acid-phosphatase and Mouth-Neoplasms

Ameloblastoma is the most common benign odontogenic tumor in Japan. It is believed that it expands in the jaw bone through peritumoral activation of osteoclasts by receptor activator of nuclear factor kappa-B ligand (RANKL) released from the ameloblastoma, as in bone metastases of cancer cells. However, the clinical features of ameloblastoma, including its growth rate and patterns of invasion, are quite different from those of bone metastasis of cancer cells, suggesting that different underlying mechanisms are involved. Therefore, in the present study, we examined the possible mechanisms underlying the invasive expansion of ameloblastoma in the jaw bone. Expression levels of RANKL assessed by western blotting were markedly lower in ameloblastoma (AM-1) cells than in highly metastatic oral squamous cell carcinoma (HSC-3) cells. Experiments coculturing mouse macrophages (RAW264.7) with AM-1 demonstrated low osteoclastogenic activity, as assessed by tartrate-resistant acid phosphatase (TRAP)-positive multinuclear cell formation, probably because of low release of RANKL, whereas cocultures of RAW264.7 with HSC-3 cells exhibited very high osteoclastogenic activity. Thus, RANKL release from AM-1 appeared to be too low to generate osteoclasts. However, AM-1 cultured directly on calcium phosphate-coated plates formed resorption pits, and this was inhibited by application of bafilomycin A1. Furthermore, vacuolar-type H+-ATPase (V-ATPase) and H+/Cl- exchange transporter 7 (CLC-7) were detected on the surface of AM-1 cells by plasma membrane biotinylation and immunofluorescence analysis. Immunohistochemical analysis of clinical samples of ameloblastoma also showed plasma membrane-localized V-ATPase and CLC-7 in the epithelium of plexiform, follicular and basal cell types. The demineralization activity of AM-1 was only 1.7% of osteoclasts demineralization activity, and the growth rate was 20% of human normal skin keratinocytes and HSC-3 cells. These results suggest that the slow expansion of several typical types of ameloblastomas in jaw bone is attributable to its slow growth and low demineralization ability.

Topics: Acid Phosphatase; Ameloblastoma; Animals; Cell Line, Tumor; Cell Membrane; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Humans; Isoenzymes; Jaw; Jaw Neoplasms; Keratinocytes; Mice; Mouth Neoplasms; Neoplasm Invasiveness; Neoplasm Metastasis; Osteoclasts; RANK Ligand; RAW 264.7 Cells; Tartrate-Resistant Acid Phosphatase; Vacuolar Proton-Translocating ATPases

Oral squamous cell carcinoma (OSCC) often spreads from the primary tumor to regional lymph nodes in the early stage. Better understanding of the biology of lymphatic spread of oral cancer cells is important for improving the survival rate of cancer patients.. We established the cell line LNMTca8113 by repeated injections in foot pads of nude mice, which had a much higher lymphatic metastasis rate than its parental cell line Tca8113. Then, we compared the biologic behaviors of cancer cells between them. Moreover, microarray-based expression profiles between them were also compared, and a panel of differential genes was validated using real-time-PCR.. In contrast to Tca8113 cells, LNMTca8113 cells were more proliferative and resistant to apoptosis in the absence of serum, and had enhanced ability of inducing capillary-like structures. Moreover, microarray-based expression profiles between them identified 1341 genes involved in cell cycle, cell adhesion, lymphangiogenesis, regulation of apoptosis, and so on. Some genes dedicating to the metastatic potential, including JAM2, TNC, CTSC, LAMB1, VEGFC, HAPLN1, ACPP, GDF9 and FGF11, were upregulated in LNMTca8113 cells.. These results suggested that LNMTca8113 and Tca8113 cells were proper models for lymphatic metastasis study because there were differences in biologic behaviors and metastasis-related genes between them. Additionally, the differentially expressed gene profiles in cancer progression may be helpful in exploring therapeutic targets and provide the foundation for further functional validation of these specific candidate genes for OSCC.

