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PubMed1979

Comparison of rat liver and Walker 256 carcinosarcoma tRNAs.

The complete nucleotide sequences of both rat liver and Walker 256 mammary carcinosarcoma tRNAAsn reveal that they are identical except for the nucleotide present in the wobble position of the anticodon loop. The rat liver tRNAAsn contains the Q nucleoside, whereas the tumour tRNAAsn contains an unmodified guanosine. The tRNAs from both tissues also show significant quantitative differences in the chromatographic mobilities for isoaccepting species of tRNAAsp, tRNAAsn, tRNAHis and tRNATyr. In addition, chromatographic shifts upon cyanogen bromide treatment and analyses of the alkaline hydrolysates of these tRNAs demonstrate that those of tumour origin contain significantly less Q and Q nucleoside than their normal rat liver counterparts.

Animals↗
PubMed1991

Chronobiological analysis of peripheral lymphocyte dehydrogenase activities in rats with Walker 256 carcinosarcoma.

Alpha-glycerophosphate dehydrogenase (alpha-GPD) and succinate dehydrogenase (SD) activities were investigated in lymphocytes from peripheral blood of normal rats and rats bearing the Walker 256 carcinosarcoma. Computer analysis using an original algorithm revealed a hierarchy of biorhythmic patterns of dehydrogenase activities. In all rats, mean SD activity was higher than mean alpha-GPD activity. In rats without tumor, SD and alpha-GPD activities were both higher than in rats with the Walker tumor. Biorhythm spectra for both dehydrogenases were very similar in rats with or without tumor, but tumor implantation resulted in a change of the phase relationship between alpha-GPD and SD.

Animals↗
PubMed1991

Mechanism of metabolic abnormality of thyroid hormones in Walker 256 carcinosarcoma-bearing rats.

We examined the mechanism of abnormality of thyroid hormone metabolism in Walker 256 carcinosarcoma-bearing rats. The serum levels of thyroxine (T4), 3,5,3'-triiodothyronine (T3) and thyroid-stimulating hormone (TSH), and the responses of serum T4 and T3 to exogenous TSH in tumor-bearing rats on day 14 after inoculation of tumor cells were significantly less than those in pair-fed control (PFC) rats, suggesting that the metabolic abnormality of thyroid hormones may be caused by disorder of both peripheral and central functions, and that a certain tumor-derived factor may be involved in this abnormality. An active factor responsible for the metabolic abnormality was found in soluble cytosol fraction (SF) of the tumor cells. Administration of the SF to normal rats significantly reduced their serum T4 and T3 concentrations, liver 5'-deiodinase (5'-DI) activity, responsiveness of the thyroid gland to TSH and food intake compared with those of PFC rats, but, unlike the tumor, did not reduce the serum TSH level. This biologically active factor in the SF was found to be a heat-labile protein and specific to the tumor. It was tentatively named serum thyroid hormone reducing factor (STRF). STRF was partially purified from the SF by ammonium sulfate fractionation and DEAE-cellulose chromatography. Partially purified STRF preparation significantly diminished the serum T4 and T3 concentrations and liver 5'-DI activity and food intake of normal rats compared with those of PFC rats, mimicking the changes associated with the tumor in tumor-bearing animals. These results suggested that abnormality of thyroid hormone metabolism in tumor-bearing animals may partly be caused by STRF-mediated modulation at peripheral and thyroid gland levels. Whether STRF actually induces anorexia remains to be clarified.

Animals↗
PubMed1982

Purification and characterization of dihydrofolate reductase from Walker 256 carcinosarcoma.

