Primary giant cell malignant fibrous histocytoma of the lung: a case report.

A rare case of malignant fibrous histiocytoma of giant cell type originating in the lung of a 46-year-old woman is presented. The patient complained of having a cough that had lasted for a few weeks. A chest X-ray photograph showed a tumor shadow on the left lung. Histological and cytological examination of the biopsy specimen revealed that the tumor was a kind of sarcoma. An operative procedure was selected because of tumor invasion into the trunk of the left pulmonary artery, which was discovered on computed tomography examination, and because metastatic tumor was excluded clinically. The tumor was almost encapsulated and 6 x 6 x 6 cm in size; however, it also showed invasion into the pulmonary artery and bronchial lumen. A histological survey of the tumor showed a wide range of patterns such as fibrous, pleomorphic, fascicular and osteoclast-like giant cell figures; however, the osteoclast-like giant cell area was predominant. Immunohistochemically, the tumor cells were positive for vimentin, CD68 for histiocytic marker and alpha1-antichymotrypsin, and negative for keratin, epithelial membrane antigen, S-100 protein, MT-1, desmin, myoglobin and lysosome. No primary tumor was found clinically in any part of the patient's body at 2 and 4 months after operation. Consequently, she was diagnosed as having primary giant cell malignant fibrous histiocytoma of the lung.

Supercritical fluid chromatographic determination of cholesterol and cholesteryl esters in serum on ODS-silica gel column.

Cholesterol and cholesteryl esters in human serum were determined by supercritical fluid chromatography on an inert ODS-silica gel column using supercritical carbon dioxide as a mobile phase without a modifier. Chromatograms were obtained by monitoring the eluent simultaneously with an FID and UV detector at the wavelength of 190 nm. The retention behavior of cholesterol and cholesteryl esters was investigated in terms of the density of CO2 mobile phase. The separation mode was found to be reversed phase, as in liquid chromatography. The amounts of cholesterol and cholesteryl esters extracted from human serum reference material (NIST SRM 909) were determined individually using cholesteryl laurate as an internal standard to give good agreement of total cholesterol with the value certified by NIST.

Suppressive effect of aluminium chloride administration on mouse lung carcinogenesis by dimethylnitrosamine.

Dimethylnitrosamine was administered to mice by ip injection once a week for 3 weeks and a high incidence of lung tumor was found 6 approximately 8 months after the final injection. In experiment I, the incidence of mice with lung tumors was 74% and the average number of nodules per mouse was 15.6 within 6.0 months after the final injection of dimethylnitrosamine. In mice given aluminium pretreatment, these values decreased to 65% and 6.7 (P less than 0.05), respectively. In experiment II, the incidence of mice with lung tumors was 100% and the average number of nodules per mouse was 8.7 within 7.5 months after the final injection of dimethylnitrosamine. In mice given aluminium pretreatment, these values decreased to 79% and 4.6 (P less than 0.05), respectively.

Epithelial focus assay for early detection of carcinogen-altered cells in various organs of rats exposed in situ to N-nitrosoheptamethyleneimine.

The purpose of these studies was to determine a) whether epithelial cells with altered in vitro growth capacity occur not only after topical application of 7-12-dimethylbenz [a]-anthracene but also after systemic administration of a carcinogenic nitrosamine, and b) whether such cells can be isolated from tissues other than tracheal mucosa. AT 3 and 20 weeks following intragastric administration of 150, 300, or 600 mg N-nitrosohepatamethyleneimine (NHMI)/kg, cells were harvested from tracheas, esophagi, and lungs (target tissues for NHMI) of inbred F344 rats and seeded into culture dishes. Normal cells from nonexposed organs produced no proliferative epithelial foci (EF). Of those tracheas sampled 3 weeks following exposure to 150 and 300 mg/kg 10 and 20%, respectively, contained one or more EF that could be subcultured. Of these tracheas harvested 3 weeks post exposure to 600 mg/kg or 20 weeks post exposure to 150-600 mg/kg, 80-100% contained EF that could be subcultured. Twenty weeks after 600 mg NHMI/kg, the incidence of tracheas harboring cell populations with neoplastic potential (agarose-positive EF) was 80%, whereas the tracheal tumor incidence determined at 24 months was only 29%. Epithelial focus-forming units with various abnormal in vitro growth potentials were also detected in esophagi and lungs of NHMI-exposed rats.

Diagnosis of small early gastric cancer by X-ray, endoscopy, and biopsy.

Cases of early gastric cancer detected over a span of 12 years were reviewed for three periods: 1968-71, 1972-74, 1975-79. Early gastric cancers detected in each period were compared by size, type, and accuracy of diagnostic techniques consisting of barium meal double contrast radiography, gastroscopy, and biopsy. Eighty-five lesions were detected in the first period, 101 in the second, and 237 in the third, in a total of 369 patients. The number of detected early gastric cancers less than 10 mm in diameter also increased in each period. The study indicated that emphasis should be placed on careful radiographic and gastroscopic analysis of slight mucosal abnormalities in order to detect small early gastric cancer with greater accuracy.

