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Relevant bibliographies by topics / Metabolic inhibition

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Academic literature on the topic 'Metabolic inhibition'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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Journal articles on the topic "Metabolic inhibition"

1

Lee, Sung Ryul, and Jin Han. "Mitochondrial Metabolic Inhibition and Cardioprotection." Korean Circulation Journal 47, no. 2 (2017): 168. http://dx.doi.org/10.4070/kcj.2016.0401.

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Delius, Ralph E., and Daniel B. Hinshaw. "Metabolic inhibition potentiates oxidant injury." Journal of Surgical Research 50, no. 4 (April 1991): 314–22. http://dx.doi.org/10.1016/0022-4804(91)90197-t.

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Zhang, Yiru, Trang Nguyen, Junfei Zhao, Enyuan Shang, Consuelo Torrini, Peter D. Canoll, Georg Karpel-Massler, and Markus Siegelin. "CBMT-15. MET INHIBITION DRIVES PGC1A DEPENDENT METABOLIC REPROGRAMMING AND ELICITS UNIQUE METABOLIC VULNERABILITIES IN GLIOBLASTOMA." Neuro-Oncology 21, Supplement_6 (November 2019): vi36. http://dx.doi.org/10.1093/neuonc/noz175.137.

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Abstract The receptor kinase, c-MET, has emerged as a target for glioblastoma therapy. However, treatment resistance evolves inevitably. By performing a global metabolite screen with metabolite set enrichment coupled with transcriptome and gene set enrichment analysis and proteomic screening, we have identified substantial reprogramming of tumor metabolism, involving oxidative phosphorylation and fatty acid oxidation (FAO) with a substantial accumulation of acyl-carnitines accompanied by an increase of PGC1a in response to genetic (shRNA and CRISPR/Cas9) and pharmacological (crizotinib) inhibition of c-MET. Extracellular flux and carbon tracing analyses (U-13C-Glucose and U-13C-Glutamine) demonstrated enhanced oxidative metabolism, which was driven by FAO and supported by increased anaplerosis of glucose carbons. These findings were observed in concert with increased number and fusion of mitochondria and production of reactive oxygen species (ROS). Genetic interference with PGC1a rescued this oxidative phenotype driven by c-MET inhibition. Silencing and chromatin immunoprecipitation experiments demonstrated that CREB regulates the expression of PGC1a in the context of c-MET inhibition. Interference with both oxidative phosphorylation (metformin, oligomycin) and beta-oxidation of fatty acids (etomoxir) enhanced the anti-tumor efficacy of c-MET inhibition. Moreover, based on a high-throughput drug screen, we show that gamitrinib along with c-MET inhibition results in synergistic cell death. Finally, utilizing patient-derived xenograft models, we provide evidence that the combination treatments (crizotinib+etomoxir and crizotinib+gamitrinib) were significantly more efficacious than single treatment without induction of toxicity. Collectively, we have unraveled the mechanistic underpinnings of c-MET inhibitor treatment and identified novel combination therapies that may enhance the therapeutic efficacy of c-MET inhibition.

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Riley, Robert J., and Ken Grime. "Metabolic screening in vitro: metabolic stability, CYP inhibition and induction." Drug Discovery Today: Technologies 1, no. 4 (December 2004): 365–72. http://dx.doi.org/10.1016/j.ddtec.2004.10.008.

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Falezza, A., S. Cinelli, P. Ciliutti, and J. A. Vericat. "Metabolic activation in the inhibition of the metabolic cooperation assay." Mutation Research/Environmental Mutagenesis and Related Subjects 271, no. 2 (1992): 161. http://dx.doi.org/10.1016/0165-1161(92)91193-u.

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Funaki, Tomoo, Hideo Fukazawa, and Isami Kuruma. "Metabolic Kinetics of Nonproductive Binding Inhibition." Journal of Pharmaceutical Sciences 83, no. 8 (August 1994): 1181–83. http://dx.doi.org/10.1002/jps.2600830820.

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Loch‐Caruso, Rita, Isabel A. Corcos, and James E. Trosko. "Inhibition of metabolic coupling by metals." Journal of Toxicology and Environmental Health 32, no. 1 (January 1991): 33–48. http://dx.doi.org/10.1080/15287399109531463.

