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

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Published: 4 June 2021
Last updated: 8 February 2022

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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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2

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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3

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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4

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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5

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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10

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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11

Balram, C., E. H. Tan, Q. Zhou, Y. B. Cheung, C. Kibat, and S. S. Leong. "Pharmacogenetics of ABC transporters and drug metabolising enzymes and their influence on Irinotecan (CPT-11) elimination pathways in Asian cancer patients." Journal of Clinical Oncology 22, no. 14_suppl (July 15, 2004): 2063. http://dx.doi.org/10.1200/jco.2004.22.14_suppl.2063.

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12

Balram, C., E. H. Tan, Q. Zhou, Y. B. Cheung, C. Kibat, and S. S. Leong. "Pharmacogenetics of ABC transporters and drug metabolising enzymes and their influence on Irinotecan (CPT-11) elimination pathways in Asian cancer patients." Journal of Clinical Oncology 22, no. 14_suppl (July 15, 2004): 2063. http://dx.doi.org/10.1200/jco.2004.22.90140.2063.

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13

Sneha, Smarakan, Simon C. Baker, Andrew Green, Sarah Storr, Radhika Aiyappa, Stewart Martin, and Klaus Pors. "Intratumoural Cytochrome P450 Expression in Breast Cancer: Impact on Standard of Care Treatment and New Efforts to Develop Tumour-Selective Therapies." Biomedicines 9, no. 3 (March 12, 2021): 290. http://dx.doi.org/10.3390/biomedicines9030290.

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Despite significant advances in treatment strategies over the past decade, selective treatment of breast cancer with limited side-effects still remains a great challenge. The cytochrome P450 (CYP) family of enzymes contribute to cancer cell proliferation, cell signaling and drug metabolism with implications for treatment outcomes. A clearer understanding of CYP expression is important in the pathogenesis of breast cancer as several isoforms play critical roles in metabolising steroid hormones and xenobiotics that contribute to the genesis of breast cancer. The purpose of this review is to provide an update on how the presence of CYPs impacts on standard of care (SoC) drugs used to treat breast cancer as well as discuss opportunities to exploit CYP expression for therapeutic intervention. Finally, we provide our thoughts on future work in CYP research with the aim of supporting ongoing efforts to develop drugs with improved therapeutic index for patient benefit.
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14

Stein, Katrin, Anke Borowicki, Daniel Scharlau, and Michael Glei. "Fermented wheat aleurone induces enzymes involved in detoxification of carcinogens and in antioxidative defence in human colon cells." British Journal of Nutrition 104, no. 8 (June 28, 2010): 1101–11. http://dx.doi.org/10.1017/s0007114510001881.

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Dietary fibre is fermented by the human gut flora resulting mainly in the formation of SCFA, for example, acetate, propionate and butyrate. SCFA, in particular butyrate, may be important for secondary cancer prevention by inducing apoptosis and inhibiting cell growth of cancer cells, thereby inhibiting the promotion and/or progression of cancer. Furthermore, SCFA could also act on primary cancer prevention by activation of detoxifying and antioxidative enzymes. We investigated the effects of fermented wheat aleurone on the expression of genes involved in stress response and toxicity, activity of drug-metabolising enzymes and anti-genotoxic potential. Aleurone was digested and fermented in vitro to obtain samples that reflect the content of the colon. HT29 cells and colon epithelial stripes were incubated with the resulting fermentation supernatant fractions (fs) and effects on mRNA expression of CAT, GSTP1 and SULT2B1 and enzyme activity of glutathione S-transferase (GST) and catalase (CAT) were measured. Fermented aleurone was also used to study the protection against H2O2-induced DNA damage in HT29 cells. The fs of aleurone significantly induced the mRNA expression of CAT, GSTP1 and SULT2B1 (HT29) and GSTP1 (epithelial stripes), respectively. The enzyme activities of GST (HT29) and CAT (HT29, epithelial stripes) were also unambiguously increased (1·4- to 3·7-fold) by the fs of aleurone. DNA damage induced by H2O2 was significantly reduced by the fs of aleurone after 48 h, whereupon no difference was observed compared with the faeces control. In conclusion, fermented aleurone is able to act on primary prevention by inducing mRNA expression and the activity of enzymes involved in detoxification of carcinogens and antioxidative defence.
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15

Robertson, Holly, Albena T. Dinkova-Kostova, and John D. Hayes. "NRF2 and the Ambiguous Consequences of Its Activation during Initiation and the Subsequent Stages of Tumourigenesis." Cancers 12, no. 12 (December 2, 2020): 3609. http://dx.doi.org/10.3390/cancers12123609.

