Prof. Lee Jae-woong of Korea University's School of Biosystems and Biomedical Science, left, and his partner researcher for the study, Prof. Markus Muschen of Yale University / Courtesy of Korea University
A Korea University research study is claiming to have identified a mechanism that allows leukemia cells to survive despite excessive growth signals, offering a potential new strategy for related cancer treatment.
The study, led by Lee Jae-woong of the university’s School of Biosystems and Biomedical Science, was released Feb. 10 through Science Signaling, a sister journal of the American Association for the Advancement of Science. The paper was selected as the issue’s cover article.
Leukemia occurs when cