Basaloid-squamous carcinoma of the esophagus is rare and similiar to the solid type of adenoid cystic carcinoma of the salivary gland. The origin of this tumor is unknown. The tumor was located in the lower third of the esophagus. The case of basaloid-squamous carcinoma consisted of submucosal tumor showing carcinoma with a basaloid pattern and focal squamous differentiation associated with squamous cell carcinoma or carcinoma in situ of the esophageal mucosa. A few submucosal tumor cells were positive for cytokeratin.

To determine the prevalence of lymphoid follicles in Helicobacter pylori(H. pylori) positive and negative gastritis and its relationship to age, biopsy site, gastritis activity, degree of gastritis, number of H. pylori and gastritis score in H. pylori associated gastritis, we examined the gastric tissue of patients with 121 nonulcer dyspepsia and 99 peptic ulcers. The gastritis score was obtained by adding together the figures for gastritis degree, gastritis activity and number of H. pylori. H. pylori was detected in 75.2% of nonulcer dyspepsia, 84.5% of gastric ulcers and 90.3% of duodenal ulcers. Lymphoid follicles were found in 63.3% of H. pylori associated gastritis and 4.7% of H. pylori negative gastritis, and there was a strong relationship between the prevalence of lymphoid follicles and H. pylori infection(P<0.01). Lymphoid follicles were found in 100% of H. pylori associated gastritis, showing severe chronic inflammatory cell infiltration, and strong relationship between the prevalene of lymphoid follicles and the degree of gastritis (P<0.01). There was no significant difference among lymphoid follicles, age, biopsy site, clinical diagnosis, gastritis activity and number of H. pylori. Lymphoid follicles were found in 58.3% of gastritis score 4, 67.6% of gastritis score 7 and 100% of gastritis score 9, and there was significant correlation between the prevalence of lymphoid follicles and a gastritis score(P<0.01, R=0.85). In summary, gastric lymphoid follicle is significantly associated with H. pylori infection and its presence in H. pylori associated gastritis is related to chronic inflammatory cell infiltration.
Humans ; Biopsy

Many studies have shown that angiogenesis plays an important role in the growth, the progression, and the metastasis of a solid tumor. The vascular endothelial growth factor(VEGF) is thought to be a selective mitogen for endothelial cells. Twenty eight advanced gastric carcinomas and twenty early gastric carcinomas were investigated by staining with polyclonal antibody against the VEGF. Correlation between the expression of the VEGF and the clinicopathologic features of gastric carcinoma were studied. The VEGF was mainly localized to the cytoplasm of carcinoma cells. Normal gastric foveolar epithelium was not immunoreactive, but some endothelial cells were weakly immunoreactive with an anti-VEGF antibody. Expression of the VEGF was significantly higher in advanced gastric carcinoma than in early gastric carcinoma (p=0.003). Expression of the VEGF was correlated with the depth of tumor, the lymph node metastasis, and the stage (p<0.05). The VEGF positivity was significantly higher in moderately and poorly differentiated gastric carcinoma than in well differentiated gastric carcinoma. The VEGF scores of the metastatic foci in the lymph nodes were higher than that of the primary tumors, which were followed by deep and superficial portions of the primary tumors in a descending order (p<0.05). In summary, the expression of the VEGF may be associated with progression and metastasis of a gastric carcinoma and may also be a good prognostic factor in a gastric carcinoma.
Cytoplasm ; Endothelial Cells ; Epithelium ; Lymph Nodes ; Neoplasm Metastasis ; Prognosis ; Vascular Endothelial Growth Factor A*