Topics: Acid Phosphatase; Animals; Apoptosis; Carcinoma, Squamous Cell; Cathepsin C; Cell Adhesion; Cell Adhesion Molecules; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Extracellular Matrix Proteins; Female; Fibroblast Growth Factors; Gene Expression Profiling; Growth Differentiation Factor 9; Laminin; Lymphatic Metastasis; Mice; Mice, Inbred BALB C; Mice, Nude; Mouth Neoplasms; Oncogenes; Protein Tyrosine Phosphatases; Proteoglycans; Up-Regulation; Vascular Endothelial Growth Factor C

Squamous cell carcinoma (SCC) is the most common form of oral cancer. Destruction and invasion of mandibular and maxillary bone frequently occurs and contributes to morbidity and mortality. We hypothesized that the bisphosphonate drug zoledronic acid (ZOL) would inhibit tumor-induced osteolysis and reduce tumor growth and invasion in a murine xenograft model of bone-invasive oral SCC (OSCC) derived from an osteolytic feline OSCC. Luciferase-expressing OSCC cells (SCCF2Luc) were injected into the perimaxillary subgingiva of nude mice, which were then treated with 100 μg/kg ZOL or vehicle. ZOL treatment reduced tumor growth and prevented loss of bone volume and surface area but had no effect on tumor invasion. Effects on bone were associated with reduced osteolysis and increased periosteal new bone formation. ZOL-mediated inhibition of tumor-induced osteolysis was characterized by reduced numbers of tartrate-resistant acid phosphatase-positive osteoclasts at the tumor-bone interface, where it was associated with osteoclast vacuolar degeneration. The ratio of eroded to total bone surface was not affected by treatment, arguing that ZOL-mediated inhibition of osteolysis was independent of effects on osteoclast activation or initiation of bone resorption. In summary, our results establish that ZOL can reduce OSCC-induced osteolysis and may be valuable as an adjuvant therapy in OSCC to preserve mandibular and maxillary bone volume and function.

Topics: Acid Phosphatase; Animals; Bone Density Conservation Agents; Bone Resorption; Calcium; Carcinoma, Squamous Cell; Cats; Diphosphonates; Disease Models, Animal; Imidazoles; Isoenzymes; Luciferases; Male; Mice; Mice, Nude; Mouth Neoplasms; Osteoclasts; Osteolysis; Tartrate-Resistant Acid Phosphatase; Transplantation, Heterologous; X-Ray Microtomography; Zoledronic Acid

Green tea polyphenols (GTP) has been used as a chemopreventive agent world wide against chemically induced cancer. The present study is aimed to understand the therapeutic action of GTP on glycoconjugates and immunological markers in 4-Nitroquinoline 1-oxide (4-NQO)-induced oral cancer over a period of 30 days at 200mg/kg, p.o., Oral cancer was induced by painting 4-NQO for 8 weeks followed by administration of GTP after 22 weeks, for 30 days. Glycoconjugates such as hexose, hexosamine, sialicacid, fucose and mucoprotein were analysed. Expression of glycoconjugates was examined through histology and SDS-PAGE. Immunological markers such as circulating immune complex and mast cell density were studied. Oral cancer-induced animals showed a significant increase in levels of glycoconjugates and its expression, similar to that observed for immunological markers. Treatment with GTP altered the expression of glycoconjugates as well as immunological markers. The results suggest that GTP modulates both the expression of glycoconjugates and immunological markers resulting in regression of oral cancer.

Topics: 4-Nitroquinoline-1-oxide; Acid Phosphatase; Animals; Antineoplastic Agents, Phytogenic; beta-Galactosidase; Camellia sinensis; Flavonoids; Glucuronidase; Glycoconjugates; Hexoses; Immunoglobulins; Male; Mouth; Mouth Neoplasms; Mucoproteins; N-Acetylneuraminic Acid; Phenols; Phospholipases; Phytotherapy; Plant Extracts; Polyphenols; Rats; Rats, Wistar; Tongue; Tongue Neoplasms

We quantified telomerase activity (TA) in patients with oral and maxillofacial malignant and nonmalignant lesions, and compared it with their clinical status and grade of malignancy. Fifty-two malignant and 52 nonmalignant lesions were analyzed. All malignant lesions were pathologically diagnosed as oral squamous cell carcinoma (OSCC). Normal gingival tissue served as a control. These specimens were obtained by biopsy or surgical resection, and stored at -80 degrees C until use. TA was quantified by a fluorescence-based TRAP method. TA levels ranged from 0.00 to 95.24 (average 33.24)U/microgP in 52 malignant lesions, and from 0.00 to 79.35 (average 11.91)U/microgP in 52 nonmalignant lesions (P < 0.0001). TA was detected in 96.2% of malignant and 65.4% of nonmalignant lesions. There was no relationship between TA levels and clinical stages or YK classification. However, under WHO classification, there were significant differences (P < 0.05) between Grades I and III or II + III. Among nonmalignant lesions, epithelial dysplasia showed a significantly higher TA level than that of oral lichen planus (P < 0.05) and other benign lesions (P < 0.0001). Oral lichen planus also significantly differed from other benign lesions (P < 0.05). These results suggest that TA is related to the histological grade of malignancy, and is also useful as a prognostic predictor for precancerous lesions and conditions.

