While research has led to effective agents for killing cancer cells, they come with a high price: some of these drugs, such as Doxorubicin (DOX), can also damage the heart. DOX is a common chemotherapy drug used to treat many cancers, including leukemias, lymphomas, breast, uterine, ovarian, bladder, and lung cancers.
“When patients undergo chemotherapy, drugs like DOX act like sledge hammers,” explains Dr. Lorrie Kirshenbaum, Director of the Institute of Cardiovascular Sciences (ICS) at the Albrechtsen Research Centre at St. Boniface Hospital. “They attack all cells that divide – cancerous or healthy. And because heart cells stop dividing at birth, they can’t repair themselves when damaged, and the pumping activity of the heart can become impaired.”
Dr. Kirshenbaum has discovered the source of this side effect. “DOX turns on a suicide gene called Bnip3, and when Bnip3 is turned on, it’s a killer. It’s the same gene that programs heart cells to die when a person suffers a heart attack.”
With the mechanism of Bnip3 understood, Dr. Kirshenbaum is now working to solve the problem through the development of an ‘inhibitor’ drug that can be taken with DOX to keep the Bnip3 gene dormant in the heart, without comprising the drug’s ability to kill the cancer cells.
Implications for cancer treatment
The road to developing this inhibitor also points to new lines of cancer research. Cancer cells have typically lost their ability to STOP dividing, and Dr. Kirshenbaum has been able to demonstrate that this is because the Bnip3 gene is not turned on in cancer cells. His team is now interested in understanding how they can trigger the Bnip3 gene to switch on, and stop cancer cells from growing.
While other laboratories are investigating the process of cell death in heart disease and cancer, St. Boniface Hospital is the only facility translating this work directly into a clinical setting.
Dr. Kirshenbaum believes that when the control mechanisms that would otherwise instruct normal cells to stop growing or dividing become damaged, these normal cells grow uncontrollably, and become cancerous. His team has discovered that Bnip3, which regulates cell death, can be re-introduced into cancer cells to stop them from dividing. In fact, the team has demonstrated that by genetically manipulating Bnip3 to turn on in cancer cells, we can re-program those cells to die and prevent them from growing.
Translating into a clinical setting
While other laboratories are investigating the process of cell death in heart disease and cancer, St. Boniface Hospital is the only facility translating this work directly into a clinical setting, with great potential to help patients.
Patients like Alina.
In 2017, Alina was experiencing what she thought was an extremely difficult pregnancy; she was exhausted, and found it hard to look after her two children. She also had the flu, with a cough that would not subside.
She made numerous trips to St. Boniface Hospital for treatment. While no diagnosis was confirmed, she received extraordinary care from the nurses each time. On her fourth trip, her obstetrician insisted Alina be admitted to St. Boniface Hospital for a battery of tests, to find a diagnosis.
At 32 weeks pregnant she received the worst news of her life: it was cancer.
The next two and a half weeks in hospital were a blur as she underwent more tests. Meanwhile, her third son was delivered at 34 weeks via C-section, and was immediately admitted to the Neonatal Intensive Care Unit (NICU).
She will never forget the excellent care her son received, and the cooperation between all the departments that helped her family. When her diagnosis was confirmed as Hodgkin’s lymphoma, Alina began chemotherapy treatment.
Today, Alina has hope for the future – hope that she will see her young sons through to adulthood. She has a lot of life ahead and many more memories to make with her family
Cancer research underway at St. Boniface Hospital Research Centre has vast potential to improve the treatment Alina is receiving, and to give Alina and her family a more-certain future.
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