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Zarrinpar, Ali. "Metabolic Pathway Inhibition in Liver Cancer." SLAS TECHNOLOGY: Translating Life Sciences Innovation 22, no. 3 (March 17, 2017): 237–44. http://dx.doi.org/10.1177/2472630317698683.

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Liver cancer is fundamentally physiologically different from the surrounding liver tissue. Despite multiple efforts to target the altered signaling pathways created by oncogenic mutations, not many have focused on targeting the altered metabolism that allows liver cancer to develop and grow. Still to be resolved is the question of whether the altered metabolic pathways in this cancer differ enough from the surrounding noncancerous cells to allow for the development of potent and specific compounds. Clinical studies of metabolic modulators would provide some more information with regard to the feasibility of this approach. Furthermore, as it appears that oncogenic signaling is essential to this cancer’s altered metabolism, it stands to reason that targeting this altered signaling may allow the exploitation of specific metabolic vulnerabilities in combination with other drugs for enhanced efficacy. The identification of biomarkers of metabolic sensitivity will also be essential to determine whether these drugs will have the desired effect.

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Thibonnier, Marc, and Christine Esau. "Metabolic Benefits of MicroRNA-22 Inhibition." Nucleic Acid Therapeutics 30, no. 2 (April 1, 2020): 104–16. http://dx.doi.org/10.1089/nat.2019.0820.

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Fern, Robert. "Metabolic Inhibition and Selective Axonal Injury." Neuroscientist 2, no. 6 (November 1996): 313–14. http://dx.doi.org/10.1177/107385849600200608.

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The selective injury of CNS axons produced by exposure to Cd2+, an environmental contaminant, is a result of disruption of mitochondrial respiration (oxidative phosphorylation). An examination of the literature reveals some other poisons that have a similar effect upon oxidative phosphorylation and that also produce CNS lesions typified by damage of axons with selective sparing of neurons. These include cyanide, CO, CS2, arsenic, and azide. The neurological injuries produced by these toxins appear to constitute a distinct class of pathology in which axonal injury is dominant. Such an observation is paradoxical, considering that ischemia tends to produce selective injury of neurons with relative sparing of axons, the mirror image of the injury associated with disruption of oxidative phosphorylation by these toxins. This paradox may be resolved by considering the extent to which energy utilization is disrupted during these two classes of metabolic insult. It appears likely that low levels of cytochrome oxidase, which is required for oxidative phosphorylation, endow white matter with a relatively high sensitivity to insults that disrupt oxidative phosphorylation.

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Dissertations / Theses on the topic "Metabolic inhibition"

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Bullock, Anthony James. "Metabolic inhibition in the ureter." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.366420.

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Gibb, Fraser Wilson. "Metabolic effects of aromatase inhibition." Thesis, University of Edinburgh, 2015. http://hdl.handle.net/1842/15838.

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Aromatase, a member of the cytochrome P450 superfamily, catalyses the conversion of androgens to estrogens; specifically, testosterone to estradiol and androstenedione to estrone. Aromatase is widely expressed across a range of tissues and deleterious metabolic effects are observed in both murine aromatase knock-out models and in rare human cases of aromatase deficiency. The effects of pharmacological inhibition of aromatase, as employed in the treatment of breast cancer, are not well characterised. This thesis addresses the hypothesis that aromatase inhibition, and consequent changes in sex steroid hormone action (higher androgen:estrogen ratio), results in disadvantageous changes in body composition and reduced insulin sensitivity. In a cohort study of 197 community-dwelling men, lower testosterone and SHBG concentrations were observed in those fulfilling criteria for metabolic syndrome, although no relationship with estrogens was observed. The strongest determinant of circulating estrogens was substrate androgen concentration. A case-control study of aromatase inhibitor treated breast cancer patients and age-matched controls (n=40) demonstrated decreased insulin sensitivity and increased body fat in those treated with aromatase inhibitors; serum leptin concentration and leptin mRNA transcript levels (in subcutaneous adipose tissue) were elevated in this group. In healthy male volunteers (n=17), 6 weeks of aromatase inhibition (1 mg anastrozole daily) resulted in reduced glucose disposal during a hyperinsulinaemic euglycaemic clamp study, with d2-glucose and d5-glycerol tracers. No effects upon hepatic insulin sensitivity, lipolysis or body composition were noted, although serum leptin concentration was reduced following aromatase inhibitor administration. In conclusion, aromatase inhibition is associated with increased insulin resistance and, in women, increased body fat. This may be relevant for patients receiving aromatase inhibitor therapy, where more careful monitoring of glucose tolerance may be warranted.