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NF-E2 p45-related factor 2 (NRF2, encoded in the human by NFE2L2) mediates short-term adaptation to thiol-reactive stressors. In normal cells, activation of NRF2 by a thiol-reactive stressor helps prevent, for a limited period of time, the initiation of cancer by chemical carcinogens through induction of genes encoding drug-metabolising enzymes. However, in many tumour types, NRF2 is permanently upregulated. In such cases, its overexpressed target genes support the promotion and progression of cancer by suppressing oxidative stress, because they constitutively increase the capacity to scavenge reactive oxygen species (ROS), and they support cell proliferation by increasing ribonucleotide synthesis, serine biosynthesis and autophagy. Herein, we describe cancer chemoprevention and the discovery of the essential role played by NRF2 in orchestrating protection against chemical carcinogenesis. We similarly describe the discoveries of somatic mutations in NFE2L2 and the gene encoding the principal NRF2 repressor, Kelch-like ECH-associated protein 1 (KEAP1) along with that encoding a component of the E3 ubiquitin-ligase complex Cullin 3 (CUL3), which result in permanent activation of NRF2, and the recognition that such mutations occur frequently in many types of cancer. Notably, mutations in NFE2L2, KEAP1 and CUL3 that cause persistent upregulation of NRF2 often co-exist with mutations that activate KRAS and the PI3K-PKB/Akt pathway, suggesting NRF2 supports growth of tumours in which KRAS or PKB/Akt are hyperactive. Besides somatic mutations, NRF2 activation in human tumours can occur by other means, such as alternative splicing that results in a NRF2 protein which lacks the KEAP1-binding domain or overexpression of other KEAP1-binding partners that compete with NRF2. Lastly, as NRF2 upregulation is associated with resistance to cancer chemotherapy and radiotherapy, we describe strategies that might be employed to suppress growth and overcome drug resistance in tumours with overactive NRF2.
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16

Soo, R. A., S. C. Lee, S. S. Ng, P. Y. Chong, L. S. Tham, L. Z. Wang, H. S. Lee, R. Soong, and B. C. Goh. "Analysis of gemcitabine pathway genotypes in ethnic Asians and their relationship with outcome in non-small cell lung cancer (NSCLC) patients." Journal of Clinical Oncology 24, no. 18_suppl (June 20, 2006): 2008. http://dx.doi.org/10.1200/jco.2006.24.18_suppl.2008.

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2008 Background: Genotypic variation for drug metabolising enzymes, targets and transporters is associated with inter-patient and inter-ethnic variability in toxicity and efficacy. Gemcitabine is a nucleoside anti-metabolite used in a range of solid tumors. Aims: 1) to determine genotype distribution of genes involved in gemcitabine pharmacology pathway in ethnic groups; 2) to evaluate the association between genotypes and treatment related outcomes in patients with chemo-naive, advanced NSCLC receiving gemcitabine based chemotherapy on a prospective study. Methods: Candidate genes involved in gemcitabine pharmacology were identified from a comprehensive search of public databases (NCBI, PharmGKB), and publications. 25 variants of 9 candidate genes (RRM-1, SLC28A1, SLC28A2, SLC28A3, SLC29A2, POLA2, DCTD, CDA, TS) were genotyped from blood in 94 healthy donors and 76 cancer patients (breast 22, NSCLC 54) with pyrosequencing. Chi-squared, Kruskall-Wallis, and Kaplan-Meier analysis were used to evaluate associations between genotypes and ethnic groups and clinical end points. Results: Significant differences in genotype distribution between Chinese, Malay and Indian were seen in 5/25 loci (see table ). In NSCLC patients, POLA2 2089 (G > A) was associated with neutropenia (p = 0.022), SLC28A1-1576 (C > T) with neutropenia nadir (p = 0.030) and thrombocytopenia nadir (p = 0.037), RRM-1 -524 (T > C) with neutropenia (p = 0.024) and SLC28A2–283 (CA 18.3 vs CC 8.5 months, p = 0.004), and SLC28A2–22 (CC 8.0 vs CT 18.3 months, p = 0.002) with survival. Conclusions: Our results suggest there is significant genotypic variability among ethnic groups. Variants in gemcitabine transporters and targets may be useful indicators of gemcitabine related toxicity and survival. Further studies should be performed to confirm these preliminary findings. [Table: see text] No significant financial relationships to disclose.
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17

Stankovic, Tatjana, and Eliot Marston. "Molecular mechanisms involved in chemoresistance in paediatric acute lymphoblastic leukaemia." Srpski arhiv za celokupno lekarstvo 136, no. 3-4 (2008): 187–92. http://dx.doi.org/10.2298/sarh0804187s.

