Keiji Fujii

Lymphocytic infiltration in juvenile thyroid carcinoma.

In this study, the significance of lymphocytic infiltration in juvenile thyroid carcinoma is clarified. We examined nine patients younger than 20 years of age. Histopathologically, there was good correlation between lymphocytic infiltration and the development and spread of carcinoma. It is believed that lymphocytic infiltration around the tumor is an immunologic reaction induced by antigens from the carcinoma itself, and also that the reaction may progress according to tumor development. Immunocytochemically, we determined what type of inflammatory cells infiltrated the thyroid and demonstrated HLA‐DR expression in the cancer cells. These findings are similar to autoimmune thyroiditis in which antibody‐dependent cellular cytotoxicity (ADCC) works as a main immunomechanism.

Venous tumor thrombosis and cavernous transformation of the portal vein in a patient with gastric carcinoma

A case of extensive extra-and intrahepatic portal tumor thrombosis, with no metastatic foci in liver parenchyma, secondary to advanced gastric carcinoma in a 69-year-old man is reported. The portal tumor thrombosis was characterized by enlargement of the thrombosed segment of the vein, decreased density mass without intraluminal enhancement of the involved vein, nonvisualization of the portal venous branch in the involved lobe, and the so-called cavernous transformation of the portal vein. The surgically resected gastric specimen showed Borrmann type 3 advanced papillary adenocarcinoma. The portal tumor thrombus is presumed to have arisen from vascular invasion in the primary foci of gastric carcinoma, and then to have permeated the portal vein without invasion of liver parenchyma.

Comparative study of tumorigenicity in mice administered transplacentally or neonatally with metabolites of tryptophan and its related compounds

SummaryIntermediate metabolites of tryptophan, 3-hydroxy-l-kynurenine (3-OHKY), 3-hydroxyanthranilic acid (3-OHAA) and anthranilic acid (AA), and an enzyme inhibitor from 3-OHKY to 3-OHAA, isonicotinic acid hydrazide (INH) with or without 3-OHKY at the maximum tolerated dose were injected s.c. to infant CDF1 mice. AA and 3-OHAA were tested tranplacentally for tumorigenicity. Animals treated were observed for 1 year.Hepatocelluar adenoma was developed at the incidence of 21.7% in male mice administered with 3-OHKY and INH as compared with 5.6% incidence in control males, but no leukemia was induced. Incidences of lung (3.4–15.0%) and liver tumors (4–5%) in other groups treated at infant stage were comparable to that in controls (lung: 11.1%; liver: 5.6%). Other tumors were one angiogenic sarcoma in a female treated with 3-OHAA, and one granulosa cell tumor of ovary in female treated with INH.Transplacentally the 10.3% incidence of liver tumor in male offspring, whose mothers were treated with AA, was slightly higher than that in male control (5.6%).However, the incidences of tumor were apparently in a critical level in these experimental conditions.

Inhibitory effect of cold stress on lung tumours induced by 7,12-dimethylbenz[a]anthracene in mice

The effect of cold stress on lung tumours induced by 7,12-dimethylbenz[a]anthracene (DMBA) was investigated in ICR male and female mice. When mice were exposed to cold stress at 0±1°C for 2 h, three times per week (every other day) for 3 months, the rectal temperatures and hepatic glutathione levels were significantly decreased. On the other hand, when DMBA (10 mg/kg) was subcutaneously injected into neonatal mice, lung tumours were observed in 81.8% of non-stressed mice of both sexes 4 months after injection. However, when mice treated with the same dose of DMBA were exposed to cold stress under the same conditions, lung tumours were observed in 53.3% and 30.3% of the male and female mice 4 months after DMBA injection. In addition, although DMBA (1 mg/kg) caused lung tumours in 20% or 40% of the treated male or female mice 4 months after injection, it did not cause lung tumours in all of the male and female mice exposed to cold stress. These results suggest that cold stress may inhibit lung tumours induced by chemicals.