Balancing the rates of cell proliferation and cell death is important in maintaining normal tissue homeostasis. The relationship among apoptosis, cell proliferation and factors influencing apoptosis according to the histologic types in chemically induced mammary tumorigenesis appears important in understanding the pathogenesis of breast carcinoma. In this study, we investigated alterations in the kinetics of cell proliferation and apoptosis during rat mammary tumorigenesis induced by 7, 12-dimethylbenzanthracene (DMBA) and we related these changes to the expressions of bcl-2, p53, and TGF-beta. Seven-week-old female Sprague-Dawley rats were divided into an experimental group (20 mg/ml DMBA by oral intubation) and a control group. The results were as follows. 1. In the experimental group, breast tumors occurred in twenty two of fifty nine rats(37.3%, 22/59), and the total number of tumors was 100 (4.5 2.0/rat). The histological classification was infiltrating ductal carcinomas (n=5), ductal carcinomas with focal invasion (n=10), intraductal carcinomas (n=36), adenomas accompanied with intraductal proliferation (n=35), intraductal proliferation (n=9), and adenomas (n=5); 2. The differentiation of terminal end bud into alveolar bud (AB) in the experimental group was significantly lower than that of the control group (p<0.05); 3. BrdU labeled tumor cells were mainly located at the peripheral portion of tumor cell nests. BrdU labeling indices were highest in ductal carcinomas, less pronounced in intraductal proliferation, and lowest in adenomas, whereas apoptosis levels were highest in adenomas, less pronounced in intraductal proliferation, and lowest in ductal carcinomas (p<0.05); 4. p53 protein was not expressed in any breast tumors. Although the expression of bcl-2 protein was highest in infiltrating and focal infiltrative ductal carcinomas (58.3%), compared with adenomas, intraductal proliferation, and intraductal carcinomas (p<0.05), the extent of its expression was less than 1% of all tumor cells; 5. TGF-beta was mainly expressed in the central portion of tumor cell nests rather than in peripheral portion, and TGF-beta immunoreactive tumor cells displayed good differentiation and did not reveal BrdU immunoreactivity. TGF-beta labeling index of infiltrating and focal infiltrative ductal carcinomas was significantly higher than that of intraductal carcinomas, intraductal proliferation, and adenomas (p<0.05). Based on these results, it is thought that high cell proliferation and the suppression of apoptosis are closely associated with DMBA-induced rat mammary carcinogenesis. However, the suppression of apoptosis is not related to p53 mutation, bcl-2, and TGF-beta. TGF-beta seems to be reversely related to tumor cell proliferation but closely associated with the progression of the tumor, especially an invasion of breast carcinomas.
9,10-Dimethyl-1,2-benzanthracene ; Adenoma ; Animals ; Apoptosis* ; Breast Neoplasms ; Bromodeoxyuridine ; Carcinogenesis* ; Carcinoma, Ductal ; Carcinoma, Intraductal, Noninfiltrating ; Cell Death ; Cell Proliferation* ; Classification ; Female ; Homeostasis ; Humans ; Kinetics ; Rats* ; Rats, Sprague-Dawley ; Transforming Growth Factor beta

Heat shock protein 70 (HSP70) is a chaperone that binds to mutant p53 and consequently can regulate its accumulation or localization. Its expression is upregulated in tumor cells. We studied 44 adenomas and 29 carcinomas of colorectum to evaluate the expression of HSP70, and to assess the correlation among p53 protein and other clinical prognostic parameters. HSP70 expression was scored according to staining intensity and extent. p53 protein expression was 45.5%(20/44) in adenomas and 79.3%(23/29) in carcinomas(P<0.01). p53 protein expression of carcinomas was 57.1%(4/7) in diploidy tumors, 100.0%(8/8) in aneuploidy tumors(P=0.07), 100.0%(8/8) in well-differentiated tumors, and 50.0%(2/4) in poorly differentiated tumors(P= 0.09). HSP70 expression mainly revealed a fine granular cytoplasmic staining pattern in tumor cells. HSP70 was focally detected in some lymphocyte, ganglion cell and normal mucosa. HSP70 expression was 46.3%(19/41) in adenomas and 93.1%(27/29) in carcinomas. HSP70 score was 0.9+/-1.3 in adenomas(n=41) and 5.5+/-3.5 in carcinomas(n=29)(P<0.0005). Its score was 1.7+/-1.6 in p53 positive adenomas and 0.3+/-0.6 in p53 negative adenomas(P<0.005), and its expression rate was higher in p53 positive carcinomas than p53 negative carcinomas (P>0.05). There was no significant correlation among HSP70, tumor size, Dukes'stage, nodal metastasis, depth of tumor invasion, DNA ploidy and tumor differentiation. In conclusion, HSP70 and p53 protein appear to be correlated to each other, and that HSP70 and p53 protein may play a certain role in the progression of colorectal tumor. Further studies are needed for determining their prognostic factors in colorectal carcinoma.
Adenoma* ; Aneuploidy ; Colorectal Neoplasms ; Cytoplasm ; Diploidy ; DNA ; Ganglion Cysts ; Heat-Shock Proteins* ; Hot Temperature* ; HSP70 Heat-Shock Proteins* ; Lymphocytes ; Mucous Membrane ; Neoplasm Metastasis ; Ploidies

