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Relevant bibliographies by topics / Cancer; Drug metabolising enzymes; DMEs

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Academic literature on the topic 'Cancer; Drug metabolising enzymes; DMEs'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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Journal articles on the topic "Cancer; Drug metabolising enzymes; DMEs"

1

Feng, Siqi, Anqi Li, Yi-Chao Zheng, and Hong-Min Liu. "Role of Drug-metabolizing Enzymes in Cancer and Cancer Therapy." Current Drug Metabolism 21, no. 1 (May 14, 2020): 67–76. http://dx.doi.org/10.2174/1389200221666200103111053.

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Background: Cancer is one of the most serious diseases threatening human health with high morbidity and mortality in the world. For the treatment of cancer, chemotherapy is one of the most widely used strategies, for almost all kinds of tumors and diverse stages of tumor development. The efficacy of chemotherapy not only depends on the activity of the drug administrated but also on whether the compound could reach the effective therapeutic concentration in tumor cells. Therefore, expression and activity of drug-metabolizing enzymes (DMEs) in tumor tissues and metabolic organs of cancer patients are important for the dispositional behavior of anticancer drugs as well as the clinical response of chemotherapy. Methods: This review summarizes the recent advancement of the DMEs expression and activity in various cancers, as well as the potential regulatory mechanisms of major DMEs in cancer and cancer therapy. Results: Compared to normal tissues, expression and activity of major DMEs are significantly dysregulated in patients by various factors including epigenetic modification, ligand-activated transcriptional regulation and signaling pathways. Additionally, DMEs play an important role in anticancer drug efficacy, chemoresistance as well as the activation of prodrugs. Conclusion: This review reinforces a more comprehensive understanding of DMEs in cancer and cancer therapy, and provides more opportunities for cancer therapy.

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Dmitriev, Alexander V., Alexey A. Lagunin, Dmitry А. Karasev, Anastasia V. Rudik, Pavel V. Pogodin, Dmitry A. Filimonov, and Vladimir V. Poroikov. "Prediction of Drug-Drug Interactions Related to Inhibition or Induction of Drug-Metabolizing Enzymes." Current Topics in Medicinal Chemistry 19, no. 5 (April 18, 2019): 319–36. http://dx.doi.org/10.2174/1568026619666190123160406.

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Drug-drug interaction (DDI) is the phenomenon of alteration of the pharmacological activity of a drug(s) when another drug(s) is co-administered in cases of so-called polypharmacy. There are three types of DDIs: pharmacokinetic (PK), pharmacodynamic, and pharmaceutical. PK is the most frequent type of DDI, which often appears as a result of the inhibition or induction of drug-metabolising enzymes (DME). In this review, we summarise in silico methods that may be applied for the prediction of the inhibition or induction of DMEs and describe appropriate computational methods for DDI prediction, showing the current situation and perspectives of these approaches in medicinal and pharmaceutical chemistry. We review sources of information on DDI, which can be used in pharmaceutical investigations and medicinal practice and/or for the creation of computational models. The problem of the inaccuracy and redundancy of these data are discussed. We provide information on the state-of-the-art physiologically- based pharmacokinetic modelling (PBPK) approaches and DME-based in silico methods. In the section on ligand-based methods, we describe pharmacophore models, molecular field analysis, quantitative structure-activity relationships (QSAR), and similarity analysis applied to the prediction of DDI related to the inhibition or induction of DME. In conclusion, we discuss the problems of DDI severity assessment, mention factors that influence severity, and highlight the issues, perspectives and practical using of in silico methods.

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Camici, Garcia-Gil, Pesi, Allegrini, and Tozzi. "Purine-Metabolising Enzymes and Apoptosis in Cancer." Cancers 11, no. 9 (September 12, 2019): 1354. http://dx.doi.org/10.3390/cancers11091354.

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The enzymes of both de novo and salvage pathways for purine nucleotide synthesis are regulated to meet the demand of nucleic acid precursors during proliferation. Among them, the salvage pathway enzymes seem to play the key role in replenishing the purine pool in dividing and tumour cells that require a greater amount of nucleotides. An imbalance in the purine pools is fundamental not only for preventing cell proliferation, but also, in many cases, to promote apoptosis. It is known that tumour cells harbour several mutations that might lead to defective apoptosis-inducing pathways, and this is probably at the basis of the initial expansion of the population of neoplastic cells. Therefore, knowledge of the molecular mechanisms that lead to apoptosis of tumoural cells is key to predicting the possible success of a drug treatment and planning more effective and focused therapies. In this review, we describe how the modulation of enzymes involved in purine metabolism in tumour cells may affect the apoptotic programme. The enzymes discussed are: ectosolic and cytosolic 5′-nucleotidases, purine nucleoside phosphorylase, adenosine deaminase, hypoxanthine-guanine phosphoribosyltransferase, and inosine-5′-monophosphate dehydrogenase, as well as recently described enzymes particularly expressed in tumour cells, such as deoxynucleoside triphosphate triphosphohydrolase and 7,8-dihydro-8-oxoguanine triphosphatase.

