Hypoxia signalling in cancer and approaches to enforce tumour regression
By J. Pouysségur, Frédéric Dayan, N. Mazure. Nature, 2006
1,720 citations recorded by the source corpus.
Subfields: Cancer Research, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/5bbdcf74ee4cdf263a532b6dbae0b8dd5efb9722
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
- Dai Fukumura
- Guido Kroemer
- Claudiu T. Supuran
- Rakesh K. Jain
- J. Pouysségur
- J. Chiche
- M. Brahimi-Horn
- N. Mazure
In Molecular Biology
- G. Semenza
- Rakesh K. Jain
- Dai Fukumura
- J. Pouysségur
- Guido Kroemer
- Claudiu T. Supuran
- J. Chiche
- M. Brahimi-Horn
Citations in the corpus
- Interfering with pH regulation in tumours as a therapeutic strategy (2011, background): “In addition, H + ions are directly extruded from the cells, either in exchange for other cations (such as Na + ) or by means of the vacuolar ATPase (V-ATPase”
- Tumour hypoxia induces a metabolic shift causing acidosis: a common feature in cancer (2009, background): “This study reinforced the idea that manipulating hypoxic tumour metabolism by targeting specific HIFinduced glycolytic enzymes could participate in bringing about a metabolic deficiency through an indirect block in ATP production [10, 123].”
- Therapeutic targeting of hypoxia and hypoxia-inducible factors in cancer. (2016, background): “The affinity of PHDs and FIH-1 for oxygen differs and, since FIH-1 has a higher affinity (lower Km) for oxygen, PHDs are thought to be more rapidly inhibited in low oxygen conditions (Pouyssegur et al., 2006).”
- Hypoxia-induced autophagy: cell death or cell survival? (2010, background): “Why would an apoptotic gene be fully induced by HIF in conditions where HIF induces a cell survival response? We thus questioned its function in a hypoxic tumor environment and demonstrated, for the first time, that rapid and full induction of BNIP3 could instead protect from cell death through an a”
- Principles of Cancer Therapy: Oncogene and Non-oncogene Addiction (2009, neutral): “Consequently many tumors upregulate the transcription factor hypoxia-inducible factor HIF-1 (Pouyssegur et al., 2006).”
- Hypoxia promotes expansion of the CD133-positive glioma stem cells through activation of HIF-1α (2009, background): “Although hypoxia may be an inevitable outcome of the rapidly growing tumor outstripping its vascular supply, it confers certain advantages on tumor cells (Pouyssegur et al., 2006).”
- Hypoxia and cancer (2007, background): “synthesis, allowing for cellular adaptation and subsequent survival [12].”
- Regulation of Autophagy by Reactive Oxygen Species (ROS): Implications for Cancer Progression and Treatment (2009, neutral): “Under these conditions, gene expression is altered to facilitate adaptation and survival in hypoxia (89).”
- Hypoxia-induced lysyl oxidase is a critical mediator of bone marrow cell recruitment to form the pre-metastatic niche (2009, background): “Increased metastases, enhanced tumor progression, and decreased patient survival have been associated with primary tumors that contain large numbers of poorly oxygenated (hypoxic) tumor cells (Cairns et al., 2003; Hockel and Vaupel, 2001; Pouyssegur et al., 2006).”
- Tumor microenvironment abnormalities: Causes, consequences, and strategies to normalize (2007, background): “There are at least two sources of Hþ ions in tumors—lactic acid and carbonic acid [Helmlinger et al., 2002; Pouyssegur et al., 2006].”
- Oxygen in stem cell biology: a critical component of the stem cell niche. (2010, background): “Hypoxic microenvironments within tumors have long been appreciated to be a product of aberrant vasculature and due to a rapidly dividing tumor mass that outstrips its vascular supply (Figure 2) (Carmeliet and Jain, 2000; Pouyssegur et al., 2006).”