Angiogenesis is a crucial step in tumor growth and progression. Scarce data is available on angiogensis in gastrointestinal tumors. We studied 16 normal colon, 44 adenomas and 29 carcinomas to evaluate angiogenesis in colorectal tumors and to assess the correlation among p53 protein, proliferative activity and other clinical prognostic parameters. Endothelial cells were immunostained with an anti-Factor VIII mAb; in each case three microscopic fields(x 200) were counted: average number of the three fields was defined as microvessel density (MVD). p53 protein expression was 45.5%(20/44) in adenomas, and 79.3%(23/29) in carcinomas (p<0.01). p53 protein expression of carcinomas was 57.1%(4/7) in diploid tumors, 100%(8/8) in aneuploid tumors (p=0.07), 100%(8/8) in well differentiated tumors, and 50%(2/4) in poorly differentiated tumors (p=0.09). MIB-1 score was 2.3+/-0.7(38) in adenomas, 3.4+/-0.5(29) in carcinomas (p<0.01). There was no significant correlation between p53 protein and MIB-1 score. MVD was 10.4+/-4.1(16) in the normal mucosa, 21.5+/-7.9(39) in the adenomas, 35.3+/-9.7(26) in carcinomas (normal versus adenomas, p<0.01; adenomas versus carcinomas, p<0.01). MVD was 25.8+/-5.4(2) in carcinomas confined to mucosa, and 36.1+/-9.6(24) in carcinomas with transmural invasion. The higher MIB-1 score was in carcinomas the more MVD increased but there was no statistical significance (r=0.38, p=0.055). MVD of carcinomas was not associated with nodal metastasis, p53 expression, and DNA ploidy. p53 protein and MIB-1 expression are useful methods for the evaluation of malignancy, and tumor angiogenesis is an early event in a colorectal tumor but MVD does not correlate with prognostic parameters except for the tumor depth.
Adenoma* ; Aneuploidy ; Colon ; Colorectal Neoplasms ; Diploidy ; DNA ; Endothelial Cells ; Microvessels* ; Mucous Membrane ; Neoplasm Metastasis ; Ploidies

TO evaluate the histopathologic features of gastric mucosa by Helicobacter pylori (HP), we reviewed 70 endoscopically biopsied chronic gastritis and peptic ulcer. The results are as fonows. l. HP was detected in 923% (48/52) of active gastritis, 8l8% (9/l l) of peptic ulcer and l43% (1/7) of chronic gastritis. The prevalence of HP infection was significantly higher in active gastritis and peptic ulcer than chronic gastritis (P<0005). 2. The infiltration of intraepithelial neutrophil of the 58 HP-positive cases was significantly more than of the l2 HP-negative cases (P<0005). 3. The infiltration of neutrophil and chronic inflammatory cells in the lamina propria of the 58 HP positive cases were significantly more than of 12 HP-negative cases (P<0.005, P<0.01) 4. The gastric epithelium of 58 HP positive case showed characteristic degenerative change, such as epithelial pits (93.l%), irregular surface (84.4%), individua1 cell drop-out (46.5%) and microerosion (27.6%). The similiar changes were not seen in l2 HP-negative cases. In summary, HP is significantly correlated with inflammatory reaction of the gastric mucosa. It is also significantly correlated with the epithelial degenerative changes that is considered to the precursor of peptic ulcer.

