Gene, Год журнала: 2021, Номер 798, С. 145796 - 145796
Опубликована: Июнь 25, 2021
Язык: Английский
Gene, Год журнала: 2021, Номер 798, С. 145796 - 145796
Опубликована: Июнь 25, 2021
Язык: Английский
Nature Reviews Clinical Oncology, Год журнала: 2016, Номер 14(1), С. 11 - 31
Опубликована: Май 4, 2016
Язык: Английский
Процитировано
1331Cell chemical biology, Год журнала: 2017, Номер 24(9), С. 1161 - 1180
Опубликована: Сен. 1, 2017
Язык: Английский
Процитировано
829Nature reviews. Cancer, Год журнала: 2017, Номер 17(10), С. 577 - 593
Опубликована: Сен. 15, 2017
Язык: Английский
Процитировано
794Science, Год журнала: 2016, Номер 352(6286), С. 658 - 660
Опубликована: Май 6, 2016
Visualizing the state of cancer–immune system interactions may spur personalized therapy
Язык: Английский
Процитировано
688Pharmacology & Therapeutics, Год журнала: 2016, Номер 164, С. 152 - 169
Опубликована: Апрель 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.
Язык: Английский
Процитировано
609Carcinogenesis, Год журнала: 2016, Номер unknown, С. bgw127 - bgw127
Опубликована: Дек. 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.
Язык: Английский
Процитировано
549CA A Cancer Journal for Clinicians, Год журнала: 2021, Номер 71(4), С. 333 - 358
Опубликована: Май 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.
Язык: Английский
Процитировано
498Molecular Cancer, Год журнала: 2017, Номер 16(1)
Опубликована: Янв. 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.
Язык: Английский
Процитировано
486Clinical & Experimental Metastasis, Год журнала: 2019, Номер 36(3), С. 171 - 198
Опубликована: Апрель 11, 2019
Язык: Английский
Процитировано
478Pharmacological Research, Год журнала: 2019, Номер 150, С. 104511 - 104511
Опубликована: Ноя. 3, 2019
Язык: Английский
Процитировано
478