rifampin has been researched along with Adenocarcinoma* in 17 studies
17 other study(ies) available for rifampin and Adenocarcinoma
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A coordinated ruthenium-rifampicin complex reprogramming the colon carcinoma micro-environment mediated by modulation of p53/AkT/mTOR/VEGF pathway.
WHO suggests that colon cancer incidences are rising steadily, propelling researchers to search for novel chemotherapeutic options. Metal-based chemotherapy is a potential forte to explore ruthenium-based complexes, exhibiting the capability to influence a variety of cellular targets. We discovered the chemotherapeutic effects of ruthenium-rifampicin complex on HT-29 and HCT-116 human colorectal cell lines and on a chemically developed murine colorectal cancer model. Complex was synthesized and characterized by analytical techniques and evaluation of antioxidant potential along with DNA binding capabilities. The complex minimizes cellular propagation and initiates apoptotic events in the colon cancer cell lines of HT-29 and HCT-116. The results of the in vivo study suggest that the complex has been successful in minimizing the wide spectrum of aberrant crypt foci and hyperplastic lesions, as well as encouraging elevated amounts of CAT, SOD and glutathione. Along with that, p53 could be modulated by the ruthenium-rifampicin complex to interfere with apoptosis in colon carcinoma, initiated by the intrinsic apoptotic trail facilitated through Bcl2 and Bax, thus controlling the Akt/mTOR/VEGF pathway coupled through the WNT/β-catenin trail. Ruthenium-rifampicin chemotherapy could interrupt, retract or interrupt the progression of colorectal cancer through modifying intrinsic apoptosis including the antiangiogenic pathway, thereby achieving the function of a potential contender in chemotherapy in the near future. Topics: Adenocarcinoma; Animals; Antineoplastic Agents; Apoptosis; Cell Cycle; Colon; Colonic Neoplasms; Drug Combinations; Female; HCT116 Cells; HT29 Cells; Humans; Male; Mice, Inbred BALB C; Proto-Oncogene Proteins c-akt; Rats, Wistar; Rifampin; Ruthenium Compounds; Signal Transduction; TOR Serine-Threonine Kinases; Tumor Microenvironment; Tumor Suppressor Protein p53; Vascular Endothelial Growth Factor A | 2021 |
'A most malignant malady': a rare case of laryngeal tuberculosis in epidermal growth factor receptor mutant lung adenocarcinoma.
Topics: Adenocarcinoma; Adenocarcinoma of Lung; Adult; Antibiotics, Antitubercular; Drug Therapy, Combination; Dysphonia; ErbB Receptors; Ethambutol; Female; Gene Expression Regulation, Neoplastic; Humans; Isoniazid; Lung Neoplasms; Pyrazinamide; Rifampin; Treatment Outcome; Tuberculosis, Laryngeal | 2017 |
In Vitro Evaluation of Inhalable Verapamil-Rifapentine Particles for Tuberculosis Therapy.