Topics: Acid Phosphatase; Adolescent; Adult; Aged; Aged, 80 and over; Biomarkers, Tumor; Carcinoma, Squamous Cell; Case-Control Studies; Child; Epithelium; Female; Humans; Isoenzymes; Lichen Planus, Oral; Lymphatic Metastasis; Male; Middle Aged; Mouth Neoplasms; Neoplasm Staging; Precancerous Conditions; Tartrate-Resistant Acid Phosphatase; Telomerase

Saliva is the first body fluid to confront inhaled cigarette smoke (CS) which is injurious to the oral cavity and is associated with several oral diseases and cancer. We have recently demonstrated in an In vitro model that an exposure of saliva to nine 'puffs' of CS induced a distinct increase in protein carbonyls. This elevation of protein carbonyls caused by CS may be the result of aldehydes presented in the CS reacting with sulphydryl (-SH) groups of the proteins. Moreover, following the exposure to CS, the activities of several salivary enzymes amylase, lactate dehydrogenase (LDH) and acid phosphatase (ACP) were found to be significantly reduced by 83%, 57% and 77%, respectively. However, CS had no effect on the activities of aspartate aminotransferase and alkaline phosphatase. In the current study we found that CS also reduced salivary peroxidase activity by no less than 80% which may be of a great importance to the clinical set up as peroxidase is considered a pivotal enzyme of the the salivary protecting system. Furthermore, in contrast to LDH findings in saliva, the LDH activity in plasma was not reduced following its exposure to CS.. Hence, we concluded that the loss of salivary enzyme activities may be due to various agents in the CS that affect the enzyme via different mechanisms.

Topics: Acid Phosphatase; Amylases; Humans; L-Lactate Dehydrogenase; Models, Biological; Mouth Neoplasms; Peroxidases; Reference Values; Saliva; Smoking

Giant cell lesions of the oral cavity are a well recognized entity. However, the histogenesis of these lesions is still the subject of controversy, with support for both histiocyte/macrophage and osteoclast origins being found in the literature. This study evaluated a set of peripheral giant cell lesions (PGCLs) and central giant cell lesions (CGCLs) for characteristics of both cell types to address this dilemma.. Detection of histiocyte/macrophage characteristics was accomplished immunohistochemically by evaluating for markers specific for this cell type, namely alpha-1 -antichymotrypsin (1 -ACT) and factor XIIIa antibodies. Detection of osteoclast characteristics made use of the fact that osteoclasts possess a unique enzyme, tartrate-resistant acid phosphatase, which can be appreciated by histochemical procedures.. A large percentage of the multinucleated cells stained with the 1-ACT (38.08% in PGCLs and 15.84% in CGCLs), while only isolated cells stained for factor XIIIa (1.20% PGCLs, 0.99% CGCLs). Isolated stromal cells also were stained. Virtually all multinucleated cells reacted with the tartrate-resistant acid phosphatase stain (99.26% PGCLs, 98.34% CGCLs), as did a number of the mononuclear stromal cells.. This study supports the contention that GCLs of the oral cavity may arise from precursor cells related to the granulocyte/macrophage line, and may originate from mononuclear cells that express markers for both macrophages and osteoclasts.

