While modern cancer treatments have reduced cancer deaths, they often have adverse effects on the cardiovascular system. “Among breast cancer survivors, cardiovascular disease is actually the number one cause of death now,” says Professor Andreas Beyer.
Professor of Medicine and Physiology at the Medical College of Wisconsin (MCW), Beyer collaborates with Minna Kaikkonen-Määttä, Professor of Cardiovascular Genomics at the University of Eastern Finland (UEF), to gain a better understanding of how cancer therapies affect blood vessels depending on patients’ genes. Beyer currently holds a Fulbright–Saastamoinen Foundation Distinguished Chair in Health Sciences at UEF, after which he has been invited to continue as a University of Eastern Finland Distinguished Professor, UEFDiPro.
Beyer represents an emerging field, cardio-oncology, the aim of which is to promote cancer patients’ cardiovascular health. “We have gotten good at treating cancer, which also means patients live long enough to develop cardiovascular disease. In addition, some are more affected than others, and we need to understand why.”
Microvascular changes predict long-term problems
According to Beyer, heart damage caused by anti-cancer therapies has already been studied extensively, but it doesn’t entirely explain the progression of cardiovascular disease. “That’s why we started looking at the vasculature, and more specifically the microvasculature – the smallest blood vessels in the body. And there we are starting to see minute differences that may in part explain different cardiovascular outcomes between cancer survivors.”
His research has shown that the first adverse cardiovascular effects of cancer treatments may not be seen in the heart but in the microvascular endothelium – the inside layer of blood vessels that regulates many important functions in the cardiovascular system. “In fact, microvascular endothelial dysfunction is a very good predictor for major long-term cardiovascular problems.”
This dysfunction is aggravated by damage to mitochondria in endothelial cells, impairing endothelial mitochondrial signalling and energy production, which is more important to the functioning of blood vessels than previously thought.
“Obviously, genetics and the environment both play a role in the outcome. The technology at UEF as well as the Finnish FinnGen biobank data and national health registers offer outstanding opportunities to understand these interactions, whereas my lab is in a position to establish the clinical relevance of any potential findings. It’s quite a nice match,” Beyer says.
His lab at MCW studies human vascular physiology on a mechanistic level using human tissue samples. Kaikkonen-Määttä’s research group, on the other hand, uses single-cell and functional genomics to investigate the genetic basis of cardiometabolic diseases.
With his research, Beyer hopes to contribute to future solutions not only to predict, but also to prevent and treat cardiovascular complications in cancer patients. “Once the problem is better understood, preventive treatments could be developed. At the very minimum, we could be able to suggest which medications are safe for some patients, but not for others.”
Another way in which cancer and cardiovascular disease are linked is via similar risk factors, such as obesity and type 2 diabetes. In addition, recent studies suggest that cardiovascular disease may increase cancer risk or accelerate tumour progression.
During his first visit to UEF earlier this year, Beyer also took the time to teach. He gave a lecture course to students and researchers on current concepts in vascular physiology, including cardio-oncological and microvascular aspects.
“On a scientific level, I met a lot of researchers doing outstanding science and was impressed by the genetics and imaging entities at their disposal. With Minna’s team, we were already able to get answers to some questions and to formulate some hypotheses. I’m looking forward to continuing doing good science together.”