Recent studies have demonstrated that efflux pumps of Mycobacterium tuberculosis (M. tb) provide a crucial mechanism in the development of drug resistant to antimycobacterial drugs. Drugs that inhibit these efflux pumps, such as verapamil, have shown the potential in enhancing the treatment success. We therefore hypothesized that the combined inhaled administration of verapamil and a first-line rifamycin antibiotic will further improve the treatment efficacy. An inhalable dry powder consisting of amorphous verapamil and crystalline rifapentine with l-leucine as an excipient was produced by spray drying. The in vitro aerosol characteristic of the powder, its microbiological activity and stability were assessed. When the powder was dispersed by an Osmohaler, the total fine particle fraction (FPFtotal, wt % of particles in aerosol <5 μm) of verapamil and rifapentine was 77.4 ± 1.1% and 71.5 ± 2.0%, respectively. The combination drug formulation showed a minimum inhibitory concentration (MIC90) similar to that of rifapentine alone when tested against both M. tb H37Ra and M. tb H37Rv strains. Importantly, the combination resulted in increased killing of M. tb H37Ra within the infected macrophage cells compared to either verapamil or rifapentine alone. In assessing cellular toxicity, the combination exhibited an acceptable half maximal inhibitory concentration (IC50) values (62.5 μg/mL) on both human monocytic (THP-1) and lung alveolar basal epithelial (A549) cell lines. Finally, the powder was stable after 3 months storage in 0% relative humidity at 20 ± 3 °C. Topics: Adenocarcinoma; Administration, Inhalation; Aerosols; Anti-Arrhythmia Agents; Antibiotics, Antitubercular; Cell Survival; Chemistry, Pharmaceutical; Humans; In Vitro Techniques; Lung Neoplasms; Microbial Sensitivity Tests; Monocytes; Mycobacterium tuberculosis; Particle Size; Rifampin; Tuberculosis; Verapamil | 2016 |
Fucoxanthin attenuates rifampin-induced cytochrome P450 3A4 (CYP3A4) and multiple drug resistance 1 (MDR1) gene expression through pregnane X receptor (PXR)-mediated pathways in human hepatoma HepG2 and colon adenocarcinoma LS174T cells.
Pregnane X receptor (PXR) has been reported to regulate the expression of drug-metabolizing enzymes, such as the cytochrome P450 3A (CYP3A) family and transporters, such as multiple drug resistance 1 (MDR1). Fucoxanthin, the major carotenoid in brown sea algae, is a putative chemopreventive agent. In this study, we determined whether fucoxanthin could overcome drug resistance through attenuation of rifampin-induced CYP3A4 and MDR1 gene expression by PXR-mediated pathways in HepG2 hepatoma cells. We found that fucoxanthin (1-10 μM) significantly attenuated rifampin (20 μM)-induced CYP3A4, MDR1 mRNA and CYP3A4 protein expression at 24 h of incubation. Mechanistically, fucoxanthin strongly attenuated the PXR-mediated CYP3A4 promoter activity in HepG2 cells. In addition, fucoxanthin attenuated constitutive androstane receptor (CAR)- and rPXR-mediated CYP3A4 promoter activity in this cell line. Using the mammalian two-hybrid assay, we found that fucoxanthin significantly decreased the interaction between PXR and SRC-1, a PXR co-activator. Thus, fucoxanthin can decrease rifampin-induced CYP3A4 and MDR1 expression through attenuation of PXR-mediated CYP3A4 promoter activation and interaction between PXR and co-activator. These findings could lead to potentially important new therapeutic and dietary approaches to reduce the frequency of adverse drug reactions. Topics: Adenocarcinoma; ATP Binding Cassette Transporter, Subfamily B; ATP Binding Cassette Transporter, Subfamily B, Member 1; Cell Line, Tumor; Colonic Neoplasms; Constitutive Androstane Receptor; Cytochrome P-450 CYP3A; Hep G2 Cells; Humans; Pregnane X Receptor; Promoter Regions, Genetic; Receptors, Cytoplasmic and Nuclear; Receptors, Steroid; Rifampin; RNA, Messenger; Transcriptional Activation; Xanthophylls | 2012 |
Human PXR-mediated induction of intestinal CYP3A4 attenuates 1α,25-dihydroxyvitamin D₃ function in human colon adenocarcinoma LS180 cells.
