Breast cancer metastasis is shown to be associated with increased levels of stress hormones in a mouse study reported in Nature this week. In addition, a synthetic stress hormone derivative (used to combat the side effects of chemotherapy) is found to reduce the efficiency of a chemotherapy drug in mice. If these findings can be translated to humans, they may have implications for treatment choices for patients with breast cancer.
The success of cancer treatment is sometimes hindered by changes that occur between tumours and metastases as the disease progresses, which alter the profiles of diagnostic markers and affect responses to therapy. To explore this variation, Mohamed Bentires-Alj and colleagues profile the activity of genes in tumours and metastases in a mouse model of breast cancer. They find metastases have increased glucocorticoid receptor activity, which seems to contribute to the spread of cancer and shortens survival compared with control mice. Concentrations of cortisol or corticosterone were higher in mice with metastases than in those with no metastases, and the authors show that increased levels of these stress hormones activate the glucocorticoid receptors.
Dexamethasone is a synthetic glucocorticoid that is used to treat symptoms related to advanced cancer and the adverse effects of chemotherapy. Bentires-Alj and colleagues show that in mice with metastatic cells, treatment with paclitaxel (a chemotherapy drug) and dexamethasone resulted in reduced survival compared with treatment with paclitaxel alone. These findings suggest that caution should be taken used prescribing glucocorticoids to patients with breast cancer.
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