European Journal of Cancer (1965)最新文献

The mitotic response following a partial hepatectomy, the nyctohemeral rhythm of these mitoses and the ‘chalone activity’ measured by the inhibitory effect of liver extracts on the normal liver regeneration have been studied in order to estimate the evolution of mitotic control in the liver of rats treated by DENA for 2, 4, 6 and 10 weeks. These parameters and the pathological lesions (preneoplastic foci, neoplastic nodules and hepatomas) have been followed up after stopping the DENA feeding. A good correlation has been found between the malignant transformation of preneoplastic foci and the breakdown of the mitotic control. In animals treated by DENA for two weeks, the homeostatic control of mitoses remains normal for a minimum of 14 months and ‘preneoplastic foci’ persist without any further malignant transformation. After DENA feeding for 4 and 6 weeks, the subsequent malignant transformation occurs as a function of the mitotic disturbance: the longer the DENA feeding, the faster the homeostatic disturbance, the earlier the conceration. After DENA treatment for 10 weeks, the homeostatic regulation is lost and the neoplastic growth is triggered at the time of the DENA feeding cessation. In this case, the pattern of canceration is the same as when DENA is given continuously up to the time of death. It is concluded that ‘preneoplastic foci’ induced during the first two weeks of treatment cannot by themselves transform into a malignant tumor. To commit them irreversibly into malignancy, a subsequent action of the carcinogen is necessary; it may consist of the irreversible breakdown of the normal homostatic regulatory mechanism of liver cell proliferation.

Hormone-responsive mammary tumors of GR mice were treated with tamoxifen, cyclophosphamide, or with both drugs combined. Tamoxifen alone or cyclophosphamide alone caused inhibition of tumor growth, but more growth inhibition was obtained with the combined therapy.

Mouse leukemias arising after neonatal inoculation of Moloney MuLV (M-MuLV) are of two main types. One is characterized by enlargement of spleen and lymph nodes, and has a normal diploid karyotype. Thymus enlargement is the most prominent feature of the second type, with or without spleen involvement. About half of the thymomas are trisomic with an extra chromosome 15. C-type viruses isolated from the two leukemia types differed with regard to their p30 peptide maps. The p30s isolated from the preleukemic tissues of a 4-weeks-old, neonatally MuLV-inoculated mouse were either of the ‘thymic’ or the ‘splenic’ type. These results suggest that the two virus types were already present in the original inoculum and had homed to different tissues. The peptide maps of the corresponding gp70 molecules showed no organ-related pattern: each virus isolate had a distinct gp70 profile.

The sensitivity to adriamycin, prednisolone, bleomycin and vincristine of human lymphoma cells in short-term culture was studied in 30 non-Hodgkin lymphomas (NHL). As indicators of drug action, the interference on [³H]thymidine and [³H]uridine incorporation was studied. The in vitro sensitivity to the drugs was then compared with the clinical response to treatment. On the basis of the retrospective analysis the in vitro sensitivity indexes were defined taking into account the biologic aggressivity of the tumor. A statistically significant correlation between the in vitro sensitivity to adriamycin and prednisolone and complete remission, relapse-free time and survival was observed in highly proliferative NHL, while in low proliferative NHL the in vitro sensitivity was statistically associated only to relapse-free survival within 22 months.

This study demonstrates that the survivial of patients with UICC category T3 and T4 bladder cancer is strongly correlated with pre-treatment levels of serum acute phase reactant proteins and albumin. A more accurate assessment of the prognosis is obtained than by considering stage and the type of operation alone.

Several dimethylbenz[c]acridines and their isomers dimethylbenz[a]acridines were studied for their capacity to induce malignant transformation in secondary hamster embryo cells. Transformation was evaluated by the ability of transformed cells to provoke tumor formation in syngenic animals. 7,8-Dimethylbenz[c]acridine, 7,10-dimethylbenz[c]acridine, as well as a mixture of both, caused malignant transformation of hamster embryo cells, but not 7,9-dimethylbenz[c]acridine. Cultures treated with 10,12-dimethylbenz[a]acridine and 9,12-dimethylbenz[a]acridine did not become malignant and showed a decreased life-span in vitro. Untreated control cells retained their original characteristics and when injected in animals did not produce tumors throughout the whole experiment.

Serial CEA assays on serum using the direct radioimmunoassay method (Marcoule, France) were performed on 76 breast cancer patients with node involvement or rapid local development of tumors who were undergoing chemotherapy. The patients were followed up for a mean period of 28 months, and assays were repeated every 2.5 months on average. Out of 521 assays performed on 49 patients who remained in complete remission, there were 37 instances of significant, but transitory, rise in CEA level which, in 8 cases, could be attributed to intercurrent benign inflammation. In 15 out of 27 patients who had relapses, there was a significant and persistent rise in CEA level which, in 11 cases, preceded clinical signs by 6 months on average. In the 12 other cases, CEA level remained constant and normal despite relapse.

In a disease-oriented phase II study, thirty-three patients with advanced non-seminomatous testicular cancer were treated with oral VP-16-213 175 mg/m²/day for three consecutive days repeated every week. All patients had previously received extensive chemotherapy and twenty patients also had prior radiotherapy, Of 30 evaluable patients, 6 experienced partial remission for a median duration of 3.5 months, whereas minor regression or stabilization of the disease was achieved in 7 patients for a median duration of 2.5 months. Leukopenia was dose-limiting and resulted in dose reduction or treatment delay in 55% of the scheduled courses. The definite antitumor activity of VP-16-213 in non-seminomatous testicular cancer warrants its incorporation into combination chemotherapy for this disease.