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Biomedical subjects

P Sur

Publications and source records attributed to P Sur.

At least 37 records · Page 2Linked to original sources
PubMed1993

Interrelationship among prognostic factors in carcinoma breast.

Presentation of breast cancer at an advanced stage is a rule than exception in rural West Bengal. It was observed that 65.6% of fresh cases presented with history of breast lump with a duration of over 12 months. Of the total 32 cases, 27 (84.4%) had breast lump of more than 5 cm size and had 4 or more pathologically positive axillary nodes. In 28 cases (87.5%) largest node measured was 2 cm or more. In histology of breast specimen, 12 (37.5%) showed high degree of lymph vessel invasion while 31 (96.9%) had at least some lymphatic invasion. Blood vessel invasion of high degree was observed in 18 cases (56.2%) while 29 cases (90.6%) showed at least some blood vessel invasion.

Adult↗
PubMed1991

Modulation of methotrexate cytotoxicity with natural interferon upon human leukemia cell line HL-60.

The effect of alpha- and gamma-interferon on methotrexate cytotoxicity against human promyelocytic cell line HL-60 has been evaluated. Synergistic inhibition of proliferation is observed with the combination of methotrexate and gamma-interferon. Enhanced cytotoxic effect of methotrexate with alpha- or gamma-interferon is removed by adding thymidine to the growth medium. The depletion of folate pools caused by methotrexate is enhanced in presence of interferons, this depletion is also removed by adding thymidine to the growth media. Synchronization of HL-60 cells in 'S' phase of cell cycle caused by methotrexate is enhanced in the presence of interferons. These results suggest that specially gamma-interferon changes the cellular environment of HL-60 cells in such a way as to make methotrexate more potent cytotoxic agent to HL-60 cells causing cell death. This study also clearly indicates the biochemical role of thymidine in modulating the activity of methotrexate in combination with interferons.

Biological Transport↗
PubMed1990

Studies on the antineoplasticity of Schiff bases containing 5-nitrofuran and pyrimidine.

Antineoplastic properties of different Schiff bases obtained by the interaction of 5-nitrofuran with substituted pyrimidines have been examined both in vitro and in vivo. In vitro studies on L 5178Y/asparaginase sensitive, HL 60 and P 388 cell lines and in vivo studies on the P 388 cell line indicate that all the compounds are potential antineoplastic agents. However, 2-(5-nitro-2-furfurylidene-amino)-pyrimidine (SBP1) is the most effective, and 2-(5-nitro-2-furfurylidene-amino)-6-hydroxypyrimidine (SBP3) is the least effective agent. Doubling time, rates of protein and DNA synthesis inhibition and LD50 values-1,000 mg/kg body weight for SBP1 and 1,275 mg/kg body weight for 2-(5-nitro-2-furfurylidene-amino)-4- methylpyrimidine (SBP2)- in the oral route support the activity and use of SBP1 and SBP2 as future anticancer agents.

Animals↗
PubMed1989

Experience with danazol in the treatment of advanced breast cancer.

Danazol, a known effective agent for the treatment of benign breast disease and in endometriosis, was used in cases of advanced breast cancer with metastasis in bone, lung or in soft tissues. Out of 17 patients who received danazol, only 4 (23%) responded well. Postmenopausal patients responded better than premenopausal. Three out of the 4 responder received full course of radiotherapy and chemotherapy prior to danazol treatment. Out of the 13 non-responders, treatment could not be continued in 10 patients, either due to inability to meet up with the recurrent expenses of the cost of drugs or the patient was lost to follow-up or due to death. The rest 3 patients did not show any response at all to this drug, among them 2 were premenopausal.

Adult↗
PubMed1988

Proliferation-dependent cytotoxicity of methotrexate in murine L5178Y leukemia.

