MILWAUKEE_There’s no drug that reliably helps fractured or damaged bones regenerate. And, for patients recovering from bone cancer, the environment inside the body is working against healing.
Priya Premnath, assistant professor of biomedical engineering, has received the 2026 Shaw Early Career Research Award to study a dual approach to bone cancer treatment and recovery. With $200,000 in seed funding, she will explore how stem cells can be directed to heal bone after surgery without triggering new cancer growth.
The annual award, established by the Greater Milwaukee Foundation, supports research in biochemistry, biological sciences and cancer by early career scientists at UW-Madison and UW-Milwaukee. The award is made possible by the late James D. and Dorothy Shaw, donors to the foundation.
How to stop stems cells from turning cancerous
Stem cells are the body’s shapeshifters. In a healthy environment, they begin as generic cells and mature into specific kinds, such as bone, liver or kidney cells. But in a cancer-promoting environment, the same process might reignite the disease instead.
Premnath has a novel idea to guide stem cells to become committed bone cells instead of new cancer cells.
She will study whether a certain drug designed to kill cancer could also help rebuild bone after removal of tumors. For it to work, stem cells in the location would have to be commissioned to mature into bone cells in a cancer-primed environment.
What is UC2288?
A compound used by researchers to kill cancer cells, UC2288 works by inhibiting a gene known as p21. Premnath suspects the gene causes stem cells to mature differently depending on what environment they are surrounded by.
Even before Premnath became aware of the drug, she and her lab members had already found that inhibiting p21 had an effect on stem cells in healthy tissue. It seemed to help bone fractures heal because the stem cells in the location of injury were being nudged into becoming bone cells.
In searching for a non-invasive treatment for bone fractures, Premnath looked for existing drugs that blocked the gene – and uncovered UC2288.
Potential for patients
Now she wants to see if UC2288 can accomplish both staving off cancer expansion while also fostering healing after bone surgery.
The approach has shown potential.
In lab studies, Premnath found that she didn’t need high, cancer-killing doses of the drug to see an effect on stem cells. At much lower concentrations, UC2288 still changed how the cells behaved – even in environments designed to mimic cancer conditions.
For patients, especially young people with bone cancers like osteosarcoma, the implications could be significant. These cancers often strike near growth plates – areas where bones are actively lengthening during puberty.
New insight into bone regeneration
The project could also verify a new idea about bone regeneration.
Evidence from other recent research suggests that stem cells have a middle stage in the transformation to bone cells. They first become cartilage cells. The cartilage serves as a kind of template that is later replaced by bone.
Premnath hopes to uncover what is happening during this process.
Along with chemical signals, Premnath’s team suspects that mechanical forces also help trigger cartilage cells to become bone cells. That insight has inspired her team to investigate a second question.
“Why not just go straight to using cartilage cells and use our mechanical methods to prompt them into bone cells?” she asked. “This would make it much safer to use stem cells, opening the door for their increased use in cancer treatment.”
It would mark a shift in thinking, from trying to control stem cells that have a high propensity to revert to cancer, to working with more stable, committed cells, she said.
