplasia of the stomach, and in Paneth cell-rich adenomas. Differentiation and function of Paneth cells was monitored by Ki67, lysozyme, and morphologic features. Using a newly established monoclonal antibody, we found that calnexin is regularly synthesized by Paneth cells of normal small intestine. In these cells, the staining intensity of calnexin was inversely correlated with their content of secretory granules (lysozyme). In contrast, Paneth cells of intestinal metaplasia and Paneth cell-rich adenomas showed a reduced immunostaining of both calnexin and lysozyme. Moreover, these Paneth cells synthesized the proliferation marker Ki67, a phenomenon that was never observed in Paneth cells of normal small intestine. In vitro experiments using CaCo2 cells showed that the expression of calnexin is not directly affected by the induction of mitosis. In conclusion, calnexin probably reflects the status of Paneth cell differentiation and function. The results do not necessarily indicate that calnexin has a function in Paneth cell proliferation.

Topics: Adenoma; Adult; Aged; Aged, 80 and over; Caco-2 Cells; Calnexin; Cell Differentiation; Female; Gastric Mucosa; Humans; Immunohistochemistry; Intestine, Small; Ki-67 Antigen; Male; Metaplasia; Middle Aged; Muramidase; Paneth Cells; Secretory Vesicles; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; Stomach; Stomach Neoplasms

The presence of lysozyme protein in some gastric adenomas and adenocarcinomas has been well documented. There have been relatively few studies investigating the presence of lysozyme in tumours of the large intestine and they show contrasting results. We aim to investigate the cellular source and expression of lysozyme in colonic adenomas and adenocarcinomas.. We randomly selected 29 and 27 colonic adenomas and adenocarcinomas, respectively. Using in-situ hybridization (ISH) and immunohistochemistry (IHC), we found an up-regulation of lysozyme in the dysplastic epithelium of all the adenomas studied, with more than 80% of cases expressing moderate to strong signals. Although the up-regulation of lysozyme was also observed in adenocarcinomas, only 30% of the cases showed moderate to strong signals, mostly with an uneven distribution. Down-regulation of lysozyme in the severely dysplastic and invasive foci were noted in some cases of adenoma with malignant transformation. Normal colonic glands were consistently negative for lysozyme at both the mRNA and the protein level, but inflamed and immature regenerative colonic epithelium at the crypt base showed positive signals in a similar pattern to those observed in the dysplastic epithelium of the adenomas.. Our results confirm that colonic epithelium can produce lysozyme and its expression is up-regulated in the dysplastic epithelium in adenomas and in invasive cancer cells. It is interesting that regenerative colonic epithelium showed a similar pattern of lysozyme expression as in adenomas. The loss of lysozyme secreting phenotype in most of the invasive tumours suggests that lysozyme may not confer an advantage to tumour progression.

Topics: Adenocarcinoma; Adenoma; Colonic Neoplasms; Humans; Immunohistochemistry; In Situ Hybridization; Intestinal Mucosa; Muramidase; Random Allocation; RNA, Messenger; Up-Regulation

We carried out an immunohistochemical analysis of nine spiradenomas and seven cylindromas. Our findings underscore the histomorphological similarities of the two adnexal neoplasms-namely, the expression of S-100 protein ascribed to eccrine differentiation within the tubular and large, pale-staining cells of both entities. Human milk fat globulin (HMFG) and lysozyme, two markers associated with apocrine differentiation, are expressed by tubular cells in spiradenomas and cylindromas. Lysozyme is also expressed in cylindromas by large, pale-staining cells. In addition, antibodies to alpha-smooth muscle actin strongly characterized the small basaloid cells of both types of neoplasm. Both spiradenomas and cylindromas expressed identical cytokeratin patterns. As with the various regions of eccrine and apocrine units, the expression by spiradenomas and cylindromas of keratins 7, 8, and 18 indicates differentiation toward the secretory tissue, whereas the expression of keratin 14 in some of the neoplastic cells points toward ductal differentiation. Malformed ductal and glandular structures in continuity with evolving spiradenomas and cylindromas in two of our cases also suggest that these tumors might arise from abortive adenxal anlagen.

Topics: Actins; Adenoma; Adenoma, Sweat Gland; Apocrine Glands; Apolipoproteins; Apolipoproteins D; Biomarkers, Tumor; Carcinoembryonic Antigen; Carrier Proteins; Cell Differentiation; Cell Lineage; Eccrine Glands; Gene Expression Regulation, Neoplastic; Glycoproteins; Humans; Immunohistochemistry; Keratins; Ki-67 Antigen; Membrane Transport Proteins; Morphogenesis; Mucin-1; Muramidase; Neoplasm Proteins; S100 Proteins; Skin Neoplasms; Sweat Gland Neoplasms; Vimentin

The authors have previously shown that duodenal adenomas in familial adenomatous polyposis (FAP) patients typically reveal abundant cells with endocrine differentiation (ED), Paneth differentiation (PD), and goblet cell differentiation (GD). However, the biological significance and proliferative potential of these cells is unknown. To study the proliferative properties of cells with ED, PD, or GD in FAP-associated duodenal adenomas, the authors used a double-labeling immunohistochemical technique to detect simultaneously the presence of proliferating cell nuclear antigen (PCNA), and either chromogranin or lysozyme in individual neoplastic cells. Adenomatous cells with GD were identified morphologically and also evaluated for the degree of PCNA expression by immunohistochemistry. Duodenal adenomas and the adjacent nonadenomatous epithelium from 10 FAP patients were studied. Cells with ED, PD, and GD were present in all adenomas, and constituted 14.1%, 11.6%, and 17.7% of adenomatous cells, respectively. The overall proliferative index of nondifferentiated adenomatous cells was 33.3%, which was similar to the proliferative index obtained for adenomatous cells with GD (31.2%) and nonadenomatous crypt goblet cells (34.9%). In contrast, adenomatous cells with ED and PD showed a significant decrease in their proliferative potential (P < .001). Only 6.0% and 7.3% of cells with ED and PD, respectively, were proliferative. Nonadenomatous crypt endocrine and Paneth cells showed no proliferative potential (proliferative index 0%). These results suggest that, in the process of proliferation and differentiation, specific subpopulations of adenomatous cells attempt to recapitulate the biological characteristics of their normal counterparts in the small intestinal crypts. Adenomatous cells with ED and PD are hypoproliferative, a finding that is consistent with their differentiated phenotype and suggests that these cells may not participate as actively in the growth of these lesions.

Topics: Adenoma; Adenomatous Polyposis Coli; Adult; Cell Differentiation; Cell Division; Chromogranins; Duodenal Neoplasms; Female; Humans; Immunoenzyme Techniques; Intestinal Mucosa; Male; Muramidase; Proliferating Cell Nuclear Antigen

Thirteen dermal cylindromas (DC) have been studied immunohistochemically using a panel of antibodies that stain different portions of normal eccrine and apocrine glands. Distinct staining patterns were found in the different cell populations of the tumor. Although the expression of cytokeratins (CK) 19 and 1/10/11 in occasional duct structures could indicate excretory (ductal) differentiation, a link between DC and apocrine secretory coil is suggested by the expression of alpha-1-antichymotrypsin, lysozyme, human milk factor globulin 1, alpha smooth muscle actin (1A4), and CK 8 and 18. The presence of intermingled S-100 protein-, HLA DR-, and CD1a-positive cells argues for the existence of Langerhans cells within the neoplasm. DC shares epithelial membrane antigen, carcinoembryonic antigen, mucin-like carcinoma-associated antigen (B12), laminin, collagen IV, fibronectin, and CD34(QBEND/10) expression with both eccrine and apocrine glands.

Topics: Actins; Adenoma; alpha 1-Antichymotrypsin; Antigens, CD1; Antigens, CD34; Antigens, Neoplasm; Antigens, Tumor-Associated, Carbohydrate; Apocrine Glands; Biomarkers, Tumor; Carcinoembryonic Antigen; Cell Differentiation; Collagen; Coloring Agents; Eccrine Glands; Fibronectins; Gene Expression Regulation, Neoplastic; HLA-DR Antigens; Humans; Keratins; Laminin; Langerhans Cells; Mucin-1; Mucins; Muramidase; Neoplasm Proteins; S100 Proteins; Sweat Gland Neoplasms

