The interplay between MYC and HIF in cancer

By C. V. Dang, Jung-whan Kim, Ping Gao, Jason T. Yustein. Nature Reviews. Cancer, 2008

628 citations recorded by the source corpus.

Subfields: Biotechnology, Cancer Research, Radiology, Nuclear Medicine and Imaging

View Paper: https://www.semanticscholar.org/paper/264d817400d2baa93a72bd4465d8eb1374607b93

How researchers see this paper

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

In Biotechnology

1. A. Mayer
2. Guido Kroemer
3. C. V. Dang
4. P. Vaupel
5. Karen H. Vousden
6. Y. Fouad
7. C. Aanei

In Cancer Research

1. C. V. Dang
2. Guido Kroemer
3. Jie Zheng
4. A. Mayer
5. Craig B. Thompson
6. Ping Gao
7. H. Schmidberger
8. Karen H. Vousden

In Radiology, Nuclear Medicine and Imaging

1. C. V. Dang
2. Guido Kroemer

Citations in the corpus

• The Warburg effect: essential part of metabolic reprogramming and central contributor to cancer progression (2019, methodology): “Warburg calculated a critical diffusion distance of 470 mm based on invalid O2 diffusion constants as part of the differential equations for calculation of O2 diffusion distances (Vaupel 1974; Dang et al. 2008).”
• p53 and metabolism (2009, background): “, but also other oncoproteins associated with deregulated proliferation (such as MYC ) or the response to O 2 starvation (such as hypoxia-inducible factor (HIF)”
• Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer. (2016, background): “The complex interplay between HIFs and Myc is reviewed in Dang et al. (2008).”
• 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).”
• Tumor suppressors and cell metabolism: a recipe for cancer growth. (2009, background): “In particular, the c-Myc proto-oncogene is a potent regulator of multiple metabolic pathways essential for cancer growth (Dang et al. 2008).”
• MYC on the Path to Cancer (2012, background): “When Myc is elevated, it could bind to the same targets that would be bound by other E box transcription factors (Dang et al., 2008; Kim et al., 2007).”
• Energy metabolism of cancer: Glycolysis versus oxidative phosphorylation (Review). (2012, background): “HIF1 cooperates with c-Myc to promote aerobic glycolysis by induction of hexokinase 2 (HK2), converting glucose to glucose 6-phosphate, and PDK1, a negative regulator of pyruvate dehydrogenase (PDH) (69).”
• Hypoxia-inducible factors in stem cells and cancer (2009, neutral): “When considering the interaction between HIF and cMyc, the cellular context can become very important [86].”
• Loss of FBP1 by Snail-mediated Repression Provides Metabolic Advantages in Basal-like Breast Cancer (2013, neutral): “Activation of Myc also induces glycolysis by inducing LDH-A and PDK1 expression, which inhibits the conversion of pyruvate to acetyl-CoA and facilitates the production of lactate (Dang et al., 2008).”
• MYC, Metabolism, and Cancer. (2015, background): “HIF1α and MYC, hence, can cooperate when MYC is overexpressed (106).”
• Foxp3 reprograms T cell metabolism to function in low glucose high lactate environments (2017, background): “Suppression of Myc also increases pyruvate dehydrogenase activity (Dang et al., 2008).”
• Anoikis molecular pathways and its role in cancer progression. (2013, background): “Likewise, c-Myc upregulates GLUT1, lactate dehydrogenase A, hexokinase 2, phosphofructokinase and glutaminase-1, the first enzymeof glutaminolysis [52].”