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Upreti, Rita. "Metabolic effects of 5α-reductase inhibition in humans." Thesis, University of Edinburgh, 2013. http://hdl.handle.net/1842/11745.

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5α-reductases (5αRs) catalyse reduction of 4-pregnene steroids, most notably the androgen testosterone to its more potent metabolite dihydrotestosterone (DHT). Well-characterised isozymes of 5αR are designated 5αR1 and 5αR2. Inhibitors of 5αR, finasteride (a 5αR2 inhibitor) and dutasteride (a dual 5αR1 and 5αR2 inhibitor), are utilised in conditions where a reduction in androgen action is desired, including benign prostatic hyperplasia. Although 5αR2 is predominantly expressed in reproductive tissues, both isozymes, but particularly 5αR1, are expressed in metabolic tissues including liver and adipose and both metabolise glucocorticoids as well as androgens; therefore inhibition of 5αR may have consequences for metabolic health. This thesis addresses the hypotheses that 5αR1 inhibition with dutasteride decreases insulin sensitivity and causes dysregulation of the HPA axis in humans. Metabolism and the HPA axis were studied in men prior to and following 3 months of dutasteride (0.5 mg daily; n=16), finasteride (5 mg daily; n=16) or control (tamsulosin MR; 0.4 mg daily; n=14). Glucose disposal during hyperinsulinaemia was the primary endpoint, measured during a hyperinsulinaemic euglycaemic clamp, with d2-glucose and d5-glycerol tracers. Peripheral insulin sensitivity for both glucose uptake and NEFA suppression decreased with dutasteride versus both finasteride and control, while hepatic insulin sensitivity was preserved. Body fat increased with dutasteride, though was not accompanied by changes in metabolic or inflammatory gene transcript abundance in subcutaneous adipose biopsies, nor any differences in abdominal adipose depots on post-treatment MRI. Subtle dysregulation of the HPA axis was evident with both 5αR inhibitors, though to a greater degree with dutasteride and changes were largely compensated for. In support of this study, this thesis also describes the development, validation and application of two novel liquid chromatography tandem mass spectrometry assays; establishing compliance by measuring serum drug levels, and demonstrating effects of 5αR inhibitors on androgen metabolism and adrenal steroidogenesis by measurement of testosterone, DHT and androstenedione. In conclusion, 5αR1 inhibition with dutasteride, but not finasteride, induces peripheral insulin resistance and increases body fat. Findings presented may have important implications for patients prescribed dutasteride for benign prostatic hyperplasia.

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何頌詩 and Chung-sze Joyce Ho. "Effects of preconditioning with metabolic inhibition or U50488H or high CA2+ on CA2+ homeostasis in ventricular myocytes subjected tosevere metabolic inhibition or high CA2+." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31226024.

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Ho, Chung-sze Joyce. "Effects of preconditioning with metabolic inhibition or U50488H or high CA2+ on CA2+ homeostasis in ventricular myocytes subjected to severe metabolic inhibition or high CA2+ /." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2359617x.

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Orr, Linda E. "Reticulocyte maturation in vitro : impaired release of vesicular activity by metabolic inhibition." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66232.

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Wamil, Małgorzata. "Protective role of 11β-HSD1 inhibition in the metabolic syndrome and atherosclerosis." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3891.