Oxidative catabolism of 1α,25-dihydroxyvitamin D(3) [1α,25(OH)(2)D(3)] is mediated by either CYP24A1 or CYP3A4. In this paper, we tested whether induction of CYP3A4 in the LS180 intestinal cell model enhances clearance of 1α,25(OH)(2)D(3) and blunts its hormonal effect on expression of the apical membrane calcium transport protein, TRPV6. Treatment with the hPXR agonist rifampin significantly increased CYP3A4 mRNA content and catalytic activity, but had no effect on CYP24A1 or TRPV6 mRNA content. Pre-treating cells with rifampin for 48h, prior to a 24h 1α,25(OH)(2)D(3) treatment phase, was associated with a subsequent 48% increase in the elimination of 1α,25(OH)(2)D(3) and a 35% reduction of peak TRPV6 mRNA. Introduction of the CYP3A4 inhibitor, 6',7'-dihydroxybergamottin, an active inhibitor in grapefruit juice, reversed the effects of rifampin on 1α,25(OH)(2)D(3) clearance and TRPV6 expression. Over-expression of hPXR in LS180 cells greatly enhanced the CYP3A4 responsiveness to rifampin pretreatment, and elicited a greater relative suppression of TRPV6 expression and an increase in 1α,25(OH)(2)D(3) disappearance rate, compared to vector expressed cells, following hormone administration. Together, these results suggest that induction of CYP3A4 in the intestinal epithelium by hPXR agonists can result in a greater metabolic clearance of 1α,25(OH)(2)D(3) and reduced effects of the hormone on the intestinal calcium absorption, which may contribute to an increased risk of drug-induced osteomalacia/osteoporosis in patients receiving chronic therapy with potent hPXR agonists. Moreover, ingestion of grapefruit juice in the at-risk patients could potentially prevent this adverse drug effect. Topics: Adenocarcinoma; Caco-2 Cells; Calcium; Cell Line, Tumor; Colonic Neoplasms; Cytochrome P-450 CYP3A; Dose-Response Relationship, Drug; Enzyme Induction; Humans; Pregnane X Receptor; Receptors, Steroid; Rifampin; Vitamin D | 2012 |
PXR-mediated induction of P-glycoprotein by anticancer drugs in a human colon adenocarcinoma-derived cell line.
The development of multidrug resistance (MDR) is one of the major limitations in the treatment of cancer. Induction of P-glycoprotein (Pgp) has been regarded as one of the main mechanisms underlying anticancer drug-induced MDR. Since the induction of Pgp is (in part) regulated by the pregnane X receptor (PXR), the ability of several widely used anticancer drugs to activate PXR-mediated Pgp induction was investigated.. A Pgp-reporter gene assay was employed to determine the ability of a panel of widely used anticancer drugs to induce Pgp. To further assess whether PXR could be involved in the induction of Pgp by anticancer drugs, Pgp protein expression after treatment with the anticancer drugs was determined in both wild-type and PXR-knocked down LS180 cells. Furthermore, the effect of the anticancer drugs on the intracellular accumulation of the Pgp-probes rhodamine 123 and doxorubicin was determined.. Our study showed that vincristine, tamoxifen, vinblastine, docetaxel, cyclophosphamide, flutamide, ifosfamide and paclitaxel activate PXR-mediated Pgp induction, and were additionally shown to affect the intracellular accumulation of the Pgp probe rhodamine 123. Moreover, PXR activation was also shown to reduce the cytotoxic activity of the Pgp substrate doxorubicin in colon cancer cells.. Our results indicate that several anticancer drugs can activate PXR-mediated induction of Pgp and affect the accumulation of Pgp substrates. Topics: Adenocarcinoma; Antibiotics, Antineoplastic; Antineoplastic Agents; Antitubercular Agents; ATP Binding Cassette Transporter, Subfamily B; ATP Binding Cassette Transporter, Subfamily B, Member 1; Blotting, Western; Cell Line, Tumor; Cell Survival; Chromatography, High Pressure Liquid; Colonic Neoplasms; Doxorubicin; Fluorescent Dyes; Humans; Plasmids; Pregnane X Receptor; Receptors, Steroid; Rhodamine 123; Rifampin; RNA Interference | 2010 |
Synthesis and cytotoxic activity of trisubstituted-1,3,5-triazines.