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Acute lymphoblastic leukaemia (ALL) is the most common paediatric cancer. Despite cure rates approaching 80%, resistance to treatment and disease relapse remain a significant clinical problem. Identification of the genes and biological pathways responsible for chemoresistance is therefore crucial for the design of novel therapeutic approaches aiming to improve patient survival. Mutations in the membrane transporter P-glycoprotein genes, genetic variations in drug-metabolising enzymes and defects in apoptotic pathways are mechanisms of chemoresistance common to a wide spectrum of cancers and also play a role in paediatric ALL. In addition, several recent microarray studies have identified transcriptional profiles specifically associated with chemoresistance and pointed to a number of potentially novel therapeutic targets. These microarray studies have shown that genes discriminating between clinically responsive and resistant leukaemias tend to be involved in cellular processes such as regulation of cell cycle, proliferation, and DNA repair. Here we review the outcomes of these microarray studies and also present our own investigations into apoptotic resistance to DNA double strand breaks (DSBs) in paediatric ALL. We present stratification of paediatric ALL by the profile of DNA damage response following ionising radiation (IR) in vitro. This approach allows classification of ALL tumours at presentation into IR-apoptotic sensitive and IR-apoptotic resistant. Furthermore, apoptotic resistant leukaemias exhibit abnormal response of NFkB pathway following irradiation and inhibition of this pathway can sensitise leukaemic cells to IR-induced DSBs.
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18

Crake, Rebekah L. I., Matthew R. Strother, Elisabeth Phillips, Matthew P. Doogue, Mei Zhang, Chris M. A. Frampton, Bridget A. Robinson, and Margaret J. Currie. "Influence of serum inflammatory cytokines on cytochrome P450 drug metabolising activity during breast cancer chemotherapy: a patient feasibility study." Scientific Reports 11, no. 1 (March 11, 2021). http://dx.doi.org/10.1038/s41598-021-85048-1.

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AbstractIndividual response to chemotherapy in patients with breast cancer is variable. Obesity and exercise are associated with better and worse outcomes, respectively, and it is known that both impact the systemic cytokine milieu. Cytochrome P450 (CYP) enzymes are responsible for the metabolism of many chemotherapy agents, and CYP enzyme activity has been shown to be modified by inflammatory cytokines in vitro and in vivo. Cytokine-associated changes in CYP metabolism may alter chemotherapy exposure, potentially affecting treatment response and patient survival. Therefore, better understanding of these biological relationships is required. This exploratory single arm open label trial investigated changes in in vivo CYP activity in twelve women treated for stage II or III breast cancer, and demonstrated for the first time the feasibility and safety of utilising the Inje phenotyping cocktail to measure CYP activity in cancer patients receiving chemotherapy. Relative CYP activity varied between participants, particularly for CYP2C9 and CYP2D6, and changes in serum concentrations of the inflammatory cytokine monocyte chemoattractant protein 1 inversely correlated to CYP3A4 activity during chemotherapy. Future use of phenotyping cocktails in a clinical oncology setting may help guide drug dosing and improve chemotherapy outcomes.Clinical Trial Registration: Trial was retrospectively registered to the Australia New Zealand Clinical Trial Registry (ANZCTR). ACTRN12620000832976, 21 Aug 2020, https://www.anzctr.org.au/ACTRN12620000832976.aspx.
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19

Presa, Daniela, Syed A. Khurram, Amir Z. A. Zubir, Sneha Smarakan, Patricia A. Cooper, Goreti R. Morais, Maria Sadiq, et al. "Cytochrome P450 isoforms 1A1, 1B1 AND 2W1 as targets for therapeutic intervention in head and neck cancer." Scientific Reports 11, no. 1 (September 23, 2021). http://dx.doi.org/10.1038/s41598-021-98217-z.

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AbstractEpidemiological studies have shown that head and neck cancer (HNC) is a complex multistage process that in part involves exposure to a combination of carcinogens and the capacity of certain drug-metabolising enzymes including cytochrome P450 (CYP) to detoxify or activate such carcinogens. In this study, CYP1A1, CYP1B1 and CYP2W1 expression in HNC was correlated with potential as target for duocarmycin prodrug activation and selective therapy. In the HNC cell lines, elevated expression was shown at the gene level for CYP1A1 and CYP1B1 whereas CYP2W1 was hardly detected. However, CYP2W1 was expressed in FaDu and Detroit-562 xenografts and in a cohort of human HNC samples. Functional activity was measured in Fadu and Detroit-562 cells using P450-Glo™ assay. Antiproliferative results of duocarmycin prodrugs ICT2700 and ICT2706 revealed FaDu and Detroit-562 as the most sensitive HNC cell lines. Administration of ICT2700 in vivo using a single dose of ICT2700 (150 mg/kg) showed preferential inhibition of small tumour growth (mean size of 60 mm3) in mice bearing FaDu xenografts. Significantly, our findings suggest a potential targeted therapeutic approach to manage HNCs by exploiting intratumoural CYP expression for metabolic activation of duocarmycin-based prodrugs such as ICT2700.
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