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Obesity is associated with an increased risk of diabetes type 2, dyslipidaemia and atherosclerosis. These cardiovascular and metabolic abnormalities are exacerbated by dietary fats such as cholesterol and its metabolites. High adipose tissue glucocorticoid levels, generated by the intracellular enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) are also implicated in the pathogenesis of obesity, metabolic syndrome and atherosclerosis. Transgenic mice over-expressing 11β-HSD1 selectively in adipose tissue develop the metabolic syndrome whereas 11β-HSD1-/- mice have a ‘cardioprotective’ phenotype, deriving in part from improved adipose tissue function. Consistent with this, prototypical therapeutic 11β-HSD1 inhibitors ameliorate metabolic disturbances associated with obesity. 11β-HSD1 also inter-converts the atherogenic oxysterols 7-ketocholesterol (7KC) and 7β-hydroxycholesterol (7β-HC). Work presented in the first part of the thesis defines the impact of these alternative substrates on the metabolism of glucocorticoids in adipocyte cell lines (3T3-L1 and 3T3-F442A). 11β-HSD1 catalyses the reduction of 7KC in mature adipocytes leading to accumulation of 7β-HC. Oxysterol and glucocorticoid conversion by 11β-HSD1 was competitive and occurred within a physiologically-relevant IC50 range of 450nM for 7KC inhibition of glucocorticoid metabolism. Working as an inhibitor of 11β-HSD1 activity, 7KC decreased the regeneration of active glucocorticoid and limited the process of preadipocyte differentiation. 7-oxysterols did not display intrinsic activation of the glucocorticoid receptor (GR). However, when co-incubated with glucocorticoid, 7KC repressed, and 7β-HC enhanced GR transcriptional activity. The effect of 7-oxysterols resulted from the modulation of 11β-HSD1 reaction direction, at least in transfected HEK293 cells, and could be abrogated by over-expression of hexose 6-phosphate dehydrogenase, which supplies NADPH to drive the reductase activity of 11β-HSD1. 11β-HSD1 inhibition protects from atherosclerosis, yet it is unknown whether it is an effect of alterations in the metabolism of 7-oxysterols. 7KC and 7β-HC did not activate the potential cognate receptor LXRα and FXR/RXR in transactivation assays. No differential regulation of key gene targets of LXRα, FXR and RORα in the liver and fat depots of high fat fed 11β-HSD1-/- and wild type mice was observed. To further determine the molecular basis for the metabolically beneficial phenotype of 11β-HSD1-/- mice I analysed global gene expression in subcutaneous and mesenteric adipose tissues of high fat-fed (4 weeks) 11β-HSD1-/- and congenic C57BL/6J mice by microarrays, followed by pathway analysis, gene clustering and realtime-PCR validation of transcripts with >1.5-fold difference between genotypes. 11β-HSD1-/- mice gained less weight and distributed adipose tissue to subcutaneous rather than visceral depots. Broadly, high fat-fed 11β-HSD1-/- mice showed up-regulation of transcripts in subcutaneous fat (70% of 1622 differentially-expressed transcripts), but down-regulation in mesenteric adipose tissue (73% of 849 transcripts). Genes up-regulated in 11β-HSD1-/- subcutaneous adipose were associated with β-adrenergic signaling, glucose metabolism, lipid oxidation, oxidative phosphorylation, MAPK, Wnt/β-catenin, EGF, and PI3K/AKT insulin signaling pathways. Increased subcutaneous fat insulin signaling was confirmed by increased IRS-1 and Akt phosphorylation in vivo. Down-regulated genes in 11β-HSD1-/- mesenteric fat were associated with immune cells, NK-kappaB, Jak/Stat, SAPK/JNK, chemokine, toll-like-receptor and Wnt signaling pathways suggesting reduced immune cell infiltration in mesenteric adipose in high fat-fed 11β-HSD1-/- mice. 11β-HSD1 deficiency protects against metabolic disease by increasing peripheral fat insulin sensitivity and through a novel mechanism involving reduction in visceral fat immune/inflammatory cell function. Data presented in this thesis contribute to the understanding of the role of 11β-HSD1 in adipose tissues in obesity and, potentially, atherosclerosis.

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Dry, Katherine L. "Catecholamine release from isolated chromaffin cells under conditions of anoxia or metabolic inhibition." Thesis, University of Edinburgh, 1990. http://hdl.handle.net/1842/18845.