Dihydrofolate reductase of Walker 256 carcinosarcoma has been purified to homogeneity by affinity chromatography. The enzyme reduced 28 mumol dihydrofolate (FAH2) . min-1 . mg protein-1 at 22 degrees C and pH 7.3. Km values with respect to FAH2 and NADPH were 21 and 29 mM, respectively. The IC50 (amount of inhibitor required for 50% loss of enzyme activity) values were 0.2 nM for MTX and aminopterin and 50 and 67 nM, respectively, for N10-formyl FA and triazinate (NSC-139105). The pH maximum is around pH 7.0 and the isoelectric point is 6.8. This reductase has an apparent molecular weight of 21 500. The N-terminal amino acid is valine and the comparison of the N-terminal 20 residues of this reductase shows very high sequence homology with other mammalian reductases. The enzyme contains two cysteine residues and one of these residues is not involved in catalysis. This reductase has four tryptophan residues and modification of one of these residues leads to loss of activity. The intrinsic circular dichroic (CD) spectrum of this reductase is very different from the CD spectra of reductase of Escherichia coli B and L1210/MTX. However, the CD spectra of the enzyme--substrate and enzyme--inhibitor complexes are very similar to that of the L1210/MTX enzyme. This suggests that the ligands may be constrained in similar conformation on the two enzymes. The fluorescence emission maximum at 314 nM when activated at 286 nM is considerably lower than other mammalian enzymes.

Animals↗
PubMed1985

A study of the adhesive, locomotory and invasive behaviour of Walker 256 carcinosarcoma cells.

We have succeeded in selecting two variant strains of the Walker 256 carcinosarcoma which display markedly different adhesive properties. Both the high (W256A) and the low (W256S) adhesive variants respond chemotactically towards 10(-8) M f-met-leu-phe (FMLP) although there is a significant difference in their locomotory ability. Nevertheless, the fact that the essentially non-adherent W256S cells can migrate in vitro argues against any simple relationship between adhesion and locomotion. We suggest that traction is important in locomotion but that it need not arise only from direct adhesive interaction. We have also tested the invasive behaviour of the W256 variants using an in vitro model system in which disruption of a cellular barrier by the invasive cells can be recorded electrophysiologically. Although leucocytes can penetrate such a barrier they do so only under chemotactic stimulation, whereas W256 tumour cells of either variant strain will do so spontaneously. The tumour variants induce cell retraction within the barrier and this may lead ultimately to cell detachment and death. The holes which arise may then be colonized by tumour cells, and in this way the invasive process could be promoted. The molecular mechanisms by which tumour cells achieve destruction of the cellular barrier are not clear, but it is likely that a number of enzymes are involved.

Animals↗
PubMed1975

Enhancement by hydrazine sulfate of antitumor effectiveness of cytoxan, mitomycin C, methotrexate and bleomycin, in walker 256 carcinosarcoma in rats.

Use of hydrazine sulfate potentiates the antitumor action of Cytoxan (cyclophosphamide), Mitomycin C, methotrexate and bleomycin against Walker 256 intramuscular carcinosarcoma in in vivo short-term studies in rats. Experimental data suggest this potentiation by hydrazine sulfate to result from a mechanism of action other than direct cytotoxicity, and further, that combination chemotherapy with hydrazine sulfate and a cytotoxic agent may be useful in the treatment of human cancer.

Animals↗
PubMed1983

Growth inhibitory activity of succinylacetone: studies with Walker 256 carcinosarcoma, Novikoff hepatoma and L1210 leukemia.

Succinylacetone (SA, 4,6-dioxoheptanoic acid) inhibits d-aminolevulinic acid dehydrase, the second enzyme of the heme biosynthetic pathway and thereby inhibits heme biosynthesis. In the present study SA is shown to inhibit the growth of the Walker carcinosarcoma (W256) in vitro and in vivo, the Novikoff hepatoma in vivo, and L1210 leukemia in vitro, but only slightly in vivo. Rats can tolerate significantly larger doses of SA for at least twice as long as were administered in the present study without gross evidence of toxicity. In contrast to findings in previously published studies with murine erythroleukemia cells, the inhibition of growth of L1210 and W256 cells by SA in vitro is not accompanied by a decrease in cellular heme and is not reversed by addition of hematin to the medium. This suggests a second mechanism of growth inhibition of tumor cells unrelated to heme biosynthesis. Although the growth of both W256 and L1210 cells was markedly inhibited by the same concentration of SA in culture, there was a great difference in responsiveness in vivo, in that much greater inhibition of the growth of the Walker tumor was produced by SA.

