Cancer metabolism: a therapeutic perspective

Nature Reviews Clinical Oncology, Journal Year: 2016, Volume and Issue: 14(1), P. 11 - 31

Published: May 4, 2016

Language: Английский

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Targeting Metabolism for Cancer Therapy

Cell chemical biology, Journal Year: 2017, Volume and Issue: 24(9), P. 1161 - 1180

Published: Sept. 1, 2017

Language: Английский

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Tumour acidosis: from the passenger to the driver's seat

Nature reviews. Cancer, Journal Year: 2017, Volume and Issue: 17(10), P. 577 - 593

Published: Sept. 15, 2017

Language: Английский

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The “cancer immunogram”

Science, Journal Year: 2016, Volume and Issue: 352(6286), P. 658 - 660

Published: May 6, 2016

Visualizing the state of cancer–immune system interactions may spur personalized therapy

Language: Английский

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Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer

Pharmacology & Therapeutics, Journal Year: 2016, Volume and Issue: 164, P. 152 - 169

Published: April 30, 2016

Insufficient tissue oxygenation, or hypoxia, contributes to tumor aggressiveness and has a profound impact on clinical outcomes in cancer patients. At decreased oxygen tensions, hypoxia-inducible factors (HIFs) 1 2 are stabilized mediate hypoxic response, primarily by acting as transcription factors. HIFs exert differential effects growth affect important hallmarks including cell proliferation, apoptosis, differentiation, vascularization/angiogenesis, genetic instability, metabolism, immune responses, invasion metastasis. As consequence, resistance chemo- radiotherapy associated with poor prognosis Intriguingly, perivascular cells can also express HIF-2α, thereby forming "pseudohypoxic" phenotype that further aggressiveness. Therefore, therapeutic targeting of the potential improve treatment efficacy. Different strategies target and/or include hypoxia-activated prodrugs inhibition HIF dimerization, mRNA protein expression, DNA binding capacity, transcriptional activity. Here we review functions progression malignant solid tumors. We highlight how may be targeted management patients therapy-resistant metastatic cancer.

Language: Английский

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Reexamining cancer metabolism: lactate production for carcinogenesis could be the purpose and explanation of the Warburg Effect

Carcinogenesis, Journal Year: 2016, Volume and Issue: unknown, P. bgw127 - bgw127

Published: Dec. 6, 2016

Herein, we use lessons learned in exercise physiology and metabolism to propose that augmented lactate production ('lactagenesis'), initiated by gene mutations, is the reason purpose of Warburg Effect dysregulated signaling are key elements carcinogenesis. Lactate-producing ('lactagenic') cancer cells characterized increased aerobic glycolysis excessive formation, a phenomenon described Otto 93 years ago, which still remains unexplained. After hiatus several decades, interest as player has been renewed. In normal physiology, lactate, obligatory product glycolysis, an important metabolic fuel energy source, most gluconeogenic precursor, molecule (i.e. 'lactormone') with major regulatory properties. lactagenic cancers, oncogenes tumor suppressor mutations behave highly orchestrated manner, apparently increasing glucose utilization for lactagenesis purposes exchange between, within among cells. Five main steps identified (i) uptake, (ii) glycolytic enzyme expression activity, (iii) decreased mitochondrial function, (iv) production, accumulation release (v) upregulation monocarboxylate transporters MTC1 MCT4 exchange. Lactate probably only compound involved necessary all sequela carcinogenesis, specifically: angiogenesis, immune escape, cell migration, metastasis self-sufficient metabolism. We hypothesize carcinogenesis explanation Effect. Accordingly, therapies limit should be priorities discovery.

Language: Английский

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Metabolomics in cancer research and emerging applications in clinical oncology

CA A Cancer Journal for Clinicians, Journal Year: 2021, Volume and Issue: 71(4), P. 333 - 358

Published: May 13, 2021

Abstract Cancer has myriad effects on metabolism that include both rewiring of intracellular to enable cancer cells proliferate inappropriately and adapt the tumor microenvironment, changes in normal tissue metabolism. With recognition fluorodeoxyglucose‐positron emission tomography imaging is an important tool for management many cancers, other metabolites biological samples have been spotlight diagnosis, monitoring, therapy. Metabolomics global analysis small molecule like ‐omics technologies can provide critical information about state are otherwise not apparent. Here, authors review how therapies interact with at cellular systemic levels. An overview metabolomics provided a focus currently available they applied clinical translational research setting. The also discuss could be further leveraged future improve patients cancer.

Language: Английский

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Induction of metastasis, cancer stem cell phenotype, and oncogenic metabolism in cancer cells by ionizing radiation

Molecular Cancer, Journal Year: 2017, Volume and Issue: 16(1)

Published: Jan. 13, 2017

Radiation therapy is one of the major tools cancer treatment, and widely used for a variety malignant tumours. Radiotherapy causes DNA damage directly by ionization or indirectly via generation reactive oxygen species (ROS), thereby destroying cells. However, ionizing radiation (IR) paradoxically promotes metastasis invasion cells inducing epithelial-mesenchymal transition (EMT). Metastasis obstacle to successful therapy, closely linked rates morbidity mortality many cancers. ROS have been shown play important roles in mediating biological effects IR. implicated IR-induced EMT, activation several EMT transcription factors—including Snail, HIF-1, ZEB1, STAT3—that are activated signalling pathways, including those TGF-β, Wnt, Hedgehog, Notch, G-CSF, EGFR/PI3K/Akt, MAPK. Cancer that undergo acquire stemness metabolic changes, although these points debated. IR known induce stem cell (CSC) properties, dedifferentiation self-renewal, promote oncogenic metabolism activating EMT-inducing pathways. Much accumulated evidence has alterations associated with CSC phenotypes; specifically, seems be required acquisition phenotypes. can also elicit various changes tumour microenvironment (TME) may affect metastasis. CSC, involved radioresistance; targeting them improve efficacy radiotherapy, preventing recurrence This study focuses on molecular mechanisms CSCs, metabolism, TME. We discuss how EMT/CSC/oncogenic resistance radiotherapy; we review efforts develop therapeutic approaches eliminate adverse effects.

Language: Английский

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The extracellular matrix in tumor progression and metastasis

Clinical & Experimental Metastasis, Journal Year: 2019, Volume and Issue: 36(3), P. 171 - 198

Published: April 11, 2019

Language: Английский

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Targeting glucose metabolism to suppress cancer progression: prospective of anti-glycolytic cancer therapy

Pharmacological Research, Journal Year: 2019, Volume and Issue: 150, P. 104511 - 104511

Published: Nov. 3, 2019

Language: Английский

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