The basis for the proliferation-dependent cytotoxicity of methotrexate has been investigated in mice bearing the L5178Y ascites leukemia. Methotrexate at 60 mg/kg i.p. reduced the viability of logarithmically growing ascites cells (55% active S phase cells) to 28% of control, whereas the viability of the slowly growing cells (18% active S phase) was decreased to only 59% of control. Log phase tumor cells accumulated 8-fold higher levels of methotrexate polyglutamates compared to cells that had approached the stationary phase. However, no differences between log phase and slowly growing tumor cells were observed in the cellular levels of unmetabolized methotrexate. Intestinal mucosa and bone marrow from non-tumor-bearing mice resembled slowly growing tumor cells and had markedly lower levels of methotrexate polyglutamates than logarithmically growing cells. The greater accumulation of methotrexate polyglutamates in the logarithmically growing tumor cells was consistent with an increased synthesis of methotrexate polyglutamates in these cells. The enhanced methotrexate polyglutamylation in log phase versus slowly growing cells was not related to changes in the rates of either cellular methotrexate transport, transmembrane efflux of methotrexate, or hydrolysis of methotrexate polyglutamates. Thymidylate synthase activity measured in situ and in extracts from log phase cells was 4- and 2-fold higher, respectively, than in the more slowly growing cells. Methotrexate produced a 2.4-fold greater depletion of poly-gamma-glutamyl derivatives of 5,10-methylenetetrahydropteroylglutamate in log phase cells compared to slowly growing cells, and this was a function of both the increased methotrexate polyglutamate accumulation and thymidylate synthase activity in the rapidly proliferating cells. These results provide further evidence that the selectivity of methotrexate for tumors with a high growth fraction is a consequence of the rapid rates of both cellular methotrexate polyglutamate synthesis and oxidation of 5,10-methylenetetrahydropteroyl polyglutamates by thymidylate synthase.

Animals↗
PubMed1988

Serum amino acid levels in leukemic mice after L-asparaginase treatment.

A rapid, reproducible HPLC method based on dansyl chloride derivatization has been developed for the determination of L-asparagine, L-aspartate, L-glutamine, and L-glutamate in mouse and human serum samples. This improved procedure has been designed for automation with an autoinjector system. Studies with mice bearing the sensitive and the asparaginase-resistant L5178Y leukemia show that this analytical method can be employed to monitor the effect of L-asparaginase on serum levels of these four amino acids. The method can be used to monitor serum amino acid levels in patients undergoing therapy with L-asparaginase.

Amino Acids↗
PubMed1987

L-asparaginase-induced modulation of methotrexate polyglutamylation in murine leukemia L5178Y.

The modulation of methotrexate polyglutamylation by L-asparaginase has been examined in mice bearing sublines of leukemia L5178Y that have different sensitivities to asparaginase. A single i.p. injection of 200 IU/kg of asparaginase completely inhibited ascites tumor cell growth in the parental L5178Y/S+ tumor for 120 h compared to 72 and 30 h in the L5178Y/S and L5178Y/S+/- sublines, respectively. Similarly, DNA and protein synthesis were completely inhibited by asparaginase for 96 h in L5178Y/S+ cells, but only for 72 and 24 h in L5178Y/S and L5178Y/S+/- cells. In each tumor the temporal patterns of depletion and recovery of S-phase cells were similar to the patterns of suppression and recovery of DNA and protein synthesis observed in that tumor. When methotrexate was administered at either 96 or 24 h after asparaginase during the asparaginase-induced S-phase nadirs of L5178Y/S+ and L5178Y/S+/- cells, respectively, subsequent methotrexate polyglutamylation was inhibited 83 and 92% compared to tumor cells exposed to methotrexate only. Recovery of methotrexate polyglutamylation in both tumors following L-asparaginase pretreatment coincided in time with the return in the fraction of S-phase cells towards the pretreatment values. The inhibition of methotrexate polyglutamate accumulation by asparaginase was associated with decreased retention of methotrexate in tumor cells. In contrast, asparaginase had no significant effect on methotrexate polyglutamate accumulation and methotrexate retention when administered after methotrexate. These data indicated that the asparaginase-induced modulation of methotrexate polyglutamylation in mice was directly related to the time course of inhibition and recovery of tumor cell proliferation by asparaginase, and thus varied with the intrinsic sensitivity of the individual tumor to the enzyme.

Animals↗
PubMed1986

Effects of methotrexate on folates in Krebs ascites and L1210 murine leukemia cells.

Changes in reduced folates upon exposure of Krebs ascites cells and L1210 murine leukemia cells to methotrexate (MTX) have been measured by stoichiometric entrapment of tissue methylenetetrahydrofolate into a stable ternary complex with thymidylate synthase and tritiated 5-fluoro-2'-deoxy-uridine-5'-monophosphate. Tetrahydrofolate and 5-methyltetrahydrofolate were determined after conversion to methylenetetrahydrofolate. In both tumor cell lines, treatment with methotrexate at levels which had little effect on methylenetetrahydrofolate and tetrahydrofolate concentrations resulted in nearly complete elimination of the methyltetrahydrofolate pool. Thus, an initial effect of methotrexate on folate metabolism appears to be on methyltetrahydrofolate.

