Epigenetics is taking on the problems of disease and aging and seeking to turn back the aging clock. The heart of it is understanding and then controlling, gene expression by learning what can block or facilitate that expression.
It’s still early stages in many respects, but you can be a part of it through epigenetic testing.
In this article:
Why You Should Give Epigenetic Diagnostic Tests a Try
How Does Pregnancy Impact Breast Cells?
In most mammals, pregnancy sets off a series of changes in breast cells in preparation for lactation. During gestation, a pregnant woman’s breast tissues begin to change.
This change includes the expansion of the epithelial cells and ductal structures. This allows the breast to accommodate milk droplets throughout gestation.
Once they stop lactating, the mammary glands go back to a nonsecretory state, but the breast tissue organization remains mostly the same and does not go back to its pre-pregnancy state.
But apart from breastfeeding, do these changes offer any other benefits? Research shows that women who get pregnant before they’re 25 years of age are less likely to develop breast cancer.
But how does pregnancy protect women from breast cancer? Dr. Camila O. dos Santos and her research team published a recent study that sheds some light on this.
What Is the Impact of Pregnancy on DNA?
The structural changes in breast cells begin at the DNA level. Pregnancy triggers a change in nucleosomes.
What are nucleosomes? They are a section of DNA that is wrapped around proteins. These proteins protect DNA.
These changes can alter how certain regions of DNA open and close. When a part of the breast cell’s DNA opens, transcription factors can combine to either activate or deactivate specific genes.
After conducting a multi-phased study on mice, Dr. dos Santos and her team found that pregnancy can trigger DNA changes that allow breast cells to block off the cMYC gene.
What is cMYC? Overexpression of the cMYC gene can cause malignancy or cancer.
Her team noted that pre-pregnancy breast cells were not resistant to this cancer-causing gene, so they were still susceptible to cancer. However, post-pregnancy breast cells resisted the adverse effects of cMYC.
The researchers believe that pregnancy can keep breast cells from interacting with cMYC. And they think that cellular senescence plays a role in all of this.
Cellular senescence is a state where cells are no longer dividing or multiplying, but they aren’t dying either. This arrested cell cycle state may protect against cancer.
After becoming pregnant, cMYC expression goes into pre-senescence where cells stop growing so cancer can’t progress. So the DNA signaling changes brought on by pregnancy may be able to shut down cancer genes before they cause malignancies in breast cells.
Dr. dos Santos is now working with her team to see if pregnancy has the same effect on human breast cells. They’re running a similar experiment, but this time, they’re using human tissue organoids.
At the same time, they’re also working on another study where they transplant pregnancy-altered breast cells in mice that have never been pregnant. They want to test the effects post-pregnancy breast cells have on non-pregnant environments.
According to the Centers for Disease Control and Prevention (CDC), approximately 250,000 women are diagnosed with breast cancer every year. On top of that, over 40,000 women die from breast cancer every year.
The field of epigenetics is full of promise, even cancer prevention. Uncovering the whys and hows behind pregnancy’s protective effects against breast cancer can help scientists develop better preventive measures and treatment options for breast cancer. In the meantime, epigenetics already offers a variety of health applications. If you want to learn more about it, visit Tru Diagnostics.
What are your thoughts on these new findings? Share them with us in the comments section below!
- BioNews: Pregnancy protects against breast cancer by changing the epigenome
- Nature Communications: Pregnancy reprograms the epigenome of mammary epithelial cells and blocks the development of premalignant lesions