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A significant release of catecholamines within the heart has been observed during myocardial ischaemia. Ischaemia-induced catecholamine release can be markedly inhibited by desipramine and other amine uptake blocking agents, allowing investigation of the importance of such release for arrhythmia production. The mechanism of this release appears to occur by a carrier-mediated efflux from neurones, which is not operative under normal conditions. The aim of the project has been to study this release process in chromaffin cells isolated from the bovine adrenal medulla, which are recognised as a model system for studying the sympathetic nervous system. Understanding this process of catecholamine release may lead to new methods of protecting the heart against ischaemia-induced arrhythmias. Isolated chromaffin cells could be maintained in primary culture for up to 7 days and retained all their normal secretory responses. Conditions designed to mimic ischaemia, that is, anoxia or metabolic inhibition, resulted in a significant release of catecholamines. This release was shown to be independent of extracellular calcium but, in contrast to the release observed in ischaemic hearts, it was not inhibited by uptake₁ blockers. One of the main criteria for exocytosis is the co-release of other secretory granule components. Polyacrylamide gel electrophoresis and Western blotting techniques were utilised to examine this following metabolic inhbition. Significant levels of the granule proteins chromogranin A, neuropeptide Y and ATP were measured following metabolic inhibition, indicative of an exocytotic mechanism. Furthermore, there was no release of the cytosolic protein lactate dehydrogenase, indicating that there was no breakdown of the cell membrane during metabolic inhibition. Over the first 10 minutes of metabolic inhibition there was a marked uptake of ²²Na⁺ by the cells. It is suggested that this Na⁺ influx triggers the catecholamine release by affecting the cytosolic Ca²⁺ concentration through a direct effect on intracellular stores. Intracellular Ca²⁺ mobilisation was measured using the calcium-sensitive fluorescent probe Fura-2. It was found that cytosolic free calcium levels were increased in response to metabolic inhibition. The conditions requird to evoke carrier-mediated efflux were also examined. Cytosolic levels of catecholarmines could be artificially raised following treatment with reserpine. Cytoplasmic catecholamine levels were measured following permeabilisation with the detergent digitonin which renders the plasma membrane leaky. Conditions designed to reverse the uptake carrier and cause carier-mediated efflux in the presence of raised cytoplasmic catecholamines such as removal of extracellular sodium, did not evoke any catecholamine overflow. These studies suggest the chromaffin cell uptake₁ carrier is not reversible and may be gated in some way. This work has, therefore, raised questions concerning the suitability of chromaffin cells as a conventional model for sympathetic nerve terminals.

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Houdi, A. A. "Studies on metabolic sulphoxidation of alkyl and aryl thioethers : Role of cytochrome P-450 and FAD-containing monooxygenases." Thesis, University of Manchester, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375073.

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Reid, John M. "Role of Kâº channels during hypoxia and metabolic inhibition in the rat brain." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308872.

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Books on the topic "Metabolic inhibition"

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Yu, Wai Haung. Desferrioxamine analysis by high performance liquid chromatography, stability and metabolic inhibition by monoamine oxidase inhibitors. Ottawa: National Library of Canada, 1994.

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Ahlström, Marie. Cytochrome P450, metabolism and inhibition: Computational and experimental studies. Göteborg: Göteborg University, 2007.

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Wagner, Sylvie. Studies on metabolism and inhibition of melanoma mouse cell line. Sudbury, Ont: Laurentian University, 1994.

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Bitnun, Ari. Metabolic abnormalities associated with protease inhibitor therapy in HIV-infected children. Ottawa: National Library of Canada, 2003.

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Fernandes, Leona Caterina. Pharmacologic effects and safety of tranylcypromine inhibition of nicotine metabolism in humans. Ottawa: National Library of Canada, 2002.

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Kathiramalainathan, Kalyani. Modification of codeing metabolism and abuse liability by inhibition of cytochrome P450 2D6. Ottawa: National Library of Canada, 1996.

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A, Stafford Jeffrey, ed. Kinase inhibitor drugs. Hoboken, N.J: J. Wiley, 2009.

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Cancer: Between glycolysis and physical constraint. Berlin: Springer, 2004.

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Huq, Rokaiya. Energy metabolism in human MCF-7 ADR and ADR-9 breast cancer cells treated with P-glycoprotein inhibitor PSC 833. Sudbury, Ont: Laurentian University, 2000.

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Cheung, Hermia. Effect of dopamine depletion on D1 receptor binding in rat brain; and metabolism studies of D1 agonist R-[11C]SKF 82957 and phosphodiesterase-4 inhibitor R-[11C}rolipram. Ottawa: National Library of Canada, 2003.

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Book chapters on the topic "Metabolic inhibition"

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Ochs, Raymond S. "Enzymes and Their Inhibition." In Metabolic Structure and Regulation, 91–120. Boca Raton : CRC Press, 2018.: CRC Press, 2017. http://dx.doi.org/10.1201/9781315373133-5.

