2012
DOI: 10.4161/cc.11.2.19006
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Is cancer a metabolic rebellion against host aging? In the quest for immortality, tumor cells try to save themselves by boosting mitochondrial metabolism

Abstract: (2012) Is cancer a metabolic rebellion against host aging? In the quest for immortality, tumor cells try to save themselves by boosting mitochondrial metabolism, Cell Cycle, 11:2, 253-263,

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Cited by 58 publications
(58 citation statements)
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“…[12][13][14][15][16][17][18][19][20][21][22][23][24] Conversely, genetic amplification of mitochondrial biogenesis in epithelial cancer cells also promotes tumor growth, independently of neo-angiogenesis. 23,[25][26][27][28] Consistent with these pre-clinical findings, we have identified a series of new stromal biomarkers and related gene signatures that are characteristic of this type of lethal cancer metabolism. [29][30][31][32][33][34] Remarkably, these diagnostics effectively predict early…”
Section: Introductionsupporting
confidence: 60%
See 1 more Smart Citation
“…[12][13][14][15][16][17][18][19][20][21][22][23][24] Conversely, genetic amplification of mitochondrial biogenesis in epithelial cancer cells also promotes tumor growth, independently of neo-angiogenesis. 23,[25][26][27][28] Consistent with these pre-clinical findings, we have identified a series of new stromal biomarkers and related gene signatures that are characteristic of this type of lethal cancer metabolism. [29][30][31][32][33][34] Remarkably, these diagnostics effectively predict early…”
Section: Introductionsupporting
confidence: 60%
“…Kaplan-Meier analysis was performed, essentially as we previously described. 28 Briefly, X-Tile software was employed to identify subpopulation cut-points to observe maximum survival differences between the high expression and low expression subpopulations. The Log-rank test was used to evaluate the significance of differences in survival curves for high vs. low expressing populations.…”
Section: Methodsmentioning
confidence: 99%
“…16 This led to the proposal of a novel two-compartment model of tumor metabolism, termed the "reverse Warburg effect." 11,[17][18][19][20][21][22][23][24] In this model, the glycolytic tumor stroma transfers energy-rich nutrients (such as, L-lactate and ketone bodies) to anabolic tumor cells, which then "fuels" mitochondrial metabolism in epithelial cancer cells. 18 Thus, we searched for new biomarker(s) of clinical outcome, by analyzing breast cancer cells co-cultured with human fibroblasts.…”
Section: Resultsmentioning
confidence: 99%
“…These studies also validate the "two-compartment tumor metabolism" model of tumorigenesis. 21,[27][28][29][30][31][32][33][34] …”
Section: Mitochondrial Dysfunction In Breast Cancer Cells Prevents Tumentioning
confidence: 99%