Animals↗
PubMed1988

Protective effects of a prophylactic treatment with the bisphosphonate 3-amino-1-hydroxypropane-1,1-bisphosphonic acid on the development of tumor osteopathies in the rat: experimental studies with the Walker carcinosarcoma 256.

The present report primarily describes protective effects of a long-term prophylactic treatment with 3-amino-1-hydroxypropane-1,1-bisphosphonic acid (APD) on the development of tumor-induced osteolytic bone destructions. Pretreatment with daily intravenous doses of APD 9.5 mg/kg for 1 week resulted in a significant reduction of Walker carcinosarcoma 256-induced bone destruction, when Walker cells were transplanted intraosseously (2 x 10(6) tumor cells/rat) 7 weeks later. Shorter pretreatment periods (4, 2 or 1 week prior to tumor inocculation) resulted in a nearly total inhibition of bone destruction as well as tumor-induced hypercalcemia. Tumor growth itself was not inhibited by APD pretreatment. Histological and microradiographical findings are reported. Consistent to our experiments and with regard to new immunocytological methods to detect single metastatic tumor cells in the bone marrow, potential risk groups may be defined which may profit from the prophylactic APD treatment to inhibit tumor-induced bone destructions.

Animals↗
PubMed1984

Production of a macromolecular bone-resorbing factor by the hypercalcemic variant of the walker rat carcinosarcoma.

The Walker rat 256 carcinosarcoma is a spontaneous rat breast tumor which has two unique variants, one of which is always associated with severe hypercalcemia and one which is not associated with hypercalcemia when the tumor is carried im. To determine the factor responsible for hypercalcemia, we established tumor cells derived from both variants in culture and found that the tumor cells from the hypercalcemic variant release an acid-soluble and acid-stable bone-resorbing factor of approximately 25,000 mol wt. Cells from the normocalcemic variant produce no bone-resorbing activity. These data are consistent with the notion that hypercalcemia in this animal model of the humoral hypercalcemia of malignancy is due to a macromolecular bone-resorbing factor which is acid and heat stable and requires disulfide bonds for biological activity.

Animals↗
PubMed1975

The hypercalcaemic syndrome in rats bearing the Walker carcinosarcoma 256.

The strain of Walker carcinosarcoma 256 described induces hypercalcaemia, hyperphosphataemia and hyperuraemia in tumour bearing rats. Changes in calcium and phosphorus excretion are observed as well as accompanying calcification of soft tissue organs and loss of bone calcium. These changes in calcium metabolism disappear after removal of the tumour, so that long-range action of the tumour can be stated. The results are discussed in comparison with three other animal models of tumour dependent hypercalcaemia.

Animals↗
PubMed2006

[Experimental model of Walker 256 carcinosarcoma in rats bladder].

PURPOSE: An animal model to study bladder tumor with Walker 256. METHODS: Bladders rats Wistar was catheterized via urethra and compression lesion of the wall bladder was realized with a little clamping after laparotomy. One total of the 0,3 ml suspension with 3 x 10(5) cels viable of the carcinosarcoma was instilled into each bladder. The animals were sacrificed after eight and 13 days. RESULTS: The index of tumor incidence was 100% and the average of surviving was 14,5 days. CONCLUSION: The model studied was efficient and will can to take subsidy the study experimental in treatment of local invasive bladder cancer.

Animals↗
PubMed2000

Enhancement of 5-fluorouracil anabolism by methotrexate and trimetrexate in two rat solid tumor models, Walker 256 carcinosarcoma and Novikoff hepatoma, as evaluated by 19F-magnetic resonance spectroscopy.