Inhibitory effect of cold stress against acetaminophen-induced hepatic injury in B6C3F1 and ICR mice

The effect of cold stress (at 0 +/- 1 degree C for 3 h) on acetaminophen-induced hepatic injury was investigated in B6C3F1 and ICR mice. When acetaminophen (250 mg/kg) was injected intraperitoneally in B6C3F1 mice, the plasma GPT activity was significantly increased by 93 or 107-fold at 6 h or 24 h after the drug injection. However, when B6C3F1 mice were exposed to cold stress, the increase in plasma GPT activity induced by acetaminophen was significantly inhibited by 53% and 44%, respectively. On the other hand, when acetaminophen at the same dose was injected in ICR mice, the activity of plasma GPT was increased by 9-fold at 6 h, or 16-fold at 24 h after the drug injection. The increased plasma GPT activity elicited a significant inhibition of 35% and 36%, respectively, by the exposure to cold stress. These results suggest that acetaminophen-induced hepatic injury may be blocked by physical stress in mice.

Prominent increase in the amount of a cytosol protein in transformed fibroblasts and ascites hepatome cells

Analysis of cytosol proteins by sodium dodecyl sulfate polyacrylamide slab gel electrophoresis revealed a prominent increase in the amount of a cytosol protein with molecular weight of 88 000 in transformed human adult, human embryo, mouse adult, and hamster embryo fibroblasts as compared with normal fibroblasts. The cytosol protein with Mr 88 000 is also increased in the cytosol of four kinds of rat ascites hepatoma cell as compared to normal and regenerating liver. The protein with Mr 88 000 exists as one of the major cytosol proteins in transformed fibroblasts hepatoma cells and HeLa cells, constituting 7--10% of total cytosol proteins. The data suggest that the cytosol protein with Mr 88 000 is associated with certain growth characteristics of cells.

Primary tubular adenocarcinoma arising in the duodenal limb of reconstructed gastroduodenostomy for signet-ring cell carcinoma of the stomach

Adenocarcinoma of the small intestine is uncommon. Due to this paucity and the lack of specificity of symptoms, patients are usually seen late in the course of their illness, when curative therapy, mainly represented by extensive surgical resection, is unlikely. The authors report a case of primary well-differentiated tubular adenocarcinoma (T4N0M0) arising in the duodenal limb of a reconstructed Billroth I gastroduodenostomy, 9 years after a distal gastrectomy for signet-ring cell carcinoma of the stomach (T4N0M0). Evidence for excluding the possibility of a recurrence of the primary gastric cancer was based on the different histologic pattern, the long disease-free interval, and other features of the second neoplasm. Relatively early diagnosis of the neoplasm, followed by curative surgical therapy was made possible by the early onset of the obstructive symptoms and the favorable anatomical location of the tumor.

Chronic toxicity of charred fish meat in Wistar rats

An experiment was performed on Wistar rats to examine the possible carcinogenic effects of charred fish meat. Each group (of 30 male rats each) was fed one of the following diets: the standard diet mixed with 50% charred fish meat (Group 1), the standard diet mixed with 25% charred fish meat (Group 2), the standard diet alone (Group 3), or the 1-methyl-3-nitro-1-nitrosoguanidine (MNNG) treatment in drinking water (Group 4); this last group served as positive control. The animals were observed for two years. No significant incidences of tumors were recorded. However, there were statistically significant incidences of nonspecific pathological lesions of the glandular stomach, such as erosion, regeneration, and hyperplastic epithelium. Also, an atypical epithelium of the stomach was found incidentally in two animals (Groups 1 and 2); this might suggest a premalignant condition.

Tumor induction by a single subcutaneous injection of 1-butyl-1-nitrosourea or 1-butylurea in newborn mice.

A subcutaneous injection of 1-butyl-1-nitrosourea (BNU) at the maximum tolerated dose (333 mg/kg body wt.) to newborn CDF1 mice induced adenocarcinoma and adenoma of the lung, adenoma of the liver, thymic or non-thymic lymphoma and neurinoma of the acusticus nerve; the total incidence of tumors was statistically significant as compared with that of control. However, in the 1-butylurea (BU) mice, one adenoma of the lung was induced in a male mouse; the total incidence of tumor was comparable to that of control.