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Zhang, Tong, Christiaan F. Labuschagne, Karen H. Vousden, and Oliver D. K. Maddocks. "Direct Estimation of Metabolic Flux by Heavy Isotope Labeling Simultaneous with Pathway Inhibition: Metabolic Flux Inhibition Assay." In Metabolic Signaling, 109–19. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8769-6_8.

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Püschel, Franziska, and Cristina Muñoz-Pinedo. "Measuring the Activation of Cell Death Pathways upon Inhibition of Metabolism." In Metabolic Signaling, 163–72. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8769-6_12.

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Demolombe, Robert, Luis Fariñas del Cerro, and Naji Obeid. "Automated Reasoning in Metabolic Networks with Inhibition." In AI*IA 2013: Advances in Artificial Intelligence, 37–47. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-03524-6_4.

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Hoang, Giang, Kiet Nguyen, and Anne Le. "Metabolic Intersection of Cancer and Cardiovascular Diseases: Opportunities for Cancer Therapy." In The Heterogeneity of Cancer Metabolism, 249–63. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65768-0_18.

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AbstractAccording to data from the World Health Organization, cardiovascular diseases and cancer are the two leading causes of mortality in the world [1]. Despite the immense effort to study these diseases and the constant innovation in treatment modalities, the number of deaths associated with cardiovascular diseases and cancer is predicted to increase in the coming decades [1]. From 2008 to 2030, due to population growth and population aging in many parts of the world, the number of deaths caused by cancer globally is projected to increase by 45%, corresponding to an annual increase of around four million people [1]. For cardiovascular diseases, this number is six million people [1]. In the United States, treatments for these two diseases are among the most costly and result in a disproportionate impact on low- and middleincome people. As the fight against these fatal diseases continues, it is crucial that we continue our investigation and broaden our understanding of cancer and cardiovascular diseases to innovate our prognostic and treatment approaches. Even though cardiovascular diseases and cancer are usually studied independently [2–12], there are some striking overlaps between their metabolic behaviors and therapeutic targets, suggesting the potential application of cardiovascular disease treatments for cancer therapy. More specifically, both cancer and many cardiovascular diseases have an upregulated glutaminolysis pathway, resulting in low glutamine and high glutamate circulating levels. Similar treatment modalities, such as glutaminase (GLS) inhibition and glutamine supplementation, have been identified to target glutamine metabolism in both cancer and some cardiovascular diseases. Studies have also found similarities in lipid metabolism, specifically fatty acid oxidation (FAO) and synthesis. Pharmacological inhibition of FAO and fatty acid synthesis have proven effective against many cancer types as well as specific cardiovascular conditions. Many of these treatments have been tested in clinical trials, and some have been medically prescribed to patients to treat certain diseases, such as angina pectoris [13, 14]. Other metabolic pathways, such as tryptophan catabolism and pyruvate metabolism, were also dysregulated in both diseases, making them promising treatment targets. Understanding the overlapping traits exhibited by both cancer metabolism and cardiovascular disease metabolism can give us a more holistic view of how important metabolic dysregulation is in the progression of diseases. Using established links between these illnesses, researchers can take advantage of the discoveries from one field and potentially apply them to the other. In this chapter, we highlight some promising therapeutic discoveries that can support our fight against cancer, based on common metabolic traits displayed in both cancer and cardiovascular diseases.

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Hodgson, Ernest, and Andrew D. Wallace. "Human Metabolic Interactions of Pesticides: Inhibition, Induction, and Activation." In ACS Symposium Series, 115–32. Washington, DC: American Chemical Society, 2012. http://dx.doi.org/10.1021/bk-2012-1099.ch008.

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Tamaddoni-Nezhad, Alireza, Antonis Kakas, Stephen Muggleton, and Florencio Pazos. "Modelling Inhibition in Metabolic Pathways Through Abduction and Induction." In Inductive Logic Programming, 305–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-30109-7_23.

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Poveda, José B., and Robin Nicholas. "Serological Identification of Mycoplasmas by Growth and Metabolic Inhibition Tests." In Mycoplasma Protocols, 105–11. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1385/0-89603-525-5:105.

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Barry, William H., and Hiroshi Ikenouchi. "Does Calcium Overload Adequately Explain Diastolic Dysfunction During Metabolic Inhibition?" In Diastolic Relaxation of the Heart, 135–48. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2594-3_15.