Animals↗
PubMed1986

Effects of growth rate and methotrexate on folate polyglutamates and folylpolyglutamate hydrolase activity in Krebs ascites cells.

The activity of folylpolyglutamate hydrolase was measured throughout intraperitoneal growth of Krebs ascites cells in mice and after exposure to methotrexate. Hydrolase activity was lowest during the log phase of growth. Methotrexate administered intraperitoneally during log growth caused a dose- and time-dependent increase in hydrolase activity. Modest changes were observed in endogenous folate polyglutamate chain length distributions throughout growth and upon exposure to methotrexate, but these changes could not be correlated with hydrolase activity.

Animals↗
PubMed1985

Determination of mouse liver 5-methyltetrahydrofolate concentration and polyglutamate forms.

The concentration and polyglutamate status of 5-methyltetrahydrofolate in mouse liver tissue extracts has been determined by enzymatic conversion to methylenetetrahydrofolate and subsequent entrapment of this cofactor form into a ternary complex with Lactobacillus casei thymidylate synthase and tritiated 5-fluorodeoxyuridylate. 5-Methyltetrahydrofolate was oxidized to methylenetetrahydrofolate using the reverse reaction of methylenetetrahydrofolate reductase with menadione as the ultimate electron acceptor. Reference 5-methyltetrahydrofolate could be quantitatively recovered from tissue extracts by this method. The polyglutamate status of enzymatically converted and complexed tissue 5-methyltetrahydrofolate was determined electrophoretically. Unlabeled 5-fluorodeoxyuridylate was used to remove endogenous methylenetetrahydrofolate prior to enzymatic oxidation of 5-methyltetrahydrofolate and subsequent electrophoretic analysis. In this manner, the 5-methyltetrahydrofolate polyglutamate pool alone could be labeled and visualized. There were no observable differences in the polyglutamate distribution of endogenous methylenetetrahydrofolate versus 5-methyltetrahydrofolate polyglutamates in extracts of normal mouse liver tissue.

Animals↗
PubMed1983

Response of methylenetetrahydrofolate levels to methotrexate in Krebs ascites cells.

Levels of methylenetetrahydrofolate in Krebs ascites cells subsequent to transplantation and the effects of methotrexate on these levels have been measured. To directly measure methylenetetrahydrofolate in tissue extracts, the cofactor was incorporated into a covalent ternary complex with thymidylate synthase and 3H-labelled fluorodeoxyuridine monophosphate. A 3-4-day lag preceded rapid growth of the tumour cells, and this same kinetic behaviour was observed for methylenetetrahydrofolate levels in the tumour cells. Liver and kidney tissue from the same animals also showed an increase in methylenetetrahydrofolate over the same time period. The impact of methotrexate on methylenetetrahydrofolate in the tumour cells depended upon concentration and the post-transplantation time at which treatment was initiated. Levels of methylenetetrahydrofolate in the tumour cells were most sensitive to the drug at the beginning of the rapid growth phase and were more sensitive to a given level of methotrexate in the presence of phospholipids. A slight but significant increase in methylenetetrahydrofolate occurred in some cases in response to the presence of methotrexate.

Animals↗
PubMed1983

Effect of liposomal encapsulation of cis-platinum diamminodichloride in the treatment of Ehrlich ascites carcinoma.

cis-Platinum diamminodichloride (II) encapsulated in neutral liposomes has been used to enhance the activity of the drug on Ehrlich ascites carcinoma in mice. Both in vitro and in vivo experiments have revealed that better regression in tumor growth and cure, could be achieved with a lower dose, having apparently no toxic effect, by liposomal encapsulation of the drug.

Animals↗
PubMed1981

Polyacrylamide gel electrophoresis and infrared spectroscopy of vibrio biotypes.

Polyacrylamide gel electrophoresis and infrared spectroscopy were used to study the relationship between Vibrio cholerae (classical), Vibrio cholerae (El Tor), and nonagglutinable (NAG) vibrios. Acid extracts of the different strains produced type-specific electrophoretic patterns, and the infrared spectra revealed broad absorption maxima which largely correspond to those found in other organisms. With the exception of the NAG vibrios, the infrared spectra of cholera El Tor vibrios were identical. Strain-specific differences were found in the exoprotein spectra of these organisms by the sodium dodecyl sulphate - polyacrylamide gel electrophoretic technique.

Bacterial Proteins↗