Pneumoconiosis caused by the inhalation of polyvinylchloride dust.
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Adult↗
Biomedical subjects
K Lapis
Publications and source records attributed to K Lapis.
Antitumour action of 1,5-dihalogeno-, and 1, 2-4, 5-dianhydro-xylitol derivatives.
The antitumour action of some xylitol compounds possessing alkylating potency at 1 and 5 position of the sugar skeleton was investigated. Unlike the hexitol derivatives, bi-halogenated xylitols showed no antitumour action. The modest therapeutic index of 1, 2-4,5-dianhydroxylitol on the NK/Ly ascites tumour could be substantially increased by the addition of a phenyl-benzoyl group at the 3 position. This latter compound appeared to be active against L1210 leukaemia, S-180, and Yoshida solid sarcoma; and furthermore, against metastasis formation of the Lewis lung tumour.
Animals↗
PMA induces shift from chondroitin to heparan sulphate on proteoglycans correlating with fibronectin adhesion of MDS human leukemia cells.
We have analysed the mechanism of PMA-induced adhesion of the MDS human leukemia cell line. Affinity to various matrix ligands indicated that PMA induced fibronectin adhesion of MDS cells. This interaction could not be inhibited by RGDS-peptide, therefore it was most probably not mediated by integrins. Rather, both the basal and PMA-induced fibronectin adhesion of MDS cells could be inhibited by heparin and much less efficiently by chondroitin sulphate, suggesting that glycosaminoglycans of proteoglycans may be responsible for the change in adhesive phenotype. PMA stimulation of MDS cells induced a significant increase in proteoglycan biosynthesis. Studies on the glycosaminoglycan pattern of the proteoglycans showed that PMA treatment initiated a shift in glycanation of the MDS-proteoglycans from the predominant chondroitin sulphate-proteoglycans in control cells to a predominant heparan sulphateproteoglycans in adherent cells. These data indicate that protein kinase C, the main target of PMA, may have a profound role in the regulation of glycanation pattern of proteoglycans. Furthermore, such alterations in the cellular proteoglycans may significantly affect the matrix adhesion potential of hematopoietic cells.
Cell Adhesion↗
The antitumor effect of Tiazofurin (TR) consists of anti-proliferative and anti-invasive elements.
We have studied the effects of the antimetabolite, Tiazofurin (TR-2-beta-D-furanosylthiazole-4-carboxamide), on the metastatization of HT168-M1 human melanoma cell line compared to 3LL-HH murine lung carcinoma. TR pretreatment of 3LL-HH cells, in a dose range 15-60 microM, caused inhibition of cell proliferation as well as adhesion to the EHS-matrix. TR inhibited the entry of adherent tumor cells to the S phase and accumulation in G1, however in non-adherent cells TR completely inhibited the entry of tumor cells to G2 phase. In contrast to these data TR treatment of HT168-M1 cells did not cause inhibition of cell proliferation, a change in cell cycle distribution or in the quantity of apoptotic cells. However, TR pretreatment did inhibit the adhesion to and migration through EHS-matrix of melanoma cells similar to 3LL-HH cells. Furthermore, in vivo TR treatment inhibited the formation of liver metastases of HT168-M1 melanoma cells without major effects on the spleen primary tumor. Since in vivo TR treatment of HT168-M1 and 3LL-HH tumor bearing mice significantly decreased the number and incidence of liver metastases though there was a different effect on the in vitro/in vivo growth (lack of inhibitory effect in case of IIT168-M1 cells), we suggest that the antiproliferative and anti-metastatic effects of TR could be separated. We also suggest that the antimetastatic effects of TR are due to inhibition of adhesion and migration of tumor cells.
Animals↗
Inhibition of the progression of human and rat Wilms' tumor by Tiazofurin.
We monitored the antitumoral and antimetastatic effects of tiazofurin (2-beta-Dribofuranosylthiazole-4-carboxamide, TR) on human (HWT) and rat (RWT) Wilms' tumor grafts transplanted orthotopically underneath the renal capsule of scid mice and in rat Wilms' tumour, immunocompetent F344 rats. Treatment with different doses of Tiazofurin, twice a week proved therapeutically effective, since they resulted in a significant decrease in inhibition of both human and rat nephroblastoma grafts. We also applied combined surgical and chemotherapeutic treatment using orthotopic rat Wilms' tumor. The primary tumor was removed 13 days after tumor implantation. TR treatment was started immediately after the implantation of the isograft or following surgical removal of the primary tumor and chemotherapy was followed for 13 days. A high cure rate was found from combined treatment compared to surgery alone. TR treatment resulted in a significant inhibition of the growth of the primary tumor. TR decreased also the frequency and size of recurrent tumors, and appeared to exert selective antimetastatic effects, unrelated to cytotoxicity toward tumor cells. Our results indicate that TR may be a potential alternative chemotherapeutic in the treatment of human Wilms' tumor.
