Hypoxia-inducible Factor-1α Is a Positive Factor in Solid Tumor Growth

By H. E. Ryan, M. Poloni, W. McNulty, D. Elson, M. Gassmann, J. Arbeit, Richard J. Johnson. 2000

708 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/2c32c52e6ee3552b12cc7f8d225eeb4167b700ca

How researchers see this paper

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

1. R. Kaufman
2. D. Ron
3. G. Semenza
4. W. Kaelin
5. H. Harding
6. Douglas R. Green
7. Cheng-Jun Hu
8. John D. Gordan

Citations in the corpus

• HIF1α–dependent glycolytic pathway orchestrates a metabolic checkpoint for the differentiation of TH17 and Treg cells (2011, methodology): “To investigate the role of HIF1 in T cell differentiation, we crossed mice carrying a conditional HIF1 allele (HIF1flox/flox; Ryan et al., 2000) with CD4-Cre transgenic mice to delete the floxed HIF1 allele specifically in T cells (called HIF1–/– mice thereafter).”
• Hypoxia-Inducible Factor-1 (HIF-1) (2006, unknown): “In addition, injection of HIF-1 (or HIF-1 ) positive and deficient cells to immunocompromised mice revealed that HIF-1 is a positive factor to tumorigenesis (Maxwell et al., 1997; Ryan et al., 2000).”
• ER stress‐regulated translation increases tolerance to extreme hypoxia and promotes tumor growth (2005, background): “Loss-of- function studies indicate that, in most cases, HIF-1 promotes overall tumor growth (Maxwell et al, 1997; Ryan et al, 2000).”
• Vascular Endothelial Growth Factor and Angiogenesis (2004, background): “This response seems to depend on Hypoxia Regulated/ Responsive Element/Enhancer sequences in the 5 and 3 regions of the VEGF-A gene (Dachs and Tozer, 2000; Ryan et al., 2000; Tsuzuki et al., 2000).”
• Hypoxia in cartilage: HIF-1alpha is essential for chondrocyte growth arrest and survival. (2001, methodology): “Analysis of EF-5 distribution; whole-mount -galactosidase and Alizarin Red S stainings To study EF-5 distribution, pregnant females were injected with 10 mM EF5 at 1% of body weight; staining was performed as described previously (Ryan et al. 1998, 2000).”
• Targeting HIF-1 for cancer therapy (2003, background): “In these cells, HIF-1α deficiency was associated with reduced tumour mass 16–18 days after injection, although angiogenesis was not affecte”
• The role of hypoxia-induced factors in tumor progression. (2004, background): “had fewer blood vessels and impaired hemodynamics within the tumor mass, and further, that HIF-1α knockout mice died in utero with a complete lack of cephalic vasculature as a consequence of disrupted angiogenesis [ 3 , 33].”
• Hypoxia-Induced Autophagy Is Mediated through Hypoxia-Inducible Factor Induction of BNIP3 and BNIP3L via Their BH3 Domains (2009, methodology): “Cell culture. DLD1, LS174, MCF7, PC3, 786-O, HIF/ and HIF/ MEF ( 29 ), and CCL39 cells were grown in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco-BRL) supplemented with 5 or 10% inactivated fetal bovine serum (FBS) as appropriate.”
• Inhibition of HIF2α Is Sufficient to Suppress pVHL-Defective Tumor Growth (2003, background): “Most of the work performed so far with respect to the oncogenic effects of HIF has focused exclusively on HIF1a, where both prooncogenic and antioncogenic effects have been reported (Maxwell et al. 1997; Carmeliet et al. 1998; Ryan et al. 1998, 2000; Hopfl et al. 2002).”
• The transcription factor Myc controls metabolic reprogramming upon T lymphocyte activation (2011, methodology): “We generated a mouse model carrying a conditional HIF1α allele (Hif1a flox/flox) and a tamoxifen-inducible Cre recombinase (CreERT2) transgene (de Luca et al., 2005; Ryan et al., 2000) to delete HIF1α flox alleles in an acute manner.”
• Hypoxia — a key regulatory factor in tumour growth (2002, background): “HIF-1 also seems to interact with the oncogenic RAS pathway, because loss of HIF-1α negatively affects tumour growth in HRAS-transformed cell line”
• Inhibition of HIF is necessary for tumor suppression by the von Hippel-Lindau protein. (2002, background): “Additional genetic alterin model systems as does pharmacological inhibition of some ations are presumably required for conversion to a frank renal of its targets such as VEGF and TGF /EGFR (Kung et al., 2000; carcinoma. Of note, several studies have linked TGF to renal Maxwell et al., 1997, 1998; Ry”