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Li, Xiaoyan, Yiyan Lu, Xiaojun Ou, Sijing Zeng, Ying Wang, Xiaoxiao Qi, Lijun Zhu, and Zhongqiu Liu. "Changes and sex- and age-related differences in the expression of drug metabolizing enzymes in a KRAS-mutant mouse model of lung cancer." PeerJ 8 (November 18, 2020): e10182. http://dx.doi.org/10.7717/peerj.10182.

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Background This study aimed to systematically profile the alterations and sex- and age-related differences in the drug metabolizing enzymes (DMEs) in a KRAS-mutant mouse model of lung cancer (KRAS mice). Methodology In this study, the LC-MS/MS approach and a probe substrate method were used to detect the alterations in 21 isoforms of DMEs, as well as the enzymatic activities of five isoforms, respectively. Western blotting was applied to study the protein expression of four related receptors. Results The proteins contents of CYP2C29 and CYP3A11, were significantly downregulated in the livers of male KRAS mice at 26 weeks (3.7- and 4.4-fold, respectively, p < 0.05). SULT1A1 and SULT1D1 were upregulated by 1.8- to 7.0- fold at 20 (p = 0.015 and 0.017, respectively) and 26 weeks (p = 0.055 and 0.031, respectively). There were positive correlations between protein expression and enzyme activity for CYP2E1, UGT1A9, SULT1A1 and SULT1D1 (r2 ≥ 0.5, p < 0.001). Western blotting analysis revealed the downregulation of AHR, FXR and PPARα protein expression in male KRAS mice at 26 weeks. For sex-related differences, CYP2E1 was male-predominant and UGT1A2 was female-predominant in the kidney. UGT1A1 and UGT1A5 expression was female-predominant, whereas UGT2B1 exhibited male-predominant expression in liver tissue. For the tissue distribution of DMEs, 21 subtypes of DMEs were all expressed in liver tissue. In the intestine, the expression levels of CYP2C29, CYP27A1, UGT1A2, 1A5, 1A6a, 1A9, 2B1, 2B5 and 2B36 were under the limitation of quantification. The subtypes of CYP7A1, 1B1, 2E1 and UGT1A1, 2A3, 2B34 were detected in kidney tissue. Conclusions This study, for the first time, unveils the variations and sex- and age-related differences in DMEs in C57 BL/6 (WT) mice and KRAS mice.

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Bosch, Tessa, Irma Meijerman, Jos Beijnen, and Jan Schellens. "Genetic Polymorphisms of Drug Metabolising Enzymes and Drug Transporters in Relation to Cancer Risk." Current Cancer Therapy Reviews 2, no. 2 (May 1, 2006): 137–55. http://dx.doi.org/10.2174/157339406776872825.

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6

Bosch, Tessa M., Irma Meijerman, Jos H. Beijnen, and Jan H. M. Schellens. "Genetic Polymorphisms of Drug-Metabolising Enzymes and Drug Transporters in the Chemotherapeutic Treatment of Cancer." Clinical Pharmacokinetics 45, no. 3 (2006): 253–85. http://dx.doi.org/10.2165/00003088-200645030-00003.

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7

Gorbachenko, E., O. Goreva, A. Grishanova, and E. Vigovskaya. "AOSP21 GENETIC POLYMORPHISMS OF DRUG-METABOLISING ENZYMES AND CHEMOTHERAPY RESISTANCE IN PATIENTS WITH LYMPHOPROLIFERATIVE DISEASES." European Journal of Cancer 49 (March 2013): S13. http://dx.doi.org/10.1016/s0959-8049(13)70032-7.

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8

Ekhart, Corine, Sjoerd Rodenhuis, Paul H. M. Smits, Jos H. Beijnen, and Alwin D. R. Huitema. "An overview of the relations between polymorphisms in drug metabolising enzymes and drug transporters and survival after cancer drug treatment." Cancer Treatment Reviews 35, no. 1 (February 2009): 18–31. http://dx.doi.org/10.1016/j.ctrv.2008.07.003.

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9

Kragelund, C., C. Hansen, J. Reibel, B. Nauntofte, K. Brosen, S. B. Jensen, and L. A. Torpet. "Can the genotype or phenotype of two polymorphic drug metabolising cytochrome P450-enzymes identify oral lichenoid drug eruptions?" Journal of Oral Pathology & Medicine 39, no. 6 (April 14, 2010): 497–505. http://dx.doi.org/10.1111/j.1600-0714.2010.00897.x.