Animals↗
Flow cytometric studies on the relationship between DNA content and clinicopathologic features of pancreatic cancers.
The purpose of this study was to determine DNA (DI) and proliferation indices (PI) in 26 pancreatic and 10 ampulla of Vater carcinomas by flow cytometry using paraffin embedded tissue samples. Furthermore, we analysed the relationship between these parameters and the traditionally used prognostic parameters (type, stage and grade) of the tumor. Out of the 26 pancreas carcinomas 15 proved to be DNA diploid and 11 DNA aneuploid, while among the 10 ampulla of Vater tumors 7 DNA diploids and 3 DNA aneuploids were found. The PI-ces in both type of carcinomas were significantly higher than PI-ces in the surrounding nontumorous pancreatic tissue. The average of PI in aneuploid carcinomas significantly exceeded the one of diploid carcinomas. In group of grade III-IV tumors the ratio of aneuploids (59%), and the average of PI (11.59% +/- 5.27%) proved to be significantly higher (P < 0.05, both) than in grade I-II group (21%, PI = 8.16% +/- 4.03%). Among the tumors falling into the T1 class the ratio of aneuploids (29%) and of tumors (29%) characterized by a PI > 8% proved to be lower than among the tumors of T2-T3 class (46%, 62%). The ratio of aneuploids among cases with lymphnode positivity was higher (3/4), than among those without (8/22), the single case with distant metastasis was also found to be aneuploid. The results indicate a close correlation between the DNA ploidy and PI and the stage and grade of pancreatic cancers.
Adult↗
Effect of Avemar and Avemar + vitamin C on tumor growth and metastasis in experimental animals.
Because of the observed immunostimulatory actions of a new fermented wheat germ extract--with standardized benzoquinone composition--we have investigated the eventual tumor growth- and metastasis-inhibiting effects of this preparation (Avemar) applied alone or in combination with vitamin C. Tumor models of different origin [a highly metastatic variant of the Lewis lung carcinoma (3LL-HH), B16 melanoma, a rat nephroblastoma (RWT-M) and a human colon carcinoma xenograft (HCR25)]--kept in artificially immunosuppressed mice were applied. The metastasis-inhibiting effects of the treatments have been studied both in the presence and in the absence (following surgical removal) of the transplanted primary tumors. Combined treatments with Avemar and vitamin C--administered synchronously--profoundly inhibited the metastasis formation in all the applied tumor models while, treatments with vitamin C alone did not exert such an inhibiting effect on the metastasizing process. The degree of the observed metastasis inhibition in certain models was significant, while in others--although it was meaningful--did not prove to be significant. It is noteworthy that treatment with Avemar alone in certain models exerted a more pronounced inhibiting effect on metastasis formation than the synchronous combined treatment with Avemar and vitamin C. Furthermore, if the time schedule of the combined treatment was changed (vitamin C--instead of being administered synchronously--was given one hour after the treatments with Avemar), the vitamin C rather decreased the metastasis inhibiting effect of Avemar. It should be mentioned however, that in the case of rat nephroblastoma, a different response was observed: while, in the case of synchronous combination significant inhibition of metastasis formation was observed, treatment with Avemar alone did not produce metastasis-inhibition. It is noteworthy that in this model the metastasis-inhibiting effect of the synchronous combination treatment proved to be even more pronounced if Avemar was administered in a 100 times smaller dose than its regularly applied dosage. Treatment with Avemar and vitamin C--administered in combination or separately--in the majority of experimental models (with the exception of rat nephroblastoma) did not inhibit the growth of the primary tumors. It is reasonable, therefore, to suppose that in the observed metastasis-inhibiting effect the eventual proliferation inhibiting effect of these remedies does not play an important role. According to the results of other experiments--carried out in our laboratory in parallel with those described here--Avemar proved to have a meaningful immunostimulatory effect. It might therefore be suggested that the observed metastasis-inhibiting effect of this preparation may be mainly due to its immunostimulatory properties. The possible therapeutic benefits of Avemar and Avemar plus vitamin C are also discussed.
Adenocarcinoma↗