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Chitour, Yacine, Frédéric Grognard, and Georges Bastin. "Stability Analysis of a Metabolic Model with Sequential Feedback Inhibition." In Positive Systems, 143–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-540-44928-7_20.

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Conference papers on the topic "Metabolic inhibition"

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Harper, Mason, Kinan Alhallak, Lisa Rebello, Khue Nguyen, Sruthi Ravindranathan, David Lee, Nicholas Greene, et al. "Optical Metabolic Imaging of TWIST Inhibition in 4T1 Breast Cancer Cells." In Optical Molecular Probes, Imaging and Drug Delivery. Washington, D.C.: OSA, 2017. http://dx.doi.org/10.1364/omp.2017.oms2d.3.

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Alvarez-Calderon, Francesca, Vadym Zaberezhnyy, Lelisa Gemta, Mark A. Gregory, and James V. DeGregori. "Abstract 1127: Bcr-Abl inhibition in leukemia cells creates metabolic addictions." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1127.

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Mancias, Joseph D., Douglas E. Biancur, Joao A. Paulo, Maria Quiles Del Rey, Cristovão M. Sousa, Xiaoxu Wang, Gerald C. Chu, Steven P. Gygi, J. Wade Harper, and Alec C. Kimmelman. "Abstract 4986: Pancreatic cancers develop metabolic resistance pathways to glutaminase inhibition." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4986.

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Ahmad, Fahim, and Ellora Sen. "Abstract A08: Telomerase inhibition brings metabolic compromises in glioblastoma multiforme (GBM)." In Abstracts: Fourth AACR International Conference on Frontiers in Basic Cancer Research; October 23-26, 2015; Philadelphia, PA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.fbcr15-a08.

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Ray, Oliver, Ken Whelan, and Ross King. "Logic-Based Steady-State Analysis and Revision of Metabolic Networks with Inhibition." In 2010 International Conference on Complex, Intelligent and Software Intensive Systems (CISIS). IEEE, 2010. http://dx.doi.org/10.1109/cisis.2010.184.

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Sandulache, Vlad C., James A. Bankson, Heath Skinner, Yuan Wang, Yunyun Chen, Cristina T. Dodge, Thomas Ow, John D. Hazle, Jeffrey N. Myers, and Stephen Y. Lai. "Abstract 371: In vivo monitoring of metabolic inhibition in anaplastic thyroid carcinoma." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-371.

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Kishi, Shingo, Kanya Honoki, Shinji Tsukamoto, Hiromasa Fujii, Yumiko Kondo, Yasuhito Tanaka, and Hiroki Kuniyasu. "Abstract 801: Dual inhibition of distinct metabolic features targets osteosarcoma stem cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-801.

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Kishi, Shingo, Kanya Honoki, Shinji Tsukamoto, Hiromasa Fujii, Yumiko Kondo, Yasuhito Tanaka, and Hiroki Kuniyasu. "Abstract 801: Dual inhibition of distinct metabolic features targets osteosarcoma stem cells." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-801.

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Maxwell, Micah J., Brad Poore, Allison Hanaford, Jesse Alt, Rana Rais, Barbara S. Slusher, Charles G. Eberhart, and Eric H. Raabe. "Abstract 3521: Glutamine metabolic inhibition synergizes with L-asparaginase in MYCN-amplified neuroblastoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3521.

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Ray, Oliver. "Towards a Rational Approach for the Logical Modelling of Inhibition in Metabolic Networks." In 2009 International Conference on Advanced Information Networking and Applications Workshops (WAINA). IEEE, 2009. http://dx.doi.org/10.1109/waina.2009.186.

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Reports on the topic "Metabolic inhibition"

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Thomas, Ronald D. Inhibition of Mitochondrial Estrogen Metabolism as a Possible Mechanism of Breast Cancer Prevention. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/adb248605.

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Carlson, E. A., Y. Li, and J. T. Zelikoff. Inhibition of CYP1A-Mediated Metabolism of Benzo(A)Pyrene (BAP): Effects Upon BAP-Induced Immunotoxicity in Japanese Medaka (Oryzias Latipes). Fort Belvoir, VA: Defense Technical Information Center, March 2001. http://dx.doi.org/10.21236/ada402076.

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