Eighty rats out of 233 developed malignant tumors in the stomach and small intestine by administration of 100 micrograms/ml N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in drinking water for 28 weeks. Fifteen lesions (30%) among the 50 small intestinal carcinomas showed ossification in the tumor, while none in the sarcomas (12 lesions) or gastric adenocarcinomas (59 lesions) showed ossification. Multifocal heterotopic bone formation was found within stroma in close approximation to the neoplastic glands. The islands of bone trabeculae were covered by osteoblast-like cells, and abundant fibroblasts in loose stroma gathered around the bony islands which enclosed osteocytes in lacunae. Neither osteoclast nor cartilage was identified. In 5 cases, ossification was extensive, which comprised the major portion of the stroma. In contrast, intraluminal calcification without ossified foci were occasionally seen in the gastric carcinoma. Ossification of the intestinal tumors correlated to the degree of mucin content (p<0.05, chi square with Yates' correction), degree of neutrophilic infiltration (p<0.05), and size of the tumor (p<0.1). (The average size of the ossified tumor was 21.5 +/- 4.0 mm, while that of nonossified tumors was 12.5 +/- 1.9 mm). The degree of tumoral necrosis, desmoplasia or depth of invasion did not seem to be related to the ossification of the tumor. The ossification rate of this experimental model was much higher than in human cases. Various histologic alterations, such as mucin leakage, inflammatory cell infiltration, necrosis and/or fibrosis, which might be caused by continuous stimulation of the strong carcinogen, may play some role in the ossification of experimental tumors.
Adenocarcinoma/chemically induced/*pathology ; Animals ; Intestinal Neoplasms/chemically induced/*pathology ; Intestine, Small/*pathology ; Methylnitronitrosoguanidine ; Ossification, Heterotopic/*pathology ; Rats ; Rats, Sprague-Dawley ; Staining and Labeling ; Stomach Neoplasms/chemically induced/*pathology

OBJECTIVETo further explore the carcinogenic activity of Sterigmatocystin (ST) and the possible synergistic carcinogenic effect of deoxynivalenol (DON) in NIH mice.

METHODSNIH mice were randomly divided into 6 groups, 30 in each. Five groups of mice were given by gastric intubation ST 3 microg/kg, ST 30 microg/kg, ST 3 microg/kg + DON 1.5 microg/kg, ST 30 microg/kg + DON 1.5 microg/kg and DON 1.5 microg/kg respectively, 3 times a week for 24 weeks. The remaining group of mice was given normal saline accordingly, serving as control. All mice were fed with HPLC-confirmed mycotoxin-free food, analysis. The mice were killed and pathologically examined at 58th and 74th weeks.

RESULTSNo pathological changes were found in the control group of mice. Adenocarcinoma of lung was observed in 25.0%, 41.7%, 62.5%, 69.2% and 37.5% of mice given ST 3 microg/kg, ST 30 microg/kg, ST 3 microg/kg + DON 1.5 microg/kg, ST 30 microg/kg + DON 1.5 microg/kg and DON 1.5 microg/kg, respectively. In addition, dysplasia of glandular stomach was detected in 50.0%, 58.3%, 37.5%, 53.8% and 25.0% of mice similarly treated.

CONCLUSIONOral administration of ST or DON can induce adenocarcinoma in lung and dysplasia of glandular stomach in NIH mice. There is synergistic carcinogenic effect when both ST and DON are given.

Adenocarcinoma ; chemically induced ; pathology ; Animals ; Female ; Gastric Mucosa ; pathology ; Lung Neoplasms ; chemically induced ; pathology ; Male ; Mice ; Precancerous Conditions ; chemically induced ; pathology ; Sterigmatocystin ; toxicity ; Trichothecenes ; toxicity

OBJECTIVEAflatoxin G1 (AFG1) is a member of the carcinogenic aflatoxin family produced by aspergillus flavus. It is a major contaminating mycotoxin in food in areas of China with high cancer incidence. The purpose of this study is to explore the carcinogenic effects of AFG1 in NIH mice.

METHODSNIH mice were randomly divided into three groups. Two experimental groups were treated intragastrically by gavage with AFG1 3 microg/kg and AFG1 30 microg/kg respectively, 3 times a week for 24 weeks. The control group was treated with normal saline. All mice were fed with food that was free of AFGs as confirmed by HPLC analysis. The mice were weighed every week throughout the entire experiment, and then sacrificed and examined pathologically at the 58th and 74th weeks respectively.