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Weiss, Johanna, and Walter Emil Haefeli. "Interaction potential of the endothelin-A receptor antagonist atrasentan with drug transporters and drug-metabolising enzymes assessed in vitro." Cancer Chemotherapy and Pharmacology 68, no. 4 (July 31, 2011): 1093–98. http://dx.doi.org/10.1007/s00280-011-1715-8.

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Dissertations / Theses on the topic "Cancer; Drug metabolising enzymes; DMEs"

1

Delgoda, Rupika. "A study of arylamine N-acetyltransferase from Salmonella typhimurium." Thesis, University of Oxford, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302221.

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Fraser, Emily Anne. "Investigating the role of CAR and PXR in the regulation of cytochrome P450s and other drug metabolising enzymes by anti-cancer drugs using novel humanised mouse models." Thesis, University of Dundee, 2013. https://discovery.dundee.ac.uk/en/studentTheses/53400dff-cf5e-49a6-99ca-9bd95b2326bd.

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Nuclear receptor activation, particularly that of the pregnane X receptor (PXR) and constitutive androstane receptor (CAR), is increasingly recognised as a key determinant in the development of drug-drug interactions (DDIs) as a result of their key role in the transcriptional regulation of numerous drug metabolizing enzymes and drug transporters. PXR and CAR involvement in the regulation of the cytochrome P450 enzymes is of greatest concern, since these enzymes metabolise the majority of currently available therapeutics. Various methods are available to investigate the activation of these receptors in response to drug challenge, including reporter gene assays, primary human hepatocytes and transgenic mouse models. However, these models lack the sophistication to effectively assess receptor cross-talk, a key regulatory mechanism in the control of drug metabolism with the potential to impact the development of DDIs. Using a novel panel of PXR & CAR transgenic mouse models this study was designed to investigate the role of cross-talk between PXR and CAR in the metabolism and pharmacokinetics of commonly available pharmaceuticals, with particular emphasis on species-specific regulation. This study has identified potential interactions with PXR and CAR following treatment of wild-type mice with cyclophosphamide, gefitinib, anastrozole and letrozole. Data from the PXR/CAR transgenic mouse panel has also provided evidence that the aromatase inhibitors, anastrozole and letrozole, interact with PXR and CAR in a species- and gender-specific manner. Cross-talk between these receptors plays a key role in the regulation of P450 expression and drug pharmacokinetics following treatment by these agents, although the elimination of these drugs appears to be primarily renal, in contrast to data derived from humans. Of particular note is the aromatase inhibitor-induced up-regulation of Cyp2b10 expression and activity observed in all models possessing a functional CAR moiety. A corresponding induction in CYP2B6 transcriptional activation has been confirmed in a novel reporter mouse model, indicating a potential DDI risk if coadministered with a drug requiring CYP2B6 for its metabolism, i.e.cyclophosphamide. These data therefore support the use of these models as a tool to dissect the regulatory cross-talk of these receptors in the control of drug metabolism, and thus to improve the assessment of DDI risk in the development of therapeutics.

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Alandas, Mohammed N. "An investigation into the metabolic activation of novel chloromethylindolines by isoforms of cytochrome P450. Targeting drug metabolising enzymes in cancer: analysis of the role and function of selected cytochrome P450 oxidising novel cancer prodrugs." Thesis, University of Bradford, 2012. http://hdl.handle.net/10454/6289.