1,3,5-Triazine derivatives were screened for phototoxicity as well as the cytotoxic activities against leukemia and adenocarcinoma derived cell lines in comparison to the normal human keratinocytes. A simple and environmentally friendly procedure has been developed for the synthesis of 1,3,5-triazine derivatives under microwave irradiation in the presence of a HY zeolite. The catalyst can be recovered and reused. Thus, the procedure provides a simple and green synthetic methodology under environmentally friendly conditions. Structure-activity relationships between the chemical structures and antimycobacterial and photosynthesis-inhibiting activity of the evaluated compounds are also discussed. Topics: Adenocarcinoma; Antineoplastic Agents; Cell Line, Tumor; Drug Screening Assays, Antitumor; Humans; Inhibitory Concentration 50; Keratinocytes; Leukemia; Microbial Sensitivity Tests; Models, Chemical; Photosynthesis; Structure-Activity Relationship; Triazines | 2007 |
Lithocholic acid induction of the FGF19 promoter in intestinal cells is mediated by PXR.
To study the effect of the toxic secondary bile acid lithocholic acid (LCA) on the expression of fibroblast growth factor 19 (FGF19) in intestinal cells and to characterize the pregnane-X-receptor (PXR) response of the FGF19 promoter region.. The intestinal cell line LS174T was stimulated with various concentrations of chenodeoxy-cholic acid and lithocholic acid for several time points. FGF19 mRNA levels were determined with quantitative realtime RT-PCR. FGF19 deletion promoter constructs were generated and the LCA response was analzyed in reporter assays. Co-transfections with PXR and RXR were carried out to study FGF19 regulation by these factors.. LCA and CDCA strongly up-regulate FGF19 mRNA expression in LS174T cells in a time and dose dependent manner. Using reporter gene assays with several deletion constructs we found that the LCA responsive element in the human FGF19 promoter maps to the proximal regulatory region containing two potential binding sites for PXR. Overexpression of PXR and its dimerization partner retinoid X receptor (RXR) and stimulation with LCA or the potent PXR ligand rifampicin leads to a significant induction of FGF19 promoter activity in intestinal cells.. LCA induced feedback inhibition of bile acid synthesis in the liver is likely to be regulated by PXR inducing intestinal FGF19 expression. Topics: Adenocarcinoma; Base Sequence; Cell Line, Tumor; Detergents; Enzyme Inhibitors; Feedback, Physiological; Fibroblast Growth Factors; Gene Expression Regulation, Neoplastic; Humans; Intestinal Neoplasms; Lithocholic Acid; Molecular Sequence Data; Pregnane X Receptor; Promoter Regions, Genetic; Receptors, Steroid; Rifampin; RNA, Messenger; Signal Transduction; Up-Regulation | 2007 |
Effects of rifampicin on global gene expression in human small intestine.
The small intestinal wall serves as an important barrier for the entry of foreign substances into the organism. Of particular importance are enzymes and transporters that can inactivate or prevent the uptake of many xenobiotics including drugs. Some of the genes encoding these proteins are transcriptionally activated by xenobiotics, a response well studied in liver but less so in the intestine. The effect of the inducer drug rifampicin on intestinal cells was therefore evaluated both in vivo and in vitro.. Seven healthy volunteers were treated with rifampicin for 9 days and the global gene expression profile was analysed in RNA from duodenal biopsies taken before and after drug treatment. The gene expression profile was also assessed in LS174T cells derived from a human colon adenocarcinoma after exposure to 10 micromol/l rifampicin for 24 h.. We identified 32 genes that were upregulated and two genes that were downregulated by rifampicin treatment in vivo. The list of rifampicin regulated transcripts expectedly included drug metabolizing enzymes and drug transporters, but also genes involved in lipid and amino acid metabolism as well as genes not previously recognized to be part of the adaptation of intestinal cells to xenobiotic exposure. Only a limited number of these rifampicin-regulated transcripts were however also regulated by rifampicin in LS174T cells.. The similarities and differences of changes in gene expression after rifampicin treatment between duodenal biopsies and cell culture provide a new assessment of the extent and diversity of systems affected by drug exposure. Topics: Adenocarcinoma; Antibiotics, Antitubercular; Biomarkers; Colonic Neoplasms; Duodenum; Gene Expression Profiling; Gene Expression Regulation; Humans; Oligonucleotide Array Sequence Analysis; Rifampin; RNA, Messenger; Transcription, Genetic; Tumor Cells, Cultured | 2007 |
[Bilateral breast bacterial cellulite secondary to Streptococcus agalactiae septicemia].