RESULTSCompared with control mice receiving no AFG1, bronchial epithelial hyperplasia, alveolar hyperplasia and adenocarcinoma of lung were observed in mice receiving AFG1 treatment. The incidences of bronchial epithelial hyperplasia, alveolar hyperplasia and adenocarcinoma of lung were 60.0%, 10.0% and 30.0% for mice receiving 3 microg/kg AFG1 and 28.6%, 35.7%, 42.9% for mice receiving 30 microg/kg of the toxin, respectively.

CONCLUSIONOral administration of AFG1 can induce hyperplastic lesions and adenocarcinoma of lung in NIH mice.

Adenocarcinoma ; chemically induced ; pathology ; Aflatoxins ; toxicity ; Animals ; Aspergillus flavus ; Carcinogens ; toxicity ; Lung Neoplasms ; chemically induced ; pathology ; Mice ; Random Allocation

OBJECTIVETo study farm compost polluted water that may induce pharyngo-esophageal, gastric and liver carcinoma in chickens.

METHODS280 chickens were randomized into 4 groups: experiment group 100 chickens fed with compost water + NaNO(2) by stomach tube. The other 180 were evenly randomized into 3 control groups (60 each), fed with compost water, NaNO(2) and tap water in the same way. The farm compost was prepared with corn stalks, rice straws, excreta of men and livestock. The compost water, after being nitrosified and acidified, was fed through stomach tube 5 - 7.5 ml/session, twice a week. Besides, a solution consisting of the respective formula of each group added with 3 - 4 L water with pH adjusted to 3 - 4 by 1N HCL was given ad lib to all chickens in each group for 26.5 months.

RESULTSIn the experiment group, there were pharyngo-esophageal carcinoma 16 (16.3%), gastric adenocarcinoma 5 (10.4%) and liver carcinoma 3 (6.3%), in contrast to none in the 3 control groups, showing significant differences (P < 0.01, P < 0.01, P < 0.05).

CONCLUSIONSuccessful simulation of the layout of esophageal carcinoma high morbidity area and the mimic of chicken gastric fluid strongly support our compost etiological hypothesis that the nitrosified and acidified compost water are carcinogenic, very well causing esophageal, gastric and liver carcinoma.

Adenocarcinoma ; chemically induced ; pathology ; Animals ; Carcinoma, Squamous Cell ; chemically induced ; pathology ; Chickens ; Esophageal Neoplasms ; chemically induced ; pathology ; Feces ; Female ; Liver Neoplasms ; chemically induced ; pathology ; Male ; Pharyngeal Neoplasms ; chemically induced ; pathology ; Random Allocation ; Sewage ; adverse effects ; Sodium Nitrite ; toxicity ; Stomach Neoplasms ; chemically induced ; pathology ; Water Pollution, Chemical ; adverse effects

Adenocarcinoma ; pathology ; Animals ; Carcinoma, Squamous Cell ; chemically induced ; pathology ; Cell Line, Tumor ; Dimethylnitrosamine ; analogs & derivatives ; Disease Models, Animal ; Esophageal Neoplasms ; chemically induced ; pathology ; Humans ; Neoplasm Transplantation

Adenocarcinoma ; chemically induced ; pathology ; Animals ; Animals, Newborn ; Lung Neoplasms ; chemically induced ; pathology ; Mice ; Mice, Inbred BALB C ; Random Allocation ; Sterigmatocystin ; toxicity