Failure of two retinoids to inhibit tracheal carcinogenesis in hamsters.

The effect of 2 retinoids, 13-cis-retinoic acid and 4-methoxy-2,3,6-trimethylphenyl analog of retinoic acid ethyl amide (designated Roll-1430), on tracheal tumor development in hamsters exposed to N-nitroso-N-methylurea was tested. Hamsters were intratracheally exposed either 18, 20, or 23 times to 1% N-nitroso-N-methylurea before the retinoids were administered in the diet. Evidence was presented which indicates that the great majority of the animals are free of invasive neoplasia at the start of retinoid feeding. In none of the 6 retinoid-treated groups could a statistically significant inhibition of tumor development be demonstrated. Hamsters treated with 13-cis-retinoic acid (128 or 172 mg/kg of diet) tended to have an elevated cancer risk; this effect was at a statistically significant level in the group treated with 172 mg/kg of diet. The distribution of histologic tumor types seemed to be shifted in favor of adeno and mixed adeno-epidermoid tumors in the group receiving a low carcinogen dose and Roll-1430. Similar to earlier studies with retinyl acetate tested in hamsters and rats, 13-cis retinoic acid and the retinoic acid ethyl amide analog Roll-1430, failed to inhibit development of respiratory tract neoplasms. We suspect that the reason for this is the absence of significant promoting influences in the current lung cancer models and that retinoids act mostly as anti-promoters.

Tumor development in organ transplants obtained from carcinogen-exposed rats.

F344 rats were exposed intragastrically to two different dose levels of N-nitrosoheptamethyleneimine (NHMI) resulting in a cumulative dose of either 225 or 450 mg/kg body weight. Tumor development was followed either in situ in the NHMI-exposed animals or in tracheas and esophagi from NHMI-exposed donors after these organs were grafted to isogeneic recipients. Tumor responses in situ and in organ grafts were compared. The results showed that the process of carcinogenesis is not disrupted by the transplantation procedure. The carcinogen dose-response relationship observed in situ was also seen in the transplanted organs. At the high carcinogen dose, the tumor incidence was 100% in situ and transplanted esophagi and 20% in tracheas in situ compared to 25% in tracheal transplants. At the low dose, the tumor incidence was 36% in the esophagi in situ compared to 100% in transplanted esophagi, which suggests a greater sensitivity of the transplant system to detect the carcinogenicity of NHMI. The proportion of carcinomas to papillomas was markedly higher in transplanted esophagi. The tracheal tumor response at both NHMI dose levels showed the same trend but was too low to allow any firm conclusions.

Carcinogenicity of nickel subsulfide for respiratory tract mucosa.

The carcinogenicity of nickel subsulfide, Ni3S2, for respiratory tract epithelium was studied in heterotopic tracheal transplants with doses of 1 and 3 mg Ni3S2 per trachea. Chemical determinations indicated that Ni3S2 persisted in the tracheas for seven to nine months. Ni3S2 showed marked toxicity for mucociliary epithelium, resulting in widespread atrophy and focal epithelial necrosis during the first two months of exposure. The submucosa showed mononuclear infiltration and signs of fibroblastic and capillary proliferation. Tumor studies indicated that Ni3S2 can induce carcinomas in tracheal epithelium. The carcinoma incidence was 10% at 1 mg and approximately 1.5% at 3 mg. The higher dose produced a 67% incidence of fibro- and myosarcomas. The data suggest that, compared to some carcinogenic polycyclic hydrocarbons, Ni3S2 may not be a strong carcinogen for the epithelium of conducting airways. The data are discussed in light of other experimental studies and of epidemiological findings on respiratory tract cancers in nickel workers.

Effects of carcinogen dose on the characteristics of the tracheal tumor response induced by N-nitroso-N-methylurea in hamsters.

Tracheal tumors were induced by repeated intratracheal exposures to the carcinogen N-nitroso-N-methylurea (NMU), using a catheter system previously described. Carcinogen concentrations of 0.25, 0.50 and 1.0% were employed in 20 or 30 twice-weekly exposures. Most of the tumors developed in the mid-portion of the tracheas. Virtually all tumors developed after the end of the 10- to 15-week exposure period. Tumor incidence ranged from 20-94% with mean tumor induction times of 13-46 weeks, depending on NMU concentration and frequency of exposure (i.e., dose). At lower doses, mostly non-invasive tumors were induced; at higher doses, mostly invasive carcinomas of various histological types (epidermoid, adeno-, epidermoid-adeno, and anaplastic large- and small-cell carcinomas) were induced. Adenocarcinomas were most frequent at low NMU concentrations. The possible mechanisms of the carcinogen dose effects are discussed.