University of Alberta Research & Quebec Team Uncovers Growing Excitement of PARP Inhibitors

Asian scientist in the laboratory working at lab with test tube

New research from the University of Alberta Faculty of Medicine & Dentistry uncovers the mechanism behind the newest generation of cancer drugs is opening the door for better-targeted therapy. Specifically, PARP inhibitors are molecular targeted cancer drugs used to treat women with ovarian cancer who have the BRCA1 and BCRA2 gene mutations. The drugs are showing promise in late-stage clinical trials for breast cancer, prostate cancer, and pancreatic cancer.

The University of Alberta Faculty of Medicine and Dentistry has been busy at work engaged in new research uncovering the mechanisms underlying the newest generation of cancer drugs—and in the process identifying the potential for improved, targeted therapies for a number of cancer targets.

University of Alberta Research Focus

PARP inhibitors, molecular targeted cancer drugs used to treat women with ovarian cancer who have the BRCA1 and BRCA2 gene mutations.

PARP Inhibitors Updates

These drugs are evidencing promise in late-stage clinical trials for breast cancer, prostate cancer, and pancreatic cancer and are a core element in the precision medicine movement—e.g. targeting treatments based on genetic, environmental and lifestyle factors.

The team notes that PARP inhibitors are the first cancer therapies developed to exploit a process known as synthetic lethality, in which cancers with specific mutations are many times more sensitive to the drug than normal cancer cells.

BRCA1 & BRCA2 Attributes

Their research, summarized in Science Daily, center on people with BRCA1 or BCRA2 gene mutation. They possess a defect in their cells’ ability to repair double-strand breaks in the DNA, which puts them at increased risk for breast cancer development.

Apparently, the PARP inhibitors exploit a weakness and further interfere or meddle with the proteins known as poly-ADP ribose polymerase (PARP1 and PARP2), which cells use to repair the daily damage to DNA that occurs normally. When the cells can’t repair themselves, they die. Normal cells are unaffected.

Researcher Comment: We must Fully Understand

Michael Hendzel, University of Alberta oncologist and cell biologist notes “Knowing how they work will enable us to come up with new applications for them, so we can make this drug as useful as possible for as many patients as possible.” Hendzel continued “Cells often have redundancy, so for example, if they have a defect in one way they use to repair the damage, they can use a different way to do it.”

Lengthy Research Collaboration

Hendzel and the University of Alberta team have been collaborating with Guy Poirier at Laval University’s Centre de recherche sur le cancer and Jean-Yves Masson of the CHU de Quebec’s research centre.

Lead Research/Investigator

Michael Hendzel, University of Alberta lead for the genomics stability research group at the Cancer Research Institute of UA.

Guy Poirier, Laval University Centre de recherche sur le cancer

Jean-Yves Masson, CHU de Quebec’s research centre