Breast cancer: Does stress fuel its spread?

stressed woman at her desk

By Maria Cohut 

Fact checked by Jasmin Collier
New research in mouse models
shows that stress hormones can help breast cancer grow, spread, and diversify,
which makes it harder to treat.

Breast cancer is one of the
most common types of cancer.
In the United States, there
were about 266,120 new cases last year, according to the National Cancer
Although breast cancer is also
one of the most treatable types of cancer, once it metastasizes — that is,
grows and spreads — it can be quick to diversify.
When cancer tumors are so
diverse, doctors may find it hard to apply the right kind of treatment, as the
therapy that works for one type of tumor may have no effect on another.
Previous research that Medical
News Today covered suggests that exposure to chronic (long-term) stress is one
factor that contributes to cancer cell growth in breast cancer.
Now, a new study conducted by
a team from the University of Basel and the University Hospital of Basel in
Switzerland has uncovered further evidence to suggest that stress can fuel the
spread of breast cancer tumors, perhaps also supporting their diversification.
The study — which the team
carried out in a mouse model — found that stress hormones support breast cancer
metastasis. The scientists also state that the stress hormone derivatives
present in certain anti-inflammatory treatments could actually
“disarm” chemotherapy agents.
Lead author Prof. Mohamed
Bentires-Alj and colleagues explain their findings in a new study paper that
appears 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 matched metastases
that may lead to inadequate treatment.” They say that new research needs
to find a way to address this mismatch.
intricate mechanisms at play

Prof. Bentires-Alj and team
worked with a mouse model of breast cancer. They started by studying how
different the original tumors were from metastatic tumors by assessing specific
gene activity.
The researchers note that in
metastatic tumors, a type of receptor called “glucocorticoid
receptors” were very active. These receptors bind to stress hormones,
including cortisol.
Also, the team found that mice
with metastases had higher levels of cortisol and another stress hormone,
corticosterone, than rodents in which cancer had not yet spread.
The investigators also
observed that when these stress hormones are highly present, they activate
glucocorticoid receptors. This, they explain, triggers cancer cells’ spread and
supports their diversification.
Furthermore, Prof.
Bentires-Alj and colleagues saw that glucocorticoid receptors also interact
with synthetic derivatives of cortisol — for example, dexamethasone — which
doctors use as anti-inflammatories to address some of chemotherapy’s side effects.
This interaction, however,
seems to interfere with some chemotherapeutic agents, neutralizing their
effects. This is what happens with the chemotherapy drug paclitaxel, for
instance; it becomes less effective in the presence of dexamethasone.
Based on these results, the
scientists advise physicians to use caution in prescribing glucocorticoid
hormones for the treatment of breast cancer, in case they end up doing more
harm than good.
Prof. Bentires-Alj and team
also explain that by the same token, inhibiting glucocorticoid receptors could
be a helpful new approach in breast cancer treatment. “Tumor heterogeneity
is a serious hurdle for therapy,” explains Prof. Bentires-Alj.
“These findings highlight
the importance of stress management in patients — and especially those with
triple-negative breast cancer. Moderate exercise and relaxation techniques have
been shown to correlate with enhanced quality of life and greater survival in
Mohamed Bentires-Alj
Kayode Ojo
Kayode Emmanuel Ojo is the Co-Founder and Managing Director at SHEFFA Limited. He is presently studying Computer Science at the National Open University, Victoria Island, Lagos.