Health

Breast Cancer: Does Stress Fuel Its Spread?

New research in mouse models shows that stress hormones can help breast cancer grow, spread and diversify, making it difficult to treat. While breast cancer is also one of the most treatable cancers, once it metastasizes – that is, grows and spreads – it can quickly diversify.

When cancerous tumors are so diverse, it can be difficult for doctors to apply the right type of treatment, since therapy that works for one type of tumor may not have an effect on another.

Previous research that Health Consultations covered suggests that exposure to chronic (long-term) stress is a contributing factor to the growth of cancer cells in breast cancer.

Now, a new study by a team from the University of Basel and the University Hospital of Basel in Switzerland has uncovered additional evidence suggesting that stress can fuel the spread of breast cancer tumors, perhaps also supporting their diversification.

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The study, which the team conducted in a mouse model, found that stress hormones support breast cancer metastasis. Scientists also claim that stress hormone derivatives in certain anti-inflammatory treatments may actually “disarm” chemotherapy agents. Lead author Prof. Mohamed Bentires-Alj and his colleagues explain their findings in a new study paper appearing in the journal Nature.

“Intra-patient tumor heterogeneity is an obstacle to treatment,” they note, “as it causes divergence in diagnostic markers between primary tumors and paired metastases that can lead to inappropriate treatment.” They say new research must find a way to address this mismatch.

The intricate mechanisms at play

Professor Bentires-Alj and the team worked with a mouse model of breast cancer. They began by studying how different original tumors were from metastatic tumors by assessing the specific activity of genes.

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The researchers note that in metastatic tumors, a type of receptor called “glucocorticoid receptors” was very active. These receptors bind to stress hormones, including cortisol. Additionally, the team found that the metastatic mice had higher levels of cortisol and another stress hormone, corticosterone, compared to rodents in which the cancer had not yet spread.

The researchers also observed that when these stress hormones are highly present, they activate glucocorticoid receptors. This, they explain, triggers the spread of cancer cells and supports their diversification.

Additionally, Professor Bentires-Alj and his colleagues observed that glucocorticoid receptors also interact with synthetic derivatives of cortisol, for example dexamethasone, which doctors use as anti-inflammatories to treat some of the side effects of chemotherapy.

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This interaction, however, appears to interfere with some chemotherapeutic agents, neutralizing their effects. This is what happens with the chemotherapy drug paclitaxel, for example; it becomes less effective in the presence of dexamethasone.

Based on these results, scientists advise doctors to be careful when prescribing glucocorticoid hormones for breast cancer treatment, in case they end up doing more harm than good.

Professor Bentires-Alj and his team also explain that, at the same time, inhibiting glucocorticoid receptors could be a useful new approach in the treatment of breast cancer. “Tumor heterogeneity is a serious obstacle to therapy,” explains Prof. Bentires-Alj.

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