Modulation of tumour cell colony growth in soft agar by oxygen and its mechanism

Gupta, V. D.; Eberle, R.

doi:10.1038/bjc.1984.93

Cited by 19 publications

(6 citation statements)

References 27 publications

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“…In fact, this has also been shown previously for the extra-embryonic tissue of the early chick embryo [12]. In addition, tumour cell proliferation in vivo [33] as well as in vitro has been demonstrated to be enhanced by hypoxia [34].…”

Section: Discussionsupporting

confidence: 50%

Hypoxia-Induced Tumour Cell Migration in an in vivo Chicken Model

et al. 2000

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To investigate the relationship between hypoxia, neovascularisation and tumour cell spread, experiments on the area vasculosa of the early chick embryo under different oxygen concentrations were performed in vivo. Human glioblastoma cells (U-138MG) were inoculated onto the area vasculosa and the fertilised eggs were incubated under conditions of normoxia or hypoxia. For evaluation, we performed in vivo video-microscopy of the area vasculosa and determination of microvessel density (MVD), as well as a histological examination of the fixed specimen. Under hypoxia, MVD was significantly increased compared to normoxic conditions. Only under hypoxic conditions was tumour cell spread found outside the main tumour mass and within the vessels, at times followed by the subsequent development of secondary tumour cell bulks on the area vasculosa. These data lead to the conclusion that hypoxia can stimulate tumour cell migration in this in vivo model.

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Section: Discussionsupporting

confidence: 50%

Hypoxia-Induced Tumour Cell Migration in an in vivo Chicken Model

et al. 2000

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“…Although it has been generally accepted that factors in the cellular microenvironment, such as oxygen and glucose concentration, may influence the metabolism and proliferation of cells (and vice versa) (Ceccarini & Eagle, 1971;Balin et al, 1976;Gupta & Eberle, 1984). However, investigations using spherical cellular aggregates, i.e.…”

mentioning

confidence: 99%

Influence of glucose and oxygen supply conditions on the oxygenation of multicellular spheroids

Mueller‐Klieser¹,

Freyer²,

Sutherland³

1986

Br J Cancer

165

133

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Summary The interrelationship among external 02 and glucose supply, oxygenation status, oxygen consumption rates and cellular viability in tumour microregions was studied using the multicellular spheroid model. For chronic exposure to various supply conditions multicellular EMT6/Ro spheroids were cultured in stirred media equilibrated either with 20% (v/v) or 5% (v/v) oxygen and containing four different glucose concentrations ranging from 0.8mm to 16.5mM. Spheroids were investigated using histology and 02-sensitive microelectrodes for measuring oxygen tension (PO ) values. A chronic decrease of the glucose concentration in the medium is associated with a substantial reduction in the thickness of the viable rim of cells and with a persistent increase in the cellular respiration rate. In general, both viable rim size and respiration are decreased through restriction of 02 supply during spheroid growth at a given external glucose concentration. The 02 consumption in spheroids appears to decrease with increasing spheroid size under most of the growth conditions investigated. These findings provide evidence for a large capacity of the spheroid cells to chronically adapt their metabolic rates to different supply situations. The experimental data and theoretical considerations indicate that necrosis may develop in the centre of these spheroids due to the lack of 02 and/or glucose under some of the growth conditions, but central necrosis can also occur despite sufficient 02 and glucose supply. Consequently, cellular metabolism and viability in tumour microregions may not be determined by the diffusion limitation of O2 or specific substrates alone, such as glucose, but may be influenced by a complex interaction of factors in the micromilieu the majority of which are still unknown.

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“…Here, the initiated cells proliferate to fill the void left by the removal of their normal counterpart. Gupta et al (1984) and Vallyathan (1998) demonstrated increased ROS activity associated with carcinogenesis. Cellular defences may alter the level of toxicity caused by ROS and play a preventative role against carcinogenesis, according to Kemsler et al (1984) and Oberley et al (1997).…”

Section: Discussionmentioning

confidence: 97%