Comparative studies of a near-tetraploid and a near-diploid line of Ehrlich's ascites tumor propagated in vivo and in vitro I. Metabolism and growth

B, Biczowa; Kieler, J; Moore, J.L.

doi:10.1016/0014-2964(68)90071-6

Cited by 16 publications

(8 citation statements)

References 15 publications

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“…Despite the old tenet that cancer can grow at the expence of glycolysis only (Warburg, 19301, tumor cell proliferation actually depends, both in vivo and in vitro, on oxygen supply (Barach and Bickermann, 1954;Tannock, 1968;Tannock, 1969; Biczowa et al, 1968;Harris et al, 1970;Gregg et al, 1968;Gregg, 1972; Gosalves et al, 1972;Figueras and Gosalves, 1973;,Gullino, 1975).…”

mentioning

confidence: 99%

The role of respiration in tumor cell transition from the noncycling to the cycling state

Olivotto

Paoletti

1981

Journal Cellular Physiology

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Resting Yoshida AH130 hepatoma cells, harvested at the plateau of tumor development in vivo, were recruited into the cycling state following transfer to an in vitro system whereby these cells were incubated in the autologous ascites plasma diluted with buffered saline and enriched with glucose. In this system, cell recruitment into the phase of DNA synthesis (S phase) strictly depends on the activity of the respiratory chain and is abolished by anaerobiosis as well as by antimycin A, although the intracellular levels of ATP and the rate of protein synthesis are practically unaffected by these treatments. Furthermore, 2,4-dinitrophenol, at concentrations which uncouple the respiratory phosphorylation and hence enhance both glycolysis and oxygen consumption, does not hinder cell promotion into S phase. Thus, the absolute respiration dependence of cycling resumption by resting ascites cells does not seem to rely on respiratory ATP supply, but rather is linked to the electron flow through the respiratory chain.

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confidence: 99%

The role of respiration in tumor cell transition from the noncycling to the cycling state

Olivotto

Paoletti

1981

Journal Cellular Physiology

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“…These differences may be related to the chromosomal changes mentioned above, but this assumption is not supported by studies of the doubling time in vivo and iii vitvo (Biczowa et at., 1967) which showed n o significant differences between the two cell lines, either in vitro or in vivo. I n both cell lines the doubling time was somewhat longer in vitro than in vivo.…”

Section: Discussionmentioning

confidence: 93%

“…In the present work six murine cell lines of non-malignant and malignant origin were studied. The tumor-producing capacity of these six cell lines, as well as their cytological, chromosomal, metabolic and growth characteristics will be reported elsewhere (Biczowa et a/., 1967;Kieler et al, 1967;.…”

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confidence: 99%

Autoradiographic analysis of the proliferation in vitro of six murine cell lines of non‐malignant or malignant origin

Sawicki

Kieler

Briand

1967

Intl Journal of Cancer

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“…Metabolic alterations are commonly observed in aneuploid and polyploid cells [ 180 , 213 , 214 , 215 , 216 , 217 , 218 ]. Both aneuploidy and polyploidy lead to increased glycolytic activity and lactate production [ 215 , 217 , 218 , 219 , 220 ]. Metabolic byproducts, such as lactate, are thought to be a major contributor to tumor acidification [ 221 ].…”

Section: The Role Of Aneuploidy and Polyploidy In Tumor Niche Constructionmentioning

confidence: 99%

Karyotype Aberrations in Action: The Evolution of Cancer Genomes and the Tumor Microenvironment

Baudoin

Bloomfield

2021

Genes

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Cancer is a disease of cellular evolution. For this cellular evolution to take place, a population of cells must contain functional heterogeneity and an assessment of this heterogeneity in the form of natural selection. Cancer cells from advanced malignancies are genomically and functionally very different compared to the healthy cells from which they evolved. Genomic alterations include aneuploidy (numerical and structural changes in chromosome content) and polyploidy (e.g., whole genome doubling), which can have considerable effects on cell physiology and phenotype. Likewise, conditions in the tumor microenvironment are spatially heterogeneous and vastly different than in healthy tissues, resulting in a number of environmental niches that play important roles in driving the evolution of tumor cells. While a number of studies have documented abnormal conditions of the tumor microenvironment and the cellular consequences of aneuploidy and polyploidy, a thorough overview of the interplay between karyotypically abnormal cells and the tissue and tumor microenvironments is not available. Here, we examine the evidence for how this interaction may unfold during tumor evolution. We describe a bidirectional interplay in which aneuploid and polyploid cells alter and shape the microenvironment in which they and their progeny reside; in turn, this microenvironment modulates the rate of genesis for new karyotype aberrations and selects for cells that are most fit under a given condition. We conclude by discussing the importance of this interaction for tumor evolution and the possibility of leveraging our understanding of this interplay for cancer therapy.

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Comparative studies of a near-tetraploid and a near-diploid line of Ehrlich's ascites tumor propagated in vivo and in vitro I. Metabolism and growth

Cited by 16 publications

References 15 publications

The role of respiration in tumor cell transition from the noncycling to the cycling state

The role of respiration in tumor cell transition from the noncycling to the cycling state

Autoradiographic analysis of the proliferation in vitro of six murine cell lines of non‐malignant or malignant origin

Karyotype Aberrations in Action: The Evolution of Cancer Genomes and the Tumor Microenvironment

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