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Introduction Cytochromes P450 (CYPs) are the major family of enzymes responsible for detoxification and metabolism of a wide range of both endogenous and xenobiotics chemicals in living organisms. The use of CYPs to activate prodrugs to cytotoxins selectively in tumours has been explored including AQ4N, Phortress and Aminoflavone. CYP1A1, CYP1B1, CYP2W1, and CYP4F11 have been identified as expressed in tumour tissue and surrounding stroma at high frequency compared to most normal tissues. Aim is to investigate the differential metabolism of novel chloromethylindoline by high frequency expressed CYPs in tumours. This differential may be exploited to elicit a selective chemotherapeutic effect by metabolising inert small molecules to potent cytotoxins within the tumour environment. Materials and Methods Sensitive and specific LC/MS/MS techniques have been developed to investigate the metabolism of chloromethylindolines. Recombinant enzymes and transfected cell lines were used to investigate the metabolic profiles with a focus on production of the cytotoxic derivatives of chloromethylindolines. Results Detailed metabolic studies show that (1-(Chloromethyl)-1,2-dihydropyrrolo [3,2-e]indol-3(6H)-yl)(5-methoxy-1H-indol-2-yl) methanone (ICT2700) and other chloromethylindolines are converted by CYP1A1 mediated hydroxylation at the C-5 position leading to highly potent metabolites. In vitro cytotoxicity studies showed differentials of up to 1000-fold was achieved between CYP1A1 activated compared to the non-metabolised parent molecules. The reactivity of metabolites of ICT2700 was also explored using glutathione as a nucleophile. The metabolites were identified by a combination of LC/MS and LC MS/MS techniques. Investigations using mouse and human liver microsomes show that a large number of metabolites are created though none were shown to be associated with a potential anticancer effect. Studies focused on CYP2W1 show that this isoform metabolised ICT2706 to a cytotoxic species and a pharmacokinetic study showed a good distribution of ICT2706 into mouse tissues including tumour. However metabolism of ICT2726 by CYP2W1 resulted only in a non-toxic metabolite profile and may have potential as a biomarker for functional CYP2W1 in tissues. Preliminary studies show that palmitic acid hydroxylation is a useful marker of functional CYP4F11. Summary and conclusion The in vitro results show that the chloromethylindolines are a novel class of agent with potential as prodrugs that following specific hydroxylation by CYP1A1 and CYP2W1 are converted to ultra-potent cytotoxins. Other metabolites are also evident which are not cytotoxic. Studies in vivo show that selected chloromethylindolines possess a good pharmacokinetic profile and show potential as prodrug anticancer agents that require activation by CYP1A1 or CYP2W1. The methods, results, progress and suggestions for future work are presented in this thesis.

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4

Alandas, Mohammed Nasser. "An investigation into the metabolic activation of novel chloromethylindolines by isoforms of cytochrome P450 : targeting drug metabolising enzymes in cancer : analysis of the role and function of selected cytochrome P450 oxidising novel cancer prodrugs." Thesis, University of Bradford, 2012. http://hdl.handle.net/10454/6289.

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Abstract:

Introduction: Cytochromes P450 (CYPs) are the major family of enzymes responsible for detoxification and metabolism of a wide range of both endogenous and xenobiotics chemicals in living organisms. The use of CYPs to activate prodrugs to cytotoxins selectively in tumours has been explored including AQ4N, Phortress and Aminoflavone. CYP1A1, CYP1B1, CYP2W1, and CYP4F11 have been identified as expressed in tumour tissue and surrounding stroma at high frequency compared to most normal tissues. Aim is to investigate the differential metabolism of novel chloromethylindoline by high frequency expressed CYPs in tumours. This differential may be exploited to elicit a selective chemotherapeutic effect by metabolising inert small molecules to potent cytotoxins within the tumour environment. Materials and Methods: Sensitive and specific LC/MS/MS techniques have been developed to investigate the metabolism of chloromethylindolines. Recombinant enzymes and transfected cell lines were used to investigate the metabolic profiles with a focus on production of the cytotoxic derivatives of chloromethylindolines. Results: Detailed metabolic studies show that (1-(Chloromethyl)-1,2-dihydropyrrolo [3,2-e]indol-3(6H)-yl)(5-methoxy-1H-indol-2-yl) methanone (ICT2700) and other chloromethylindolines are converted by CYP1A1 mediated hydroxylation at the C-5 position leading to highly potent metabolites. In vitro cytotoxicity studies showed differentials of up to 1000-fold was achieved between CYP1A1 activated compared to the non-metabolised parent molecules. The reactivity of metabolites of ICT2700 was also explored using glutathione as a nucleophile. The metabolites were identified by a combination of LC/MS and LC MS/MS techniques. Investigations using mouse and human liver microsomes show that a large number of metabolites are created though none were shown to be associated with a potential anticancer effect. Studies focused on CYP2W1 show that this isoform metabolised ICT2706 to a cytotoxic species and a pharmacokinetic study showed a good distribution of ICT2706 into mouse tissues including tumour. However metabolism of ICT2726 by CYP2W1 resulted only in a non-toxic metabolite profile and may have potential as a biomarker for functional CYP2W1 in tissues. Preliminary studies show that palmitic acid hydroxylation is a useful marker of functional CYP4F11. Summary and conclusion: The in vitro results show that the chloromethylindolines are a novel class of agent with potential as prodrugs that following specific hydroxylation by CYP1A1 and CYP2W1 are converted to ultra-potent cytotoxins. Other metabolites are also evident which are not cytotoxic. Studies in vivo show that selected chloromethylindolines possess a good pharmacokinetic profile and show potential as prodrug anticancer agents that require activation by CYP1A1 or CYP2W1. The methods, results, progress and suggestions for future work are presented in this thesis.

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