Topics: Acid Phosphatase; alpha 1-Antichymotrypsin; Biomarkers; Biomarkers, Tumor; Cell Lineage; Coagulants; Giant Cell Tumors; Giant Cells; Granulocytes; Granuloma, Giant Cell; Histiocytes; Histocytochemistry; Humans; Immunohistochemistry; Isoenzymes; Leukocytes, Mononuclear; Macrophages; Mouth Diseases; Mouth Neoplasms; Osteoclasts; Serine Proteinase Inhibitors; Stem Cells; Tartrate-Resistant Acid Phosphatase; Transglutaminases

The activity and isoenzyme profile of lactate dehydrogenase (LDH), alkaline and acid phosphatase were studied in tumors of the tongue, cheek, oral floor, soft palate and palatine tonsils (n = 100), leukoplakia (n = 7) and in the oral mucosa at corresponding sites in healthy subjects (n = 66), to develop tests for early detection, monitoring and prognosis of oral cancer. Levels of alpha-amylase and acid phosphatase were measured in saliva and blood serum of patients with oral cancer and healthy subjects. The activity of LDH and alkaline and acid phosphatase in oral malignancies were 1.5-6 times that in normal mucosa, depending on tumor site. Changes in LDH isoenzyme profile consisted in an increased level of M-subunits (LDH-4 and 5) and a decreased concentration of N-subunits (LDH-1 and 2). With regards to acid phosphatase, an increase in the activity of its tartrate-inhibited fraction was observed. An increase in LDH and alkaline phosphatase activity was registered for oral precancer (leukoplakia), too, although it was less pronounced than in cancer. Changes in LDH isoenzyme profile matched those in cancer patients. A significant increase in the activity of alpha-amylase, acid phosphatase and the latter's tartrate-inhibited fraction was registered in saliva of oral cancer patients (86-96%). The credibility of enzyme activity measurement in saliva for evaluation of response and prognosis is discussed.

Topics: Acid Phosphatase; Alkaline Phosphatase; alpha-Amylases; Clinical Enzyme Tests; Humans; Isoenzymes; L-Lactate Dehydrogenase; Leukoplakia, Oral; Mouth Mucosa; Mouth Neoplasms; Saliva

After in vitro incubation of human squamous cell carcinomas of the head and neck region with aromatic retinoid an increased number of lysosomes can be observed in the tumor cells. It is discussed whether this accumulaion of lysosomes is due to a direct stimulation of lysosomal enzyme synthesis or whether it is consequence of cell damage by the retinoid.

Topics: Acid Phosphatase; Acitretin; Carcinoma, Squamous Cell; Culture Techniques; Dose-Response Relationship, Drug; Humans; Laryngeal Neoplasms; Lysosomes; Mouth Neoplasms; Tretinoin

Surgical specimens of oral squamous cell carcinoma were processed for cytochemistry of acid phosphatase using Gomori's substrate. Reaction product was deposited in the cytoplasmic dense bodies, autophagic vacuoles, cytoplasmic projections, and advancing cell borders. Results of this study suggest that acid phosphatase and its associated lysosomes seem to play a role in the invasiveness of cancer cells.

Topics: Acid Phosphatase; Adult; Aged; Carcinoma, Squamous Cell; Female; Histocytochemistry; Humans; Lysosomes; Middle Aged; Mouth Neoplasms

Jaw ameloblastomas produce most frequently (62%) multilocular translucences. An unilocular translucence was observed in 28% of the cases. In both forms, secondary cysts were present. This radiomorphologic finding is of pathognomonic value. Conchiform or finger-shaped translucences were seen in 10% of the cases. Such radiographic changes were observed in ameloblastomas arising from the oral mucosa. The border of the radiolucent area was always sharply defined and had a lobulate or wreathed form. The ameloblastoma spreads in an expansive or invasive way. The bone destruction is in all probability caused by the acid phosphatase activity of the tumour. Bone transformation occurs simultaneously with bone destruction and might be regarded as a morphologic sign of the defence mechanism.

Topics: Acid Phosphatase; Ameloblastoma; Bone Regeneration; Bone Resorption; Humans; Jaw Neoplasms; Mouth Neoplasms; Neoplasm Invasiveness; Radiography

Cytologic assay of metastatic involvement of lymph nodes may be used along with histological studies as a reliable adjunct for morphological diagnosis, that makes possible in many cases to determine not only the epithelial origin of the affection but also to characterize its histological pattern. However, the cytologic diagnosis of undifferentiated cancer metastases is frequently rather difficult in relation to establishing the differential diagnosis between the former and other affections of lymph nodes. A careful, and sometimes repeated analysis of the material, taking into account the clinical data and cytochemical findings, contributes to greater efficiency of a cytologic method. The perspective use of cytochemical reactions as additional criteria for the diagnosis of undifferentiated cancer necessitates their further elaboration and study.

