HIF-1 and tumor progression: pathophysiology and therapeutics.

By G. Semenza. Trends in Molecular Medicine, 2002

1,062 citations recorded by the source corpus.

Subfields: Cancer Research, Hepatology, Oncology

View Paper: https://www.semanticscholar.org/paper/d43c1c977107a35a7c03b27a1609fcbd5f4820db

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. Craig B. Thompson
4. P. Vaupel
5. Ping Gao
6. M. C. Simon
7. Jung-whan Kim
8. Eyal Gottlieb

In Hepatology

1. P. Vaupel
2. Eyal Gottlieb
3. Georgina N. Masoud
4. Wei Li
5. Ian Tomlinson
6. A. Mayer

In Oncology

1. A. Sica
2. A. Mantovani
3. P. Vaupel
4. Subhra K. Biswas
5. Eyal Gottlieb
6. Georgina N. Masoud
7. Wei Li
8. G. Semenza

Citations in the corpus

• Regulation of the Chemokine Receptor CXCR4 by Hypoxia (2003, background): “Expression of CXCR4 and VEGF mRNAs was tested by real-time PCR in the renal cancer cell line 786.0 (VHL mutated) and WT2 (in which a WT VHL has been reintroduced).”
• Direct regulation of TWIST by HIF-1α promotes metastasis (2008, background): “Intratumoural hypoxia, followed by stabilization and activation of the HIF-1α transcription complex, is one of the most important mechanisms that promotes metastasis and thereby, increases tumour aggressivenes”
• Sirtuin 1 modulates cellular responses to hypoxia by deacetylating hypoxia-inducible factor 1alpha. (2010, background): “In view of the contribution made by HIF-1a to tumor development (Semenza, 2002), we surmised that SIRT1 might be involved in the modulation of HIF-1a-mediated tumor progression.”
• 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): “The proliferation of cancer cells in a three-dimensional multicellular cluster, however, is limited by diffusion of oxygen and nutrients, such that a phase of metabolic adaptation must be endured via the activation of hypoxia-inducible factors (HIFs) and, in particular, HIF-1 (6, 25, 72).”
• Chemokine receptor CXCR4 downregulated by von Hippel–Lindau tumour suppressor pVHL (2003, background): “The best characterized function of pVHL is as a recognition subunit of an E3 ubiquitin protein ligase complex that targets the α-subunits of the DNA-binding transcription factor HIF (ref”
• Mitochondrial tumour suppressors: a genetic and biochemical update (2005, background): “HIF is a heterodimeric complex comprised of HIFα and HIFβ subunit”
• Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase. (2005, background): “This posttranslational modification is catalyzed by the HIF-(cid:1) -prolyl HIF transcription factor, a heterodimer comprised of HIF-(cid:1) and HIF-(cid:2) subunits (Pugh and Ratcliffe, 2003; Semenza, 2002).”
• HIF-1α pathway: role, regulation and intervention for cancer therapy (2015, background): “PI3K inhibitors LY294002 (5) and wortmannin (6) have been recognized for their anti-HIF activity.”
• The role of hypoxia-induced factors in tumor progression. (2004, background): “However, for hypoxic tumor cells, these adaptive responses can additionally favor cell survival, further expansion, and metastasis, as outlined below [ 19-26 ].”