TY - JOUR
T1 - Robust metabolic adaptation underlying tumor progression
AU - Vizán, Pedro
AU - Mazurek, Sybille
AU - Cascante, Marta
N1 - Funding Information:
Acknowledgments This work was supported by Grants SAF2005-01627 from the Spanish Ministery of Education and Science and ISCIII-RTICC (RD06/0020/0046), from the Spanish Ministry of Health and Consumption as well as from the Deutsche Forschungs-gemeinschaft (Ma 1760 1-2 and 2-1). We are also grateful to Michael Eaude of the University of Barcelona Language Service for valuable assistance in the preparation of the manuscript.
PY - 2008/3
Y1 - 2008/3
N2 - Tumor metabolism represents the end point of many signal cascades recruited by oncogenic activation. Energy metabolism of cancer cells attracted the attention of biochemists over eight decades ago. For example, high consume of glucose and high lactate production under aerobic conditions make up one of the most fundamental characteristics of cancer cells and has been exploited for diagnosis. At the same time, study of the metabolic status of tumor cells during tumor progression reveals characteristic adaptations during carcinogenesis. Although these metabolic adaptations are not the main defects that cause cancer, they may confer advantages to survive. In this review, we discuss the main metabolic hot spots and their relationship with main tumor progression events. An accurate metabolic map of the many tumor phenotypes could offer new options in the treatment of cancer.
AB - Tumor metabolism represents the end point of many signal cascades recruited by oncogenic activation. Energy metabolism of cancer cells attracted the attention of biochemists over eight decades ago. For example, high consume of glucose and high lactate production under aerobic conditions make up one of the most fundamental characteristics of cancer cells and has been exploited for diagnosis. At the same time, study of the metabolic status of tumor cells during tumor progression reveals characteristic adaptations during carcinogenesis. Although these metabolic adaptations are not the main defects that cause cancer, they may confer advantages to survive. In this review, we discuss the main metabolic hot spots and their relationship with main tumor progression events. An accurate metabolic map of the many tumor phenotypes could offer new options in the treatment of cancer.
KW - Acidosis and tumor progression
KW - Alternative to glycolytic energy conversion
KW - Biosynthetic pathways in tumoral metabolism
KW - Isoenzyme expression in tumor cells
KW - Regulation of glucose metabolism in tumors
KW - Tumor metabolism
KW - Tumor metabolism and apoptosis
KW - Warburg effect
UR - http://www.scopus.com/inward/record.url?scp=38949107594&partnerID=8YFLogxK
U2 - 10.1007/s11306-007-0101-3
DO - 10.1007/s11306-007-0101-3
M3 - Review
AN - SCOPUS:38949107594
SN - 1573-3882
VL - 4
SP - 1
EP - 12
JO - Metabolomics
JF - Metabolomics
IS - 1
ER -