Cancer's molecular sweet tooth and the Warburg effect.

By Jung-whan Kim, C. V. Dang. Cancer Research, 2006

1,250 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f54b505e2bfea33ee0e542e08574880d55e19cd9

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. P. Vaupel
4. A. Mayer
5. Ping Gao
6. Jung-whan Kim
7. H. Schmidberger
8. E. Michelakis

In Molecular Biology

1. C. V. Dang
2. G. Semenza
3. E. White
4. Ping Gao
5. P. Vaupel
6. Jung-whan Kim
7. Douglas R. Green
8. E. Michelakis

Citations in the corpus

• Hypoxia inducible mir-210 regulates normoxic gene expression involved in tumor initiation (2009, neutral): “However, hypoxia is also a hallmark of cancer, where cancer cells shift their energy production from the TCA cycle to glycolysis (Kim and Dang, 2006).”
• The Warburg effect: essential part of metabolic reprogramming and central contributor to cancer progression (2019, background): “In addition, Weinhouse (1956, 1976), Aisenberg (1961), Vaupel (1974, 1977), Shapot (1976), Shapot and Vaupel (1976), Zu and Guppy (2004), Kim and Dang (2006), Moreno-Sanchez et al. (2007), Christofk et al. (2008), Potter et al. (2016) and a series of other authors provided substantial evidence that…”
• MYC-induced Cancer Cell Energy Metabolism and Therapeutic Opportunities (2009, background): “Myc cooperates with E2F1 to regulate genes involved in nucleotide metabolism and with the hypoxia inducible factor 1 (HIF-1) to regulate genes involved in glucose metabolism (11, 16, 17).”
• The interplay between MYC and HIF in cancer (2008, background): “Could the Warburg effect then be misconstrued to be pure aerobic glycolysis? It is notable, however, that certain oncogenic events, such as activation of Akt and Ras, can cause a cell-autonomous change to convert glucose to lactate, but with the caveat that stationary experimental tissue culture con”
• The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation (2011, background): “The metabolic changes associated with T cell activation are reminiscent of the characteristic metabolic activities of tumor cells and may represent a general metabolic reprogramming during cell growth and proliferation (Kim and Dang, 2006; Vander Heiden et al., 2009; Warburg, 1956).”
• Hypoxia-Inducible Factor 1 and Dysregulated c-Myc Cooperatively Induce Vascular Endothelial Growth Factor and Metabolic Switches Hexokinase 2 and Pyruvate Dehydrogenase Kinase 1 (2007, background): “Because many cancer cells display the Warburg effect or have the propensity to take up glucose and convert glucose to lactate, rather than metabolizing glucose through oxidative phosphorylation (2, 7, 15, 19, 36, 76, 82, 83), we sought to understand how dysregulated expression of c-Myc might interac”
• Interpreting Expression Data with Metabolic Flux Models: Predicting Mycobacterium tuberculosis Mycolic Acid Production (2009, background): “For example, many cancer cells are known to grow glycolytically in the presence of oxygen and to develop a lipogenic phenotype [57–59].”
• Targeting lactate-fueled respiration selectively kills hypoxic tumor cells in mice. (2008, background): “Strong evidence also indicates that the glycolytic phenotype of cancer cells is a crucial component of malignancy that confers a significant growth advantage (10).”
• c-Myc and Cancer Metabolism (2012, neutral): “tumor suppressor emerged as another regulator of mitochondrial function and glycolysis, showing that loss of p53 is associated with enhanced glycolysis (59).”