Min is a fully penetrant dominant mutation that leads to the development of multiple intestinal adenomas throughout the duodenal-to-colonic axis. Min/+ C57BL6/J mice have an average life-span of 120 d. Multi-label immunocytochemical studies of these lesions demonstrate patches of differentiated enterocytes, and scattered enteroendocrine, goblet and Paneth cells. Expression of endogenous marker genes within these differentiated cells can be directly correlated with the position occupied by the adenoma along the duodenal-to-colonic axis and mirrors the regional differentiation of the normal gut epithelium. The presence of multiple lineages in adenomas together with their retention of spatial information suggests that tumorigenesis in Min/+ mice may be initiated in a multipotent stem cell normally located at the base of intestinal crypts. To study the time-dependent properties of these tumors, genetic conditions were sought in which Min/+ animals could survive for up to 300 d. Min is fully penetrant in hybrids with either AKR/J or MA/MyJ. However, the hybrids demonstrate a reduction in the number of intestinal adenomas. Preliminary backcross analysis is consistent with a single major modifier locus unlinked to Min in both the AKR/J and MA/MyJ strains. The increased lifespan of the hybrid animals is also associated with the development of invasive tumors. New tumors do not arise continuously over the lifespan of these animals; instead all adenomas appear to be established by 100 d of age or sooner. These studies indicate that the Min/+ mouse is a powerful model system for analyzing the mechanisms that establish and maintain a balance between proliferation and differentiation in the continuously renewing gut epithelium and for an assessment of the multi-step hypothesis of intestinal neoplasia.

Topics: Adenoma; Animals; Carrier Proteins; Cell Differentiation; Crosses, Genetic; Epithelium; Fatty Acid-Binding Protein 7; Fatty Acid-Binding Proteins; Fatty Acids; Intestinal Mucosa; Intestinal Neoplasms; Mice; Mice, Inbred Strains; Mice, Mutant Strains; Mucins; Muramidase; Mutation; Neoplasm Proteins; Neoplastic Stem Cells; Nerve Tissue Proteins; Phenotype; Serotonin

High levels of lysozyme have been reported to be present in the feces of patients with colorectal cancer. It has been suggested that fecal lysozyme could prove useful in the early detection of colorectal cancer, but that further work is needed. The present investigation reports on the measurement of fecal lysozyme in 23 colorectal cancer patients and 39 healthy controls. The mean fecal lysozyme level for the cases was 13.3 +/- 2.8 micrograms/g stool compared with 12.5 +/- 2.6 micrograms/g stool for the controls. The median level for the cases was 8.7 micrograms/g stool compared with 6.6 micrograms/g stool for the controls. Forty-three percent of the cases and 31% of the controls had fecal lysozyme levels above 10 micrograms/g stool. None of these differences were statistically significant. The results of this study indicate that fecal lysozyme would be of no use in the early detection of colorectal cancer.

Topics: Adenoma; Adult; Age Factors; Aged; Aged, 80 and over; Biomarkers, Tumor; Clinical Enzyme Tests; Colorectal Neoplasms; Feces; Female; Humans; Male; Middle Aged; Muramidase; Odds Ratio

We examined 12 depressed tubular adenomas of the stomach pathologically and immunohistochemically in order to clarify the difference between the depressed type and the elevated type. Depressed tubular adenomas showed shallow mucosal depression and, of the 12, nine were endoscopically diagnosed as early gastric cancer. Histologically, the adenoma cells showed dysplasia in varying degree and focal adenocarcinoma occurred in two adenomas measuring over 2 cm. The mean height of the adenoma glands was 0.63 +/- 0.31 mm in the 12 depressed adenomas and 1.32 +/- 0.43 mm in 44 elevated adenomas, while the mean heights of the subjacent mucosa were 0.18 +/- 0.19 mm and 1.07 +/- 0.71 mm, respectively. Thus, depressed adenomas resulted from paucity of the mucosa subjacent to the adenoma glands and the height of the adenomatous glands was half that found in the elevated type. Goblet cells, a variety of endocrine cells and lysozyme-containing cells were found in nine, nine and eight depressed adenomas, respectively, in variable numbers. Hyperplasia of these cells was also detected in depressed adenomas showing mild or moderate dysplasia. Immunohistochemical examination revealed no difference in the phenotypic expression of adenoma cells as between the depressed and the elevated type.

Topics: Adenoma; Antigens, Tumor-Associated, Carbohydrate; Carcinoembryonic Antigen; Glicentin; Glucagon; Glucagon-Like Peptides; Humans; Immunohistochemistry; Muramidase; Peptide Fragments; Protein Precursors; Serotonin; Somatostatin; Stomach Neoplasms

A method for the simultaneous demonstration of lysozyme and mucins in 39 cases of gastric adenomas differentiated two intermediate cell types. The first was similar to a columnar cell comprising a single cell population which covered extensive areas of the adenomas. This cell type often showed supranuclear lysozyme reactivity and apical neutral mucins, sialomucins, and sulphomucins in variable amounts. The second cell type was found in 11 adenomas, located mainly in the fundal area. It seemed to be a transitional form between the goblet cell and the Paneth cell. This cell type was scattered among columnar cells, occasional Paneth-like cells, and small goblet cells. These two types of intermediate cells may be regarded as abnormally differentiated integral elements of gastric adenomas. They may be associated with the neck stem cells in the cytogenesis of gastric adenomas.