Topics: Acid Phosphatase; Enzyme Activation; Esterases; Humans; Lung Neoplasms; Lymph Nodes; Lymphatic Metastasis; Mouth Neoplasms; Nasopharyngeal Neoplasms

During treatment of keratinizing squamous cell carcinomas with bleomycin tumor cells are devitalized by keratinization, while simple necrosis plays a minor role. Connected with this process is a marked resorptive granulomatous inflammation with numerous macrophages which is followed by a fibrous organization. In the border region of the keratinized tumor areas many multinucleated giant cells appear. The nature of these giant cells was the subject of controversy. Enzyme histochemical, electronmicroscopic, and ultrahistochemical investigations in three cases of advanced squamous cell carcinoma of the oral cavity prove that the giant cells which are formed during bleomycin treatment are not multinucleated tumor cells, but multinucleated macrophages. The enzymatic pattern is similar to macrophages with a high content of acid phosphatase and aminopeptidase. The ultrastructure of the giant cells is characterized by lysosomes with acid phosphatase activity, pinocytotic vesicles, and cytoplasmic projections on the cell surface with signs of macroendocytosis. The tumor cells show an epithelial differentiation with desmosomes, tonofibrils, and keratohyaline granula. The giant cells are formed by fusion of mononucleated (monocytogenic) macrophages. The fusions seem to be related to the functional status of the cells. It is possible, that the macrophages and the giant cells have an additional immunologic function. This is suggested by the frequent association of giant cells with lymphocytes. The importance of these facts for the evaluation of the action of bleomycin and the consequences for its therapeutic use are discussed. A combination with methods causing a dedifferentiation of the tumor or suppression of the immunologic defense seems to be problematic.

Topics: Acid Phosphatase; Aged; Bleomycin; Carcinoma, Squamous Cell; Cell Fusion; Cell Membrane; Female; Histocytochemistry; Humans; Keratins; Leucyl Aminopeptidase; Lysosomes; Macrophages; Male; Middle Aged; Mouth Neoplasms; Organoids; Phagocytosis

Topics: Acid Phosphatase; Alkaline Phosphatase; Esterases; Glucosephosphate Dehydrogenase; Hemangioma; Hemangioma, Cavernous; Histocytochemistry; Humans; Hydroxybutyrate Dehydrogenase; L-Lactate Dehydrogenase; Mouth Mucosa; Mouth Neoplasms; Succinate Dehydrogenase

Topics: Acid Phosphatase; Adenosine Triphosphatases; Blood Vessels; Cholesterol; Crystallization; Endothelium; Histocytochemistry; Humans; Microtomy; Mouth Neoplasms; Oxidoreductases; Peptide Hydrolases; Periapical Granuloma; Radicular Cyst; Staining and Labeling

Topics: Acid Phosphatase; Alkaline Phosphatase; Anus Neoplasms; Carcinoma, Squamous Cell; Cheek; Female; Histocytochemistry; Humans; Male; Mouth Neoplasms; Penile Neoplasms; Tongue Neoplasms

Topics: Acid Phosphatase; Alkaline Phosphatase; Blood; Carcinoma; Cell Line; Culture Media; Drug Stability; Enzyme Induction; Galactosidases; Hexosaminidases; Hot Temperature; Humans; Kinetics; Mouth Neoplasms; Neoplasm Proteins; Prednisolone; Sodium Chloride

Topics: Acid Phosphatase; Animals; Azo Compounds; Biological Transport; Carbon Isotopes; Carcinoma; Cell Line; Cell Membrane; Cells, Cultured; Connective Tissue; Cyclic AMP; Estranes; Humans; Hydroxysteroids; Leucine; Lysosomes; Membranes; Mice; Mouth Neoplasms; Permeability; Thymidine; Tritium; Uridine

Topics: Acid Phosphatase; Adult; Alkaline Phosphatase; Bone Neoplasms; Breast Neoplasms; False Positive Reactions; Female; Humans; Iron Isotopes; Lung Neoplasms; Male; Mandibular Neoplasms; Mouth Neoplasms; Neoplasm Metastasis; Osteosarcoma; Pelvic Neoplasms; Pharyngeal Neoplasms; Prostatic Neoplasms; Radionuclide Imaging; Spinal Neoplasms; Strontium Isotopes

Topics: Acid Phosphatase; Alkaline Phosphatase; Esterases; Humans; Leukoplakia, Oral; Lip Neoplasms; Mouth Neoplasms; Oxidoreductases; Precancerous Conditions

