SALAMON, S., E. PODBREGAR, P. KUBATKA, D. BUSSELBERG, M. CAPRNDA, R. OPATRILOVA, V. VALENTOVA, M. ADAMEK, Peter KRUŽLIAK and M. PODBREGAR. Glucose Metabolism in Cancer and Ischemia: Possible Therapeutic Consequences of the Warburg Effect. Nutrition and cancer : an international journal. Abingdon: Routledge Journals, Taylor & Francis, 2017, vol. 69, No 2, p. 177-183. ISSN 0163-5581. Available from: https://dx.doi.org/10.1080/01635581.2017.1263751.
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Basic information
Original name Glucose Metabolism in Cancer and Ischemia: Possible Therapeutic Consequences of the Warburg Effect
Authors SALAMON, S. (705 Slovenia), E. PODBREGAR (705 Slovenia), P. KUBATKA (703 Slovakia), D. BUSSELBERG (634 Qatar), M. CAPRNDA (703 Slovakia), R. OPATRILOVA (203 Czech Republic), V. VALENTOVA (703 Slovakia), M. ADAMEK (703 Slovakia), Peter KRUŽLIAK (703 Slovakia, guarantor, belonging to the institution) and M. PODBREGAR (705 Slovenia).
Edition Nutrition and cancer : an international journal, Abingdon, Routledge Journals, Taylor & Francis, 2017, 0163-5581.
Other information
Original language English
Type of outcome Article in a journal
Field of Study 30204 Oncology
Country of publisher United Kingdom of Great Britain and Northern Ireland
Confidentiality degree is not subject to a state or trade secret
Impact factor Impact factor: 2.261
RIV identification code RIV/00216224:14110/17:00098632
Organization unit Faculty of Medicine
Doi http://dx.doi.org/10.1080/01635581.2017.1263751
UT WoS 000394613600001
Keywords in English Glucose Metabolism
Tags EL OK
Tags International impact, Reviewed
Changed by Changed by: Soňa Böhmová, učo 232884. Changed: 20/3/2018 18:49.
Abstract
The Warburg effect states that the main source of energy for cancer cells is not aerobic respiration, but glycolysiseven in normoxia. The shift from one to the other is governed by mutually counteracting enzymes: pyruvate dehydrogenase and pyruvate dehydrogenase kinase (PDK). Anaerobic metabolism of cancer cells promotes cell proliferation, local tissue immunosuppression, resistance to hypoxic conditions, and metastatic processes. By switching glucose back to oxidative metabolism, these effects might be reversed. This can be achieved using PDK inhibitors, such as dichloroacetate. Patients suffering from ischemic conditions might benefit from this effect. On the other hand, the -blockers (adrenergic -antagonists) often used in these patients appear to improve cancer-specific survival, and nonselective -blockers have been shown to promote glucose oxidation. Might there be a link?
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