Topics: Adenoma; Aged; Aged, 80 and over; Antigen-Antibody Reactions; Female; Humans; Male; Middle Aged; Mucins; Muramidase; Papilloma; Staining and Labeling; Stomach Neoplasms

Immunohistochemical identification of lysozyme and lactoferrin was made in salivary pleomorphic adenomas (147 cases) and the staining patterns were evaluated with respect to the histological features and histogenesis. In normal salivary glands, the intercalated duct cells gave positive staining for lysozyme in major glands, and serous acinar cells, demilune cells, and interlobular duct cells were positive in minor glands. Lactoferrin staining was irregularly positive in serous cells and ductal epithelium. In pleomorphic adenomas, the reaction for lysozyme was positive in 14% (21/147) of the cases, and was confined to luminal cells of tubulo-ductal structures. Lactoferrin in pleomorphic adenomas was distributed in luminal tumor cells (51%; 75/147), in outer tumor cells (3%; 4/147), and in both luminal and outer tumor cells (5%; 7/147) in tubulo-ductal structures; it was also detected in plasmacytoid myoepithelial cells (5%, 8/147). However, modified myoepithelial cells and other types of neoplastic myoepithelial participants were negative for lactoferrin staining. The occurrence of both lysozyme and lactoferrin in salivary pleomorphic adenomas suggests their participation in the local defense mechanism in the tumor.

Topics: Adenoma; Humans; Immunohistochemistry; Lactoferrin; Lactoglobulins; Muramidase; Salivary Gland Neoplasms

Serum lysozyme activity (SLA) was measured in a turbidimetric assay with a microcentrifugal analyzer. In a control group of 53 healthy dogs of both sexes and ranging in age from 4 to 10 years, SLA had a mean value of 1.2 mg/l with a range (+/- 2 SD) of 0.6 - 1.8 mg/l. In 80 dogs with a variety of neoplastic diseases the histopathological diagnosis was compared with the SLA value. SLA value was increased in 83% of the cases with malignant tumors and in 29% of the cases with benign tumors. Proper clinical examination is essential in differentiating between neoplastic disease and some interfering diseases, e.g. chronic dermatitis, pyometra and chronic nephritis. Measuring of SLA in dogs may be helpful in screening those animals with suspected malignancies.

Topics: Adenoma; Animals; Carcinoma; Dog Diseases; Dogs; Female; Immunodiffusion; Male; Mammary Glands, Animal; Melanoma; Muramidase; Neoplasms; Nephelometry and Turbidimetry; Reference Values; Sarcoma; Skin Neoplasms; Soft Tissue Neoplasms

Normal and metaplastic gastrointestinal mucosa obtained at surgical resection were studied by light microscopy, using the unlabelled antibody enzyme method for immunohistochemical staining of lysozyme, pancreatic endoproteases, and pancreatic secretory trypsin inhibitor (PSTI). Paneth cells in the mucosa of normal small intestine, gastric mucosa with intestinal metaplasia, and colonic metaplastic mucosa were found to contain anionic trypsin, cationic trypsin, lysozyme, and PSTI immunoreactivity, but not chymotrypsin and elastase immunoreactivity. Normal gastric and colonic mucosa and some goblet cells in the small intestine showed positive PSTI immunoreactivity but no endoprotease immunoreactivity. The presence of immunoreactive trypsin and immunoreactive PSTI in the Paneth cells, which are of secretory type, probably indicates an important extrapancreatic source of these proteins rather than a storage of endocytosed material.