We report a case of group B streptococcal septicemia of digestive origin with secondary bilateral breast dermal-hypodermal localization.. A 71 year-old woman with a past history of bilateral breast cancer treated by conservation therapy was hospitalized because of the sudden occurrence of two clearly delimited, inflammatory, dermal-hypodermal cutaneous plaques located on each breast, associated with fever (39 degrees C), 4 days after a colonoscopy. Further investigations eliminated carcinomatous mastitis and blood cultures were positive for group B beta-hemolytic streptococcus (Streptococcus agalactiae). Histological examination of a sigmoid polyp revealed a tubular adenocarcinoma.. We report the first documented case of secondary dermal-hypodermal bacterial skin infection (cellulitis) due to group B beta-hemolytic streptococcus. The occurrence after colonoscopy examination, chronology of clinical features, bilaterality and positive blood cultures are arguments in favor of the secondary nature of the skin infection process. Topics: Adenocarcinoma; Aged; Amoxicillin; Anti-Bacterial Agents; Anti-Infective Agents; Breast Diseases; Cellulitis; Clavulanic Acid; Colonic Polyps; Colonoscopy; Drug Therapy, Combination; Female; Humans; Metronidazole; Rifampin; Sepsis; Sigmoid Neoplasms; Streptococcal Infections; Streptococcus agalactiae; Time Factors; Treatment Outcome | 2006 |
Functional induction and de-induction of P-glycoprotein by St. John's wort and its ingredients in a human colon adenocarcinoma cell line.
Continuous use of St. John's wort decreases the bioavailabilities of a variety of drugs. This interaction is attributed to the induction of cytochrome P450 3A4 and/or P-glycoprotein. In this study, we aimed to examine the chronic effects of St. John's wort and its constituents, hyperforin and hypericin, on the expression and function of P-glycoprotein in an intestinal cell line, LS 180. We also examined the acute inhibitory effect of St. John's wort on P-glycoprotein by using LLC-GA5-COL150 cells, which overexpress P-glycoprotein. St. John's wort and hyperforin but not hypericin increased the expression of P-glycoprotein in LS 180 cells. Removal of St. John's wort resulted in a restoration of P-glycoprotein level within 48 h. The content of hyperforin in St. John's wort extract was high enough to induce P-glycoprotein, suggesting that the induction of P-glycoprotein by St. John's wort can be almost attributable to hyperforin. The LS 180 cells chronically exposed to St. John's wort or hyperforin exhibited the increase in the function of P-glycoprotein assessed by the efflux of digoxin, and the activities correlated well with P-glycoprotein level. On the other hand, St. John's wort and its two constituents did not show any acute effect on P-glycoprotein-mediated transport of digoxin. St. John's wort induced P-glycoprotein in vitro that functions as a drug efflux pump. Hyperforin is considered to be a primary cause of the inductive effect of St. John's wort. Long-term administration of St. John's wort may cause clinically significant decrease in the plasma concentrations of P-glycoprotein substrates. Topics: Adenocarcinoma; Animals; Anthracenes; ATP Binding Cassette Transporter, Subfamily B, Member 1; Biological Transport; Bridged Bicyclo Compounds; Cell Line, Tumor; Colonic Neoplasms; Digoxin; Humans; Hypericum; LLC-PK1 Cells; Perylene; Phloroglucinol; Plant Extracts; Rifampin; Swine; Terpenes; Transfection | 2005 |
Rifampin reduces the analgesic effect of transdermal fentanyl.
