Cancer treatment has improved dramatically in recent decades, but one terrifying problem still remains: relapse. Many patients undergo surgery, chemotherapy or radiation and are told their cancer is gone.
They return to normal life with hope and relief. But sometimes, years later, the cancer comes back even stronger, and doctors have long struggled to understand why this happens.
Researchers now believe that one of the main reasons is a small group of cells called cancer stem cells and that these cells behave very differently from regular cancer cells.
While most cancer cells grow quickly and are attacked by chemotherapy, cancer stem cells can ‘hide’ in the body.
They remain silent and inactive for long periods of time, almost as if they were sleeping. Because chemotherapy mainly targets fast-growing cells, these dormant stem cells survive the treatment. Later they may wake up and start forming new tumors.
At Virginia Commonwealth University, Professor Umesh Desai has spent more than thirty years researching complex sugar-like molecules in the body that can help solve this problem.
His work focuses on glycosaminoglycans, often called GAGs, which are long chains of natural sugars that cover the surface of almost every human cell.
They are important for many processes, such as blood clotting, inflammation, cell growth and communication between cells.
Although scientists have known about GAGs for many years, their exact role in disease is still not fully understood.
Desai believed that GAGs could be more than just natural cell coatings. He thought they could inspire new medicines.
Natural GAGs such as heparin are already used as blood thinners, but they can vary in quality and sometimes cause side effects. Desai’s lab began creating synthetic versions that copy specific parts of GAGs in a controlled and safer manner.
This long research journey led to a new molecule called G2.2. Desai developed it together with Dr. Bhaumik Patel, a cancer doctor and researcher who studies colorectal and digestive cancers.
Desai compares cancer stem cells to a bear in hibernation. When the bear hibernates, it remains hidden in its den, sleeping and protected from danger. No matter how strong a weapon is, it cannot reach the bear while it is hibernating.
Similarly, cancer stem cells hide from chemotherapy, but G2.2 works differently. It interacts with a specific receptor on the stem cells, forcing them out of their dormant state. Once these cells are active, the molecule activates signals in them that lead to their death.
The team tested G2.2 in many laboratory models and found that it almost completely removed dormant stem cells in colorectal cancer. The molecule also showed similar effects in models of lung, brain, kidney and pancreatic cancer. This suggests that the approach may work for different types of tumors.
Another exciting finding was the safety of using G2.2, as it showed no major toxic effects in preclinical testing. It even seemed to boost the immune system by activating T cells that help the body fight cancer naturally.
G2.2 is still in the preclinical phase, but could be a beacon of hope in cancer therapy. Instead of just attacking fast-growing tumors, it targets the hidden roots that allow cancer to grow back.