Topics: Adenoma; Colitis, Ulcerative; Gastric Mucosa; Humans; Immunoelectrophoresis; Immunoenzyme Techniques; Intestinal Mucosa; Intestinal Neoplasms; Muramidase; Pancreas; Peptide Hydrolases; Trypsin; Trypsin Inhibitors

A total of 49 gastric tubular adenomas and 6 tubular adenomas with foci of adenocarcinoma from surgically resected stomachs were examined histologically and immunohistochemically for gut peptide hormones, serotonin, carcinoembryonic antigen (CEA), secretory component (SC), and lysozyme. A variety of endocrine cells were detected in tubular adenoma with mild to moderate atypia. Both the frequency and distribution density were highest for serotonin-containing EC cells, often showing hyperplasia, followed by glicentin-containing L cells, somatostatin-containing D cells and motilin-containing Mo cells in the order given. Adenoma cells with SC immunoreactivity were more dominant than those with CEA immunoreactivity. In tubular adenoma with severe atypia, endocrine cells were markedly decreased, whereas adenoma cells with CEA immunoreactivity were increased. The distribution density of lysozyme-containing cells in tubular adenoma of the intermediate zone and fundus was significantly higher than that of the antrum. In the subjacent mucosa of the adenoma, L cells and SC-positive epithelial cells were detected in 24 and 33 cases, respectively. These findings suggest that gastric tubular adenoma develops from intestinal metaplasia. In addition, gastric tubular adenoma showed a tendency to lose various intestinal markers with increase of histologic atypicality.

Topics: Adenoma; Aged; Carcinoembryonic Antigen; Endocrine Glands; Female; Gastrointestinal Hormones; Humans; Immunoenzyme Techniques; Immunoglobulin Fragments; Male; Middle Aged; Muramidase; Secretory Component; Serotonin; Stomach Neoplasms

Five thousand seven hundred seventy-eight adenomas or adenomas containing carcinoma from 3215 patients were examined by routine histologic methods for the presence of epithelial metaplasias. Three forms of epithelial metaplasia were encountered: squamous cell metaplasia (0.44%), Paneth cell metaplasia (0.20%), and melanocytic metaplasia (0.017%). In several instances multiple forms of metaplasia were encountered in the same polyp. In those cases in which the paraffin blocks were available, a Grimelius stain was performed. Grimelius-positive cells were present in 63% of the adenomas containing a metaplastic cell type. All cases with Paneth cell differentiation were immunoreactive for lysozyme; all lesions containing areas of squamous differentiation were immunoreactive for keratin except 2. The histopathologic features of these cases are discussed, and it is concluded that rather than representing a true metaplastic process, Paneth cell, squamous cell, and melanocyte differentiation represent the full range of cellular differentiation that endodermally derived tissues can exhibit, particularly when they undergo neoplastic alterations.

Topics: Adenoma; Adult; Age Factors; Aged; Cell Differentiation; Colonic Neoplasms; Female; Histocytochemistry; Humans; Intestinal Polyps; Intestine, Large; Keratins; Male; Melanocytes; Metaplasia; Middle Aged; Muramidase; Rectal Neoplasms; Retrospective Studies; Sex Factors

Enzyme histochemical and ultrastructural studies of a "dexamethasone-suppressed" virilizing adrenocortical adenoma and the attached cortex revealed that tumor cells showed little activities of some lysosomal enzymes and scarcity of lipofuscins and dense bodies of lysosomal type, forming a marked contrast to the cells of zona reticularis and the virilizing adenomas previously reported. The other findings of tumor cells, such as a pattern of activities of dehydrogenases including 3beta-hydroxysteroid dehydrogenase and the morphology of mitochondria, were those of reticularis cells. The findings showed that scantiness of lipofuscins did not rule out the possibility of adenoma producing adrenal androgen, dehydroepiandrosterone. Most of the tumor cells as well as reticularis cells were positive for alkaline phosphatase, the activity of which was interpreted as the effect of ACTH stimulation.

Topics: 3-Hydroxysteroid Dehydrogenases; Adenoma; Adrenal Cortex Neoplasms; Adult; Dehydroepiandrosterone; Endoplasmic Reticulum; Female; Glucosephosphate Dehydrogenase; Hexosaminidases; Humans; Isocitrate Dehydrogenase; L-Lactate Dehydrogenase; Mitochondria; Muramidase; Oxidoreductases; Phosphogluconate Dehydrogenase; Succinate Dehydrogenase

Topics: Adenoma; Carcinoma; Creatinine; Dysgerminoma; Female; Humans; Kidney Neoplasms; Male; Multiple Myeloma; Muramidase; Ovarian Neoplasms; Pelvic Inflammatory Disease; Penile Neoplasms; Prostatic Hyperplasia; Prostatic Neoplasms; Urinary Bladder Neoplasms; Urogenital Neoplasms; Uterine Neoplasms; Vaginal Neoplasms