Topics: Adenocarcinoma; Administration, Cutaneous; Aged; Analgesics, Opioid; Antibiotics, Antitubercular; Drug Interactions; Fentanyl; Humans; Lung Neoplasms; Male; Pain; Parotid Neoplasms; Rifampin; Tuberculosis, Pulmonary | 2005 |
Induction and regulation of xenobiotic-metabolizing cytochrome P450s in the human A549 lung adenocarcinoma cell line.
Several cytochrome P450 (CYP) enzymes are expressed in the human lung, where they participate in metabolic inactivation and activation of numerous exogenous and endogenous compounds. In this study, the expression pattern of all known xenobiotic-metabolizing CYP genes was characterized in the human alveolar type II cell-derived A549 adenocarcinoma cell line using qualitative reverse transcriptase/polymerase chain reaction (RT-PCR). In addition, the mechanisms of induction by chemicals of members in the CYP1 and CYP3A subfamilies were assessed by quantitative RT-PCR. The expression of messenger RNAs (mRNAs) of CYPs 1A1, 1B1, 2B6, 2C, 2E1, 3A5, and 3A7 was detected in the A549 cells. The amounts of mRNAs of CYPs 1A2, 2A6, 2A7, 2A13, 2F1, 3A4, and 4B1 were below the limit of detection. 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced CYP1A1 and CYP1B1 mRNAs 56-fold and 2.5-fold, respectively. CYP3A5 was induced 8-fold by dexamethasone and 11-fold by phenobarbital. CYP3A4 was not induced by any of the typical CYP3A4 inducers used. The tyrosine kinase inhibitor genistein and the protein kinase C inhibitor staurosporine blocked TCDD-elicited induction of CYP1A1, but they did not affect CYP1B1 induction. Protein phosphatase inhibitors okadaic acid and calyculin A enhanced TCDD-induction of CYP1B1 slightly, but had negligible effects on CYP1A1 induction. These results suggest that CYP1A1 and CYP1B1 are differentially regulated in human pulmonary epithelial cells and give the first indication of the induction of CYP3A5 by glucocorticoids in human lung cells. These results establish that having retained several characteristics of human lung epithelial cell CYP expression, the A549 lung cell line is a valuable model for mechanistic studies on induction of the pulmonary CYP system. Topics: Adenocarcinoma; Anti-Inflammatory Agents; Aryl Hydrocarbon Hydroxylases; Cytochrome P-450 CYP1A1; Cytochrome P-450 CYP1B1; Cytochrome P-450 CYP3A; Cytochrome P-450 Enzyme System; Dexamethasone; Enzyme Inhibitors; Epithelial Cells; Excitatory Amino Acid Antagonists; Gene Expression Regulation, Enzymologic; Gene Expression Regulation, Neoplastic; Humans; Lung Neoplasms; Phenobarbital; Pulmonary Alveoli; Rifampin; RNA, Messenger; Tumor Cells, Cultured; Xenobiotics | 2000 |
Pulmonary nodule mimicking lung cancer in a human immunodeficiency virus type-1 infected patient.
We reported a human immunodeficiency virus type 1-infected patient with a small solitary pulmonary nodule mimicking adenocarcinoma, who was treated successfully with antituberculosis therapy. We believe that high-resolution CT scans of thorax are important examinations to detect pulmonary inflammatory findings, such as ectasis of the bronchi leading to the nodules and calcifications in the nodules, and also as follow-up tests for evaluating effectiveness of treatment on pulmonary inflammatory nodules in human immunodeficiency virus type 1-infected patients. Topics: Acquired Immunodeficiency Syndrome; Adenocarcinoma; Adult; Antitubercular Agents; Diagnosis, Differential; Drug Therapy, Combination; Ethambutol; HIV-1; Humans; Isoniazid; Lung Neoplasms; Male; Pyrazinamide; Rifampin; Solitary Pulmonary Nodule; Tomography, X-Ray Computed | 1999 |
Modulators and substrates of P-glycoprotein and cytochrome P4503A coordinately up-regulate these proteins in human colon carcinoma cells.
