Researchers have found that knowing the early changes in the cells of the fallopian tubes of women carrying the genetic mutation responsible for ovarian cancer could open the way for new preventative strategies.
The study sought to understand why women with the BRCA1/2 mutations develop ovarian cancers and what happens in the cells where the cancers originate to trigger them.
The findings showed that in approximately 60 percent of women carrying the BRCA1 or BRCA2 gene, a radically altered subcellular activity occurred in the tubal cells that are closest to the ovary.
“These new findings take us a step closer to understanding how ovarian cancers develop in BRCA 1/2 gene mutation carriers, opening up new opportunities for ovarian cancer prevention,” said Martin Widschwendter, professor at University College London.
These sub-cellular changes were similar to those seen in cells from ovarian cancer specimens.
The changes were not seen in the women without BRCA mutations.
In addition, the researchers identified an enzyme (activation-induced cytosine deaminase, AID) that appears to trigger this re-programming.
“This is vital as at present the most effective method of prevention is drastic risk-reducing surgery, which deprives women of their hormones and their ability to give birth prior to the menopause,” Widschwendter added.
For the study, published in the journal Nature Communications, the team examined the post-surgical reproductive tubal tissue from 115 women, 56 with the BRCA1/2 mutation and a control group of 59 without.
They analysed the cells’ epigenetic programmes, the ‘software’ which dictates how the cells read instructions encoded within the DNA.
Also, they compared both ends of the Fallopian tubes (the fimbrial, closest to the ovary, and the uterine, closest to the womb), from the same woman.
“The next steps will be to investigate the merit of drugs that affect epigenetic reprogramming and to look for biomarkers which allow safe monitoring of the effect of such drugs,” Widschwendter concluded.
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