Topics: Acid Phosphatase; Aged; Cheek; Endoplasmic Reticulum; Epithelium; Female; Golgi Apparatus; Humans; Leukoplakia; Leukoplakia, Oral; Lysosomes; Male; Microscopy, Electron; Middle Aged; Mouth Mucosa; Mouth Neoplasms

Topics: Acid Phosphatase; Animals; Cell Nucleus; Cytoplasm; Endoplasmic Reticulum; Fishes; Golgi Apparatus; Histiocytes; Jaw Neoplasms; Lymphatic Diseases; Microscopy, Electron; Mitochondria; Mouth Neoplasms; Neoplasms; Phagocytosis; Ribosomes

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Carcinoma, Squamous Cell; Cheek; Cricetinae; Esterases; Female; Glucosephosphate Dehydrogenase; Histocytochemistry; Humans; L-Lactate Dehydrogenase; Malate Dehydrogenase; Male; Mouth Mucosa; Mouth Neoplasms; Succinate Dehydrogenase

Topics: Acid Phosphatase; Animals; Carcinoma, Squamous Cell; Cell Division; Cell Line; Cell Membrane Permeability; Cell Nucleus; Chromosomes; Culture Techniques; DNA; Ethanol; Fibroblasts; Humans; L Cells; Lysosomes; Mice; Mouth Neoplasms; RNA; Tritium; Uridine

Topics: Acid Phosphatase; Adenocarcinoma; Adult; Alkaline Phosphatase; Female; Histocytochemistry; Humans; Male; Mouth Neoplasms; Oxidoreductases

Topics: Acid Phosphatase; Adenosine Triphosphatases; Alkaline Phosphatase; Carcinoma, Squamous Cell; Culture Techniques; Cyclophosphamide; Electron Transport Complex IV; Enzymes; Esterases; Histamine H1 Antagonists; Hydrocortisone; Imidazoles; Mouth Neoplasms; Nucleotidases; Staining and Labeling; Succinate Dehydrogenase

The effect of type 5 adenovirus infection on the synthesis of host-cell proteins by suspension cultures of KB cells was investigated. Although total protein synthesis continued at a constant rate for approximately 36 hr, net synthesis of five host enzymes (lactic dehydrogenase, acid phosphatase, deoxyribonuclease, fumarase, and phosphoglucose isomerase) was found to stop 16 to 20 hr after infection. The synthesis of alkaline phosphatase stopped 9 to 12 hr after infection. The inhibition of host protein synthesis occurred shortly after the synthesis of viral antigens had begun, accounting for the continued synthesis of total protein. An investigation of the relationship between synthesis of viral antigens and inhibition of host protein synthesis yielded results which suggest that the two processes are in some way coupled.

Topics: Acid Phosphatase; Adenoviridae; Antigens; Carcinoma; Cell Line; Cell Transformation, Neoplastic; Complement System Proteins; Culture Techniques; Cytopathogenic Effect, Viral; Deoxyribonucleases; DNA Viruses; Floxuridine; Humans; Hydro-Lyases; Isomerases; L-Lactate Dehydrogenase; Mouth Neoplasms; Protein Biosynthesis; Viral Proteins

Topics: Acid Phosphatase; Adenofibroma; Alkaline Phosphatase; Ameloblastoma; Aminopeptidases; Animals; Breast Neoplasms; Carcinoma, Squamous Cell; Female; Glucosephosphate Dehydrogenase; Glucuronidase; Histocytochemistry; Humans; L-Lactate Dehydrogenase; Malate Dehydrogenase; Male; Mice; Mouth Neoplasms; Sarcoma, Experimental; Skin Neoplasms; Succinate Dehydrogenase; Tumor Virus Infections

Topics: Acid Phosphatase; Alkaline Phosphatase; Animals; Carcinoma, Squamous Cell; Cheek; Cricetinae; Esterases; Galactosidases; Histocytochemistry; Humans; Leukoplakia; Mouth Neoplasms; Neoplasms, Experimental; Pathology; Research

Topics: Acid Phosphatase; Animals; Carcinogenesis; Carcinoma; Carcinoma, Squamous Cell; Cheek; Cricetinae; Epithelial Cells; Histocytochemistry; Humans; Lysosomes; Mouth Neoplasms; Neoplasms, Experimental; Papilloma; Research