The anticarcinogenic effects and mechanisms of the biotechnological drugs of Panax ginseng C.A. Meyer cultivated in Russia, bioginseng, panaxel and panaxel- 5, were studied. Bioginseng was produced from a tissue culture of ginseng root cultured on standard medium, whereas panaxel and panaxel-5 were produced from ginseng tissue root cultures using standard mediums enriched with 2-carboxyethylgermanium sesquioxide and 1-hydroxygermatran-monohydrate respectively. All three ginseng drugs inhibited the development of mammary tumors induced by intramammary injections of N-methyl-N-nitrosourea (MNU) in rats, the development of the brain and spinal cord tumors induced by transplacental administration of N-ethyl-N-nitrosourea (ENU) in rats, and the development of uterine, cervical and vaginal tumors induced by intravaginal applications of 7,12-dimethylbenz(a)anthracene (DMBA) in mice. The ginseng drugs induced the cytotoxic activity of macrophages in mice, enhanced T-lymphocyte rosette formation in guinea pigs exposed to cyclophosphamide, and stimulated the production of thyroid hormones in rats. These mechanisms may contribute to the anticarcinogenic action of the ginseng drugs. The organic germanium compounds present in panaxel and panaxel-5 did not potentiate the anticarcinogenic or immuno- stimulatory effects as much as biogeinseng. Preliminary clinical trials with panaxel and bioginseng were carried out in patients with precancerous lesions of the esophagus and endometrium. Panaxel was found to have a strong therapeutic effect in patients suffering from chronic erosive esophagitis. Bioginseng induced the regression of adenomatous-cystic hyperplasia of the endometrium in some patients. Thus, we conclude that the drugs of ginseng appear to hold considerable promise for future cancer chemoprevention.
Adenocarcinoma/chemically induced/prevention & control ; Adult ; Animal ; Antineoplastic Agents, Phytogenic/*therapeutic use ; Cells, Cultured ; Cervix Neoplasms/chemically induced/prevention & control ; Clinical Trials ; Cytotoxicity Tests, Immunologic ; Disease Models, Animal ; Endometrial Neoplasms/pathology/prevention & control ; Endometrium/pathology ; Esophageal Neoplasms/pathology/prevention & control ; Esophagus/pathology ; Estradiol/blood ; Female ; Fibroadenoma/chemically induced/prevention & control ; Human ; Macrophages, Peritoneal/cytology/immunology ; Male ; Mammary Neoplasms, Experimental/chemically induced/prevention & control ; Mice ; Mice, Inbred C57BL ; Neoplasms, Experimental/chemically induced/*prevention & control ; Nervous System Neoplasms/chemically induced/prevention & control ; Panax/*metabolism ; Precancerous Conditions/pathology/*prevention & control ; Rats ; Tissue Culture ; Uterine Neoplasms/chemically induced/prevention & control ; Vaginal Neoplasms/chemically induced/prevention & control

OBJECTIVETo evaluate the efficacy and safety of the combination of oxaliplatin and ELF (VP16/CF/5-Fu) regimen in the treatment of patients with advanced gastric cancer.

METHODSOxaliplatin was given at a dose of 100 mg/m(2) i.v. 2 hours D1, calcium folinate (CF) 200 mg/m(2) i.v. 1/2 hour D1 approximately D3, 5-fluorouracil (5-Fu) 500 mg/m(2) i.v. 2 hours D1 approximately D3 and etoposide 100 mg/m(2) i.v. 3 hours D1 approximately D3. Cycles were repeated every 21 days. Efficacy and safety were evaluated every 2 cycles.

RESULTSSixty-nine patients were enrolled into the study. All cases were pathologically confirmed as gastric cancer (adenocarcinoma in 57 cases and signet ring cell carcinoma in 12 cases). 42 patients had newly diagnosed disease, and 27 patients had received previous chemotherapy. 62 patients were analyzed for response (7 complete responses and 25 partial responses) with total response rate 51.61%. The median time to progression was 5.7 months and the median overall survival was 9.2 months. The most common hematologic toxicities were anemia (29.0%), leucopenia (51.2%) and thrombocytopenia (21.2%). No grade 4 and grade 5 hematologic toxicities were observed. The most common non-hematologic toxicities were nausea (46.5%), vomiting (41.1%), peripheral sensory neuropathy (47.1%), and grade 2 alopecia (27.3%).

CONCLUSIONThis oxaliplatin combined with ELF regimen shows good efficacy and acceptable safety in advanced gastric cancer patients. It is worthy to be proved as a suitable alternative regimen in this indication.

Adenocarcinoma ; drug therapy ; pathology ; Adult ; Aged ; Anemia ; chemically induced ; Antineoplastic Agents ; administration & dosage ; adverse effects ; Antineoplastic Combined Chemotherapy Protocols ; adverse effects ; therapeutic use ; Carcinoma, Signet Ring Cell ; drug therapy ; pathology ; Etoposide ; adverse effects ; therapeutic use ; Female ; Fluorouracil ; adverse effects ; therapeutic use ; Humans ; Leucovorin ; adverse effects ; therapeutic use ; Leukopenia ; chemically induced ; Levoleucovorin ; Male ; Middle Aged ; Nausea ; chemically induced ; Neoplasm Staging ; Organoplatinum Compounds ; administration & dosage ; adverse effects ; Remission Induction ; Stomach Neoplasms ; drug therapy ; pathology ; Survival Rate ; Thrombocytopenia ; chemically induced ; Vomiting ; chemically induced

OBJECTIVETo evaluate the efficacy and toxicity of oxaliplatin-based regimen in patients with advanced or metastatic gastric/esophagogastric junction cancer (AGC).