TGF-beta1 expression was studied in 25 patients with tuberculosis (lung, 9 cases and lymph node, 16 cases) using a polyclonal antibody in formalin-fixed paraffin embedded tissue. Nineteen cases (76.0%) out of 25 cases showed TGF-beta1 expression. TGF-beta1 was present in cytoplasm of epithelioid cells and Langhans' giant cells. Pulmonary tuberculosis and tuberculous lymphadenitis showed different patterns of staining. Five of 9 cases of pulmonary tuberculosis were positive for TGF-beta1: four of acid-fast bacilli positive cases (4/5, 80.0%) and one of acid-fast bacilli negative cases (1/4, 25.0%). However, high expression of TGF-beta1 was detected in tuberculous lymphadenitis of both acid-fast bacilli positive group (3/4, 75.0%) and acid-fast bacilli negative group (11/12, 91.7%). TGF-beta1 was also expressed in all of 6 cases of BCG-induced tuberculous lymphadenitis: 2 acid-fast bacilli positive and 4 acid-fast bacilli negative cases. TGF-beta1 expression was shown in 19 cases (86.4%) of 22 in active tuberculosis, while no TGF-beta1 expression was detected in any cases of inactive, healed tuberculosis (p<0.008). This study supports that the TGF-beta1 expression of epithelioid cells may alter their function resulting in the impaired antimycobacterial activity. Thus the increased production of TGF-beta1 may be one of the important mechanisms by which Mycobacterium tuberculosis avoids destruction by host macrophages.
Cytoplasm ; Epithelioid Cells ; Giant Cells ; Granuloma* ; Humans ; Lymph Nodes ; Macrophages* ; Mycobacterium tuberculosis ; Paraffin ; Transforming Growth Factor beta1* ; Tuberculosis ; Tuberculosis, Lymph Node ; Tuberculosis, Pulmonary

BACKGROUND: The Helicobacter pylori(H. pylori) is associated with chronic gastritis and is now recognized to be the main factor in the pathogenesis of peptic ulcer disease. The eradication treatment of H. pylori significantly lowers ulcer relapse rate, which is accompanied by important histological change. We evaluated the prevalence of H. pylori infection in upper gastrointestinal diseases. METHODS: Total 491 patients(274 with chronic gastritis, 134 with gastric ulcer, 57 with duodenal ulcer, and 26 with gastroduodenal ulcer) were tested for H. pylori infection by the CLO test, hematoxylin-eosin stain and Giemsa stain. RESULTS: The prevalence of H. pylori infection was 74.0% in male and 58.6% in female. The prevalence of H. pylori infection was 73.2% in 30-59 year-old group and 60.2% in older age group. The sex and age adjusted prevalence of H. pylori infection was 64.7% in chronic gastritis, 69.4% in gastric ulcer, 84.5% in duodenal ulcer and 87.8% in gastroduodenal ulcer. CONCLUSIONS: The prevalence of H. pylori infection of upper gastrointestinal diseases is significantly higher in male, 30-59 year-old group, peptic ulcer and duodenal ulcer than in female, older age group(over 60), chronic gastritis and gastric ulcer, respectively.
Azure Stains ; Duodenal Ulcer ; Female ; Gastritis ; Gastrointestinal Diseases* ; Helicobacter pylori* ; Helicobacter* ; Humans ; Male ; Peptic Ulcer ; Prevalence* ; Recurrence ; Stomach Ulcer ; Ulcer

Inflammation is closely related to the progression of cancer as well as tumorigenesis. Here, we investigated the effect of prostaglandin E2 (PGE2) and interleukin-1beta (IL-1beta) on E-cadherin expression in SNU719 gastric cancer cells. E-cadherin expression decreased as the dose or exposure time of PGE2 and IL-1beta increased, whereas Snail expression increased with dose or time of PGE2 and IL-1beta. E-cadherin expression reduced by PGE2 treatment increased after the transfection of Snail siRNA. Neutralization of IL-1beta using anti-IL-1beta antibody blocked the expression pattern of E-cadherin and Snail occurred by IL-1beta treatment. However, there was no synergic effect of IL-1beta and PGE2 on the expression pattern of E-cadherin and Snail. In conclusion, inflammatory mediators reduced E-cadherin expression by enhancing Snail expression in gastric cancer cells. Inflammation-induced transcriptional regulation of E-cadherin in gastric cancer has implications for targeted chemoprevention and therapy.
Antibodies/immunology ; Antineoplastic Agents/pharmacology ; Cadherins/*metabolism ; Cell Line, Tumor ; Dinoprostone/*pharmacology ; Gene Expression Regulation/*drug effects ; Humans ; Interleukin-1beta/immunology/*pharmacology ; RNA Interference ; RNA, Small Interfering/metabolism ; Stomach Neoplasms/metabolism/pathology ; Transcription Factors/antagonists & inhibitors/genetics/*metabolism