Why do cancers have high aerobic glycolysis?

By Robert A. Gatenby, Robert James Gillies. Nature Reviews. Cancer, 2004

4,857 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/57645c2dd22a4ce9861e3b28baf26d2405751bf6

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. C. V. Dang
2. G. Semenza
3. M. V. Vander Heiden
4. Navdeep S. Chandel
5. Ralph J. Deberardinis
6. Guido Kroemer
7. J. Pouysségur
8. J. Chiche

In Molecular Biology

1. G. Semenza
2. C. V. Dang
3. M. V. Vander Heiden
4. Navdeep S. Chandel
5. Ralph J. Deberardinis
6. Guido Kroemer
7. J. Pouysségur
8. David M. Sabatini

Citations in the corpus

• The impact of O2 availability on human cancer (2008, background): “This hypothesis appears to be incorrect, but a number of other molecular mechanisms promoting 'aerobic glycolysis' have been proposed, including mutations and epigenetic changes in genes encoding tumour suppressors (for example, TP53 ), activation of oncogenes (such as MYC ) and hypoxic adapta”
• Regulation of cancer cell metabolism (2011, background): “Adaptation to the resulting acidic microenvironment that is caused by excess lactate production may further drive the evolution of the glycolytic phenotyp”
• Cancer's molecular sweet tooth and the Warburg effect. (2006, background): “Aerobic glycolysis may provide cancer cells growth advantage in the tumor microenvironment (16).”
• ROS Function in Redox Signaling and Oxidative Stress (2014, background): “While ROS play a key role in maintaining mitogenic signals to drive cancer cell proliferation, they are also integral in adapting to the metabolic stress that occurs when highly proliferative tumors outstrip their blood supply [59].”
• Metabolic competition in the tumor microenvironment is a driver of cancer progression (2015, background): “We wondered whether higher glycolysis in P tumors limited glucose in the microenvironment and contributed to TIL hyporesponsiveness. mTOR is an environmental sensor, and mTOR pathway signals decrease when nutrients are restricted (Gatenby and Gillies, 2004; Kim et al., 2002).”
• Causes and Consequences of Increased Glucose Metabolism of Cancers (2008, background): “We have previously presented evidence that the glycolytic phenotype is selected in early in situ cancers because they are faced with intermittent hypoxia (181).”
• Metabolic Modulation of Glioblastoma with Dichloroacetate (2010, background): “For example, most glycolytic enzymes also have direct antiapoptotic actions (12); lactic acid promotes angiogenesis and interstitial matrix breakdown, facilitating metastasis (11); and decreased mitochondrial function is associated with inhibition of mitochondriadependent apoptosis (3).”
• SIRT3 opposes reprogramming of cancer cell metabolism through HIF1α destabilization (2011, background): “In support of this notion, the transition from premalignant lesions to invasive cancer is often accompanied by increased tumor glucose uptake (Gatenby and Gillies, 2004).”
• Distribution and biological activities of the flavonoid luteolin. (2009, methodology): “sumption and up-regulation of glycolysis; this technique has clinical utility for detecting metastatic cancers with high sensitivity and specificity [179, 180].”
• HIF-1 inhibits mitochondrial biogenesis and cellular respiration in VHL-deficient renal cell carcinoma by repression of C-MYC activity. (2007, background): “The increase in glucose uptake is such a reliable feature of cancer cells that it provides the basis for clinical identification of occult metastases by [ 18 F]-deoxyglucose positron-emission tomography (Gatenby and Gillies, 2004).”
• Cancer as a metabolic disease (2010, background): “In addition to the six recognized hallmarks of cancer, aerobic glycolysis or the Warburg effect is also a robust metabolic hallmark of most tumors [10-14].”