Although 5-fluorouracil (5-FU) is one of the most effective single agents in treating solid tumors, its low effectiveness as a single agent has led to development of a number of modulators intended to enhance its therapeutic effectiveness. Of these, methotrexate (MTX) and trimetrexate (TMTX) have been shown to have synergistic anticancer activity with 5-FU. The effect of these two drugs on the uptake and the intratumoral metabolism of 5-FU was studied in two rat tumor models using 19F-nuclear magnetic resonance spectroscopy: on excised samples of Walker 256 carcinosarcoma and noninvasively (in vivo) in Novikoff hepatoma. In the rats bearing the Walker 256 tumor, a 4-hr pretreatment with MTX showed the maximal increase in the rate of conversion from 5-FU to its fluorinated nucleotides/nucleosides. In the rats bearing the Novikoff hepatoma, both modulators increased the amounts of cyctotoxic anabolites of 5-FU, but at the doses administered, the cumulative amounts of 5-FU anabolites formed after MTX were significantly higher than those formed after TMTX or after saline control. On the other hand, the increase in the levels of the fluorinated nucleotides/nucleosides after TMTX peaked at a later time. The possible significance of these findings is that timing of administration of a modulator is important because it affects both transport and metabolism of 5-FU. The two modulators studied, both antifolates, act differently on transport and on metabolism: MTX affects both, whereas TMTX, at the level studied, appears to affect predominantly the metabolic process. In addition, significant differences exist between tumor models. These data suggest possible mechanisms and processes that should be studied further in humans, using these noninvasive pharmacokinetic imaging methods for monitoring 5-FU targeting and metabolism.

Animals↗
PubMed1999

[Carcinosarcoma (malignant mixed Müllerian tumor) arising in an endometrial polyp. Report of a case].

Malignant degeneration of an endometrial polyp occurs rarely, i.e. approx. 0.36%. In literature the rare cases of carcinosarcomatous degeneration of an endometrial polyp described are mostly associated with a good prognosis. The following is a description of an other case of carcinosarcoma arisen and confined to an endometrial polyp, but characterised by a particularly aggressive clinical course.

Endometrial Neoplasms↗
PubMed2001

[Disorders of blood rheology in Walker's carcinosarcoma-256 and in cyclophosphamide treatment of rats].

Tumor process development in rats inoculated with cellular suspension of transplantable Walker's carcinosarcoma-256 involved enhanced thickening of blood on day 7. Treatment with 20 mg/kg cyclophosphamide, thrice a day, every other day, retarded tumor process and brought hemorheologic indices further down, at the same time. Similar treatment of intact rats with cyclophosphamide caused hemorheologic disorders too.

Animals↗
PubMed1976

Dissociation of 5-fluorouracil uptake from intracellular pH in Walker 256 carcinosarcoma.

The influence of intracellular pH (pHi) upon 5-fluorouracil (5-FU) uptake has been studied in slices of Walker 256 carcinosarcoma and rat liver. Alteration of pHi was achieved by the addition of either glucose alone or together with oxamic acid to the incubation medium. Results indicated that 5-FU uptake by the tumor slices was not dependent upon pHi, but was enhanced by the presence of glucose. Uptake of 5-FU by liver slices appeared to follow a pattern predictable from the pHi and the pK of the drug.

Animals↗
PubMed1975

[Carcinosarcoma of the larynx (author's transl)].

Case report of a 53-year-old male patient with a carcinosarcoma of the vocal cord. The diagnostic problems of these rare tumors are discussed with a review of the available literature.

Carcinoma, Squamous Cell↗
PubMed1991

[The effect of autotransfusion of photo-modified blood on the growth of Walker's carcinosarcoma].

The study deals with the influence of autotransfusion of blood treated with ultraviolet light on the growth of experimental Walker's carcinosarcoma in rats. Animals of the study group survived longer than controls. Autotransfusion of the photo-modified blood did not influence tumor growth rate. The anti-anemic action, the inhibitory effect on lipid peroxidation and retardation of immunodepression by photo-modified blood are the possible mechanisms accounting for an increase in resistance to tumor growth in rats.

Animals↗