Hypoxia, Clonal Selection, and the Role of HIF-1 in Tumor Progression

By G. Semenza. Critical reviews in biochemistry and molecular biology, 2000

688 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/2004483b61ac6c1d82dca1a1a6b693fd1f89d5e2

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Citations in the corpus

HIF-1 and human disease: one highly involved factor. (2000, background): “Novel therapeutic strategies designed to exploit the decreased O2 concentration or increased HIF-1 expression within tumors are presently being evaluated (Dachs et al. 1997; Brown 2000; Shibata et al. 2000).”
Defining the Role of Hypoxia-Inducible Factor 1 in Cancer Biology and Therapeutics (2009, neutral): “Semenza GL. (2000). Hypoxia, clonal selection, and the role of HIF-1 in tumor progression. Crit Rev Biochem Mol Biol 35: 71–103. Semenza GL. (2009a). Oxygen homeostasis. Systems Biol Med (doi:10.1002/wsbm.69). Semenza GL. (2009b). Regulation of cancer cell metabolism by hypoxia-inducible factor 1.”
Causes and Consequences of Increased Glucose Metabolism of Cancers (2008, background): “A consequence of hypoxic selection may be increased glucose consumption through stabilization of hypoxiainducible factor (HIF) 1a (HIF-1a) (30).”
Hypoxia-inducible factor-1-dependent regulation of the multidrug resistance (MDR1) gene. (2002, background): “Because of the combination of tissue mass and the particularly high rate of glycolysis in tumor cells (termed the Warburg effect), hypoxia is considered a property of many tumor types (6).”
IL‐1β mediated up‐regulation of HIF‐lα via an NFkB/COX‐2 pathway identifies HIF‐1 as a critical link between inflammation and oncogenesis (2003, background): “HIF-1 regulated gene products play essential roles in tumor progression by promotion of cell proliferation, invasion, and metastasis (24).”
Nanomedicine therapeutic approaches to overcome cancer drug resistance (2013, background): “These hypoxic cells often revert to aerobic metabolism for the production of ATP (the Warburg effect) [73,74] to maintain enough energy to continue to thrive.”
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 ].”
The Endoplasmic Reticulum: Folding, Calcium Homeostasis, Signaling, and Redox Control (2006, neutral): “These findings highlight that different members of the PDI-family can complement each other, at least to a certain degree, and therefore might fulfill similar biological functions.”
Functional classification of interferon‐stimulated genes identified using microarrays (2001, background): “HIF1a is overexpressed in some cancer types, where it is thought to be important for protecting the tumor cells from anoxia and stimulation of angiogenesis into the tumor [70].”
The role of hypoxia in cancer progression, angiogenesis, metastasis, and resistance to therapy (2015, background): “and the existing vasculature increases, hampering oxygen diffusion and creating even more hypoxic milieu.(2,3) It is generally accepted that the oxygen level in hypoxic tumor”
Expression of hypoxia-inducible cell-surface transmembrane carbonic anhydrases in human cancer. (2001, neutral): “Head and Neck not done SCC-35(2), SQ-20B(2) Lung non-small cell carcinoma NCI-H1264(1), NCIJ460(3), NCI-H1944(1), NCI-H157(1), NCIH28(1), A549(10), EKVX(1), HOP62(1), HOP92(2) NCI-H1373(1), NCIH1264(1), NCIH1466(1), NCI-H460(1), NCIH727(2) NCI-H1693, NCI-H838, NCI-H1299, NCIH226, NCI-H23, NCIH522”
Hypoxia in cartilage: HIF-1alpha is essential for chondrocyte growth arrest and survival. (2001, background): “The putative role of HIF-1 as survival factor has recently become the focus of controversy (Maxwell et al. 1997; Carmeliet et al. 1998; Ryan et al. 1998, 2000; Wood et al. 1998; Kung et al. 2000; Semenza 2000b).”
The tumour microenvironment as a target for chemoprevention (2007, background): “Although HIF1 contributes to an invasive, lethal phenotype in the cancer cel”