A ß÷ßäÉçÇø research team has identified a key protein involved in the normal growth of mammary glands during puberty that misfires in some breast cancers, and is now searching for drugs to reverse the problem.
In , the team reports on the mechanism to switch a protein called BAD from its harmful form to its helpful form, suggesting existing drugs previously used to treat melanoma and lung cancer may be useful.
“During puberty, the mammary gland goes from a little, primordial piece of tissue to a full breast that can actually end up feeding the young,” says principal investigator , professor of biochemistry and Lilian McCullough Chair in Breast Cancer Research. “It’s a pretty remarkable organ.”
When cell growth is wanted during puberty or lactation, the BAD protein is turned off, in a form known as “phosphorylated.” When normal breast growth is complete, the BAD protein turns on in its “non-phosphorylated” form, acting as a kind of growth referee.
Goping’s research has shown that .
“Breast cancer can reawaken that signal to allow the cells to start moving again, and that’s called metastasis,” Goping says. “We found that the BAD protein is important to regulate that process.”
Goping’s team found that administering a drug to turn the BAD protein into its non-phosphorylated form can give the referee back its whistle and stop unwanted cell growth and metastasis.
Goping notes that about one-quarter of breast cancers have this problem of BAD phosphorylation. Her research team found that patient survival is worse among those with phosphorylated BAD in their tumours.
“We asked, if a tumour has high levels of the phosphorylated form, can we convert it to the non-phosphorylated form so it does its job and blocks metastasis?” says Goping. “We’ve identified the mechanism for that conversion and identified a drug that could reawaken the good non-phosphorylated BAD.”
The advantage of using a drug that is already approved for other forms of cancer is that it would not need to go through the same regulatory hurdles before being made available to patients.
Goping and her team received a Game Changer Award from the ß÷ßäÉçÇø Cancer Foundation in 2024 for their work growing patient-derived at the U of A. Organoids are like 3D models grown from individual tumours that can be used to study the effects of drugs on tumour growth.
The organoids allow the team to find the personalized “signature” of each tumour at the molecular level to target treatment. The living biobank has collected donated tissue from 36 patients so far. The Goping team is conducting extensive molecular characterization with the goal of making these valuable resources available to other breast cancer researchers.
In her role as the Lilian McCullough Chair in Breast Cancer Research, Goping is developing the U of A’s breast cancer research program in collaboration with colleagues across the university and beyond. She has run seed grant competitions and supported faculty renewal, and leads multidisciplinary groups to bring teams together and share knowledge.
She gives credit to her lab colleagues and collaborators for creating a supportive research community.
“The more authentic our relationships are, I think the better it is for research in general and for the community as a whole,” Goping says. “Community is really important — it is the ignition and the engine for everything we do.”
Goping says she is inspired by the McCullough family to push her basic biological research forward to make life better for patients.
“The goal of the chair is really to foster breast cancer research at the university and then have that start making ripples past the university’s walls,” she says. “Interacting with the McCulloughs has been a privilege and helps me reflect on the broader picture and things that are important.”
Goping is a member of the Cancer Research Institute of Northern ß÷ßäÉçÇø and the . A portion of this work was completed in the Faculty of Medicine & Dentistry’s Cell Imaging Core.