METHODSThe clinicopathological data of a total of 180 patients with AGC were retrospectively analyzed. Responses was evaluated by RECIST criteria, and toxicity were assessed according to the NCI-CTC AE version 3.0.

RESULTS155 patients received mFOLFOX regimen, and 25 patients received regimens of mEOF and CapOX, with a total chemotherapy of 717 cycles with a median of 3 cycles. The therapeutic response was evaluated in 150 patients, showing response rate (RR) of 30.0% and disease control rate (DCR) of 74.0%. The response was evaluated in 103 of 124 patients who received the therapy as 1st line, with RR of 34.0%, DCR of 74.8%, and overall survival of 11.3 months. The major grade III/IV adverse events were leucocytopenia (14.4%), neutropenia (17.8%), thrombocytopenia (3.8%), nausea/vomiting (8.9%), and peripheral neuropathy (2.2%), with no treatment related death.

CONCLUSIONOxaliplatin-based regimen is active and well tolerated in patients with advanced or metastatic gastric/esophagogastric junction cancer.

Adenocarcinoma ; drug therapy ; pathology ; Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols ; adverse effects ; therapeutic use ; Esophagogastric Junction ; Female ; Fluorouracil ; adverse effects ; therapeutic use ; Follow-Up Studies ; Humans ; Leucovorin ; adverse effects ; therapeutic use ; Leukopenia ; chemically induced ; Male ; Middle Aged ; Nausea ; chemically induced ; Neoplasm Staging ; Neutropenia ; chemically induced ; Organoplatinum Compounds ; administration & dosage ; adverse effects ; therapeutic use ; Remission Induction ; Retrospective Studies ; Stomach Neoplasms ; drug therapy ; pathology ; Survival Rate ; Thrombocytopenia ; chemically induced ; Vomiting ; chemically induced

OBJECTIVETo investigate the early efficacy of nedaplatin combined with megestrol in concurrent chemoradiotherapy for advanced cervical cancer.

METHODSForty-two cases of cervical cancer (FIGO IIb to IVa) were divided randomly into two groups: radiotherapy alone (21 cases) and radiation plus chemotherapy (Nedaplatin) group. The same radiotherapy was given to the two groups. Patients of the RT + C group received nedaplatin 30 mg/m2 in intravenous drip infusion once weekly on day 1, for 4 to 5 weeks, and megestrol 160 mg orally every day during the radiation therapy.

RESULTSThe early outcome: the complete remission rate was 81.0% and partial remission rate was 19.0% in the RT + C group, significantly better than the CR (38.1%) and PR (42.9%) in the RT group. The 1-year survival rates in the two groups were 100% (21/21) and 81.0% (17/21), respectively, with a significant difference between the two groups (P<0.05).

CONCLUSIONSThe combination of nedaplatin and megestrol with concurrent chemoradiotherapy can improve the early outcome of advanced cervical cancer, with somewhat increased but tolerable adverse effects.

Adenocarcinoma ; drug therapy ; pathology ; radiotherapy ; Adult ; Alopecia ; chemically induced ; Anemia ; chemically induced ; Antineoplastic Combined Chemotherapy Protocols ; adverse effects ; therapeutic use ; Brachytherapy ; Chemoradiotherapy ; adverse effects ; Diarrhea ; chemically induced ; Female ; Follow-Up Studies ; Humans ; Iridium Radioisotopes ; therapeutic use ; Leukopenia ; chemically induced ; Megestrol ; administration & dosage ; Middle Aged ; Neoplasm Staging ; Organoplatinum Compounds ; administration & dosage ; Particle Accelerators ; Radiotherapy, High-Energy ; Remission Induction ; Survival Rate ; Thrombocytopenia ; chemically induced ; Uterine Cervical Neoplasms ; drug therapy ; pathology ; radiotherapy