Control of cell proliferation in human glioma by glucocorticoids

Freshney, R. Ian; Sherry, A. Dean; Hassanzadah, M; Freshney, M; Crilly, Peter J.; Morgan, D

doi:10.1038/bjc.1980.161

Cited by 45 publications

(26 citation statements)

References 10 publications

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“…On the contrary, lower DEX concentrations (1.6 to 1000 nM), resembling more plasma levels of patients receiving antiemetic GC therapy, 27 increased the proliferation of GR-positive but not of -negative cells. 28 Langeveld et al 29 investigated the effect of DEX on the proliferation of seven human glioma cell lines. In two of them DEX consistently stimulated the proliferation which may be associated with a relatively high expression level of GR.…”

Section: The Effect Of Gcs Is Dependent On Gr Levelsmentioning

confidence: 99%

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Mattern¹,

Büchler²,

Herr³

2007

Cancer Biology & Therapy

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ABBrevIAtIons DEX ABstrActGlucocorticoids have been widely used as cotreatment for patients with cancer due to potent pro-apoptotic properties in lymphoid cells, reduction of nausea and diminishing acute toxicity on normal tissue. There are now data from preclinical and, to some extent, clinical studies, demonstrating that these medicaments are highly suspicious to induce therapy resistance in the majority of malignant solid tumors-irrespective of tumor origin and the nature of specific anticancer drugs or irradiation used for treatment. Despite these huge amounts of data, the underlying mechanisms of cell type-specific signaling by these steroid hormones are just beginning to be described. This review summarizes our present understanding of a relationship between glucocorticoid-induced reversible cell cycle arrest and therapy resistance in solid tumors. We give a summary of our current knowledge of decreased proliferation rates in response to glucocorticoid pre and combination treatment which are suspicious to be involved not only in protection of normal tissues, but also in protection of solid tumors from cytotoxic effects of anticancer agents. The inhibition of cell cycle progression by pretreatment with GCs may be crucially involved in switching the balance of several interacting pathways to survival upon treatment with GCs.

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Section: The Effect Of Gcs Is Dependent On Gr Levelsmentioning

confidence: 99%

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Mattern¹,

Büchler²,

Herr³

2007

Cancer Biology & Therapy

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“…Cell cultures in the plateau growth phase were established as described by Freshney et al (1980) and treated similarly. The cultures were incubated at 37°C with 5% carbon dioxide for 44 h (one doubling time for exponentially growing cells).…”

Section: Clonogenic Assaymentioning

confidence: 99%

Differential cytotoxicity of [123I]IUdR, [125I]IUdR and [131I]IUdR to human glioma cells in monolayer or spheroid culture: effect of proliferative heterogeneity and radiation cross-fire

Neshasteh-Riz

Mairs²,

Angerson³

et al. 1998

Br J Cancer

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Radioiodinated iododeoxyuridine (IUdR) is a novel, cycle-specific agent that has potential for the treatment of residual malignant glioma after surgery. As only cells in S-phase incorporate IUdR into DNA, a major limitation to this therapy is likely to be proliferative heterogeneity of the tumour cell population. Using a clonogenic end point, we have compared the toxicities of three radioiodoanalogues of IUdR--[123I]IUdR, [125I]IUdR and [131I]IUdR--to the human glioma cell line UVW, cultured as monolayers in the exponential and the plateau phase of growth and as multicellular spheroids. Monolayers treated in the exponential growth phase were most efficiently sterilized by [125I]IUdR (concentration resulting in 37% survival (C37) = 2.36 kBq ml(-1)), while [123I]IUdR and [131I]IUdR were less effective eradicators of clonogens (C37 = 9.75 and 18.9 kBq ml(-1) respectively). Plateau-phase monolayer cultures were marginally more susceptible to treatment with [123I]IUdR and [125I]IUdR (40% clonogenic survival) than [131I]IUdR (60% clonogenic survival). In cells derived from glioma spheroids, both [125I]IUdR and [123I]IUdR were again more effective than [131I]IUdR at concentrations up to and including 20 kBq ml(-1). However, the survival curve for [131I]IUdR crossed the curves for the other agents, resulting in lower survival for [131I]IUdR than [123I]IUdR and [125I]IUdR at concentrations of 40 kBq ml(-1) and higher, the clonogenic survival values at 100 kBq ml(-1) were 13%, 45% and 28% respectively. It was concluded that IUdR incorporating the Auger electron emitters 123I and 125I killed only cells that were in S-phase during the period of incubation with the radiopharmaceutical, whereas the superior toxicity to clonogenic cells in spheroids of [131I]IUdR at higher concentration was due to cross-fire beta-irradiation. These findings suggest that [131I]IUdR or combinations of [131I]IUdR and [123I]IUdR or [125I]IUdR may be more effective than Auger electron emitters alone for the treatment of residual glioma, if proliferative heterogeneity exists.

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“…Cell density in glioma culture markedly affects the response to glucocorticoids as first demonstrated by Freshney et al [26]. Using a primary culture derived from a human anaplastic astrocytoma in a 20% serum medium, they found that low-density cultures (below 50 cells per colony) proliferate in response to betamethasone at 25 µM, whilst cell proliferation is inhibited at higher cell density.…”

Section: Glioma Cell Proliferation: In Vitro Studiesmentioning

confidence: 84%

Treating gliomas with glucocorticoids: from bedside to bench

et al. 2006

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Glucocorticoids are used in the treatment of gliomas to decrease tumour-associated oedema and to reduce the risk of acute encephalopathy associated with radiotherapy. However, the mechanisms by which glucocorticoids work are still largely unknown. In this paper, we survey the experimental and clinical evidence for the effects of glucocorticoids on tumour cell proliferation, apoptosis and sensitivity to chemotherapy, angiogenesis and vascular permeability. We then review current guidelines on the choice of molecule, dose and duration of glucocorticoid treatment for gliomas.

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Control of cell proliferation in human glioma by glucocorticoids

Cited by 45 publications

References 10 publications

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Cell Cycle Arrest by Glucocorticoids May Protect Normal Tissue and Solid Tumors from Cancer Therapy

Differential cytotoxicity of [123I]IUdR, [125I]IUdR and [131I]IUdR to human glioma cells in monolayer or spheroid culture: effect of proliferative heterogeneity and radiation cross-fire

Treating gliomas with glucocorticoids: from bedside to bench

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