Xenobiotics frequently induce proteins involved in their detoxification. Because many drugs that are metabolized by human cytochromes P450 (CYP) 3A4 and 3A5 are also transported by the drug efflux pump P-glycoprotein, we determined whether expression of these proteins was altered by a variety of drugs in a cell line derived from a human colon adenocarcinoma, LS180/WT, and its adriamycin-resistant subline, LS180/AD50. P-glycoprotein and CYP3A4 were constitutively expressed in both LS180/AD50 and LS180/WT cells, and both proteins were up-regulated after treatment with many drugs, including rifampicin, phenobarbital, clotrimazole, reserpine, and isosafrole. However, there were some exceptions because P-glycoprotein was up-regulated by midazolam and nifedipine, whereas CYP3A4 was not. CYP3A5, which is also constitutively expressed in these cells, remained unchanged with most drug treatments but was up-regulated by reserpine and clotrimazole. The apparent coordinated coexpression of the CYP3A gene family and P-glycoprotein in the LS180 cells suggests that for common orally administered drugs, P-glycoprotein may play an important role in net drug absorption and drug/drug interactions of shared CYP3A4/P-glycoprotein substrates. Topics: Adenocarcinoma; ATP Binding Cassette Transporter, Subfamily B, Member 1; Base Sequence; Blotting, Northern; Cell Line; Clotrimazole; Colonic Neoplasms; Cytochrome P-450 CYP2E1; Cytochrome P-450 Enzyme System; Dexamethasone; DNA Primers; Doxorubicin; Gene Expression Regulation, Neoplastic; Humans; Midazolam; Mixed Function Oxygenases; Molecular Sequence Data; Multigene Family; Phenobarbital; Phenytoin; Polymerase Chain Reaction; Rifampin; Tumor Cells, Cultured; Verapamil | 1996 |
Cytocidal effect of rifamycin derivatives on ascites tumor cells: studies with [125I]iododeoxyuridine.
The cytotoxicity of 2 rifamycin derivatives, rifazone-82 and rifampicin, on mouse ascites cells was studied, using the [125I]iododeoxyuridine (IUDR) method of labeling the tumor cells. This technique allows a distinction to be made between a cytocidal and cytostatic effect. The 2 drugs exerted a cytocidal effect against 2 non-leukemic cell lines, but had no effect against 3 leukemic lines. Topics: Adenocarcinoma; Animals; Carcinoma, Ehrlich Tumor; Cell Line; Cell Survival; Female; Idoxuridine; Iodine Radioisotopes; Leukemia, Experimental; Mice; Neoplasm Transplantation; Neoplasms, Experimental; Rifampin; Rifamycins; Transplantation, Homologous | 1979 |
Inhibition of adenocarcinoma TA3 ascites tumor growth by rifamycin derivatives.
A growth inhibitory effect on adenocarcinoma TA3 ascites tumors in LAF1/J mice resulted from the repeated IP administration of subtoxic doses of 3 rifamycin derivatives: rifampicin (Rif)1, dimethylbenzyldesmethylrifampicin (DMB), and rifazone-82 (R-82). A high-viscosity methylcellulose vehicle was found to be essential for obtaining a uniform drug suspension and a significant antitumor effect by the least water soluble derivatives, DMB and R-82. The more hydrophilic derivative, Rif, was found to have a comparable growth inhibitory effect on TA3 cells when prepared in 0.9% NaCl solution with or without added methylcellulose. Oral or SC drug injections did not have an antitumor effect. The results of this study point to the importance of vehicle and route of administration in chemotherapy trials with these compounds. Topics: Adenocarcinoma; Administration, Oral; Animals; Cell Line; Injections, Intraperitoneal; Injections, Subcutaneous; Methylcellulose; Mice; Neoplasms, Experimental; Pharmaceutical Vehicles; Rifampin; Rifamycins | 1978 |