Targeting classical but not neurogenic inflammation reduces peritumoral oedema in secondary brain tumours

Lewis, Kate M.; Harford-Wright, Elizabeth; Vink, Robert; Ghabriel, M. N.

doi:10.1016/j.jneuroim.2012.06.001

Cited by 7 publications

(10 citation statements)

References 58 publications

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“…Besides Emend having a much greater binding capacity for the NK1 receptor because of its lipophilicity, a plausible explanation for this may be that this cell line does not secrete SP into the culture medium in vitro and is thus unable to exert a stimulatory autocrine effect on the NK1-expressing cells. It has been reported previously that Walker 256 breast carcinoma cells do not express SP in this model when injected directly into the brain [57]. However, tumours induced from this cell line do show increased SP immunoreactivity in the peritumoral neuropil in two different models of metastatic brain tumours [57,81].…”

Section: Discussionmentioning

confidence: 47%

“…These tumours showed a prominent cystic component and extensive central necrosis and haemorrhage, as described previously in the literature [57]. The model used in the current study is advantageous in that it is used in immune-competent animals, thus allowing the study of the interaction of tumour cells with the host microenvironment and immune system.…”

Section: Discussionmentioning

confidence: 53%

“…It has been reported previously that Walker 256 breast carcinoma cells do not express SP in this model when injected directly into the brain [57]. However, tumours induced from this cell line do show increased SP immunoreactivity in the peritumoral neuropil in two different models of metastatic brain tumours [57,81]. Thus, it is plausible that exogenous SP from the brain microenvironment may exert a stimulatory effect on these tumour cells in vivo.…”

Section: Discussionmentioning

confidence: 56%

“…This is likely to be because of impaired accumulation of fluid, as found in previous studies [57], rather than a decrease in the growth of the tumour cells. Evidence of this is the absence of change in tumour cell replication and apoptosis with dexamethasone treatment in the current study.…”

Section: Discussionmentioning

confidence: 58%

“…Briefly, tumour cells were implanted into the striatum at coordinates 0.5 mm anterior and 3 mm lateral to the bregma over the right hemisphere, under isoflurane inhalation general anaesthesia at 3%, as was described previously [57].…”

Section: Tumour Inoculationmentioning

confidence: 99%

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NK1 receptor antagonists and dexamethasone as anticancer agents in vitro and in a model of brain tumours secondary to breast cancer

et al. 2013

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Emend, an NK1 antagonist, and dexamethasone are used to treat complications associated with metastatic brain tumours and their treatment. It has been suggested that these agents exert anticancer effects apart from their current use. The effects of the NK1 antagonists, Emend and N-acetyl-L-tryptophan, and dexamethasone on tumour growth were investigated in vitro and in vivo at clinically relevant doses. For animal experiments, a stereotaxic injection model of Walker 256 rat breast carcinoma cells into the striatum of Wistar rats was used. Emend treatment led to a decrease in tumour cell viability in vitro, although this effect was not replicated by N-acetyl-L-tryptophan. Dexamethasone did not decrease tumour cell viability in vitro but decreased tumour volume in vivo, likely to be through a reduction in tumour oedema, as indicated by the increase in tumour cell density. None of the agents investigated altered tumour cell replication or apoptosis in vivo. Inoculated animals showed increased glial fibrillary acidic protein and ionized calcium-binding adapter molecule 1 immunoreactivity indicative of astrocytes and microglia in the peritumoral area, whereas treatment with Emend and dexamethasone reduced the labelling for both glial cells. These results do not support the hypothesis that NK1 antagonists or dexamethasone exert a cytotoxic action on tumour cells, although these conclusions may be specific to this model and cell line.

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Section: Discussionmentioning

confidence: 47%

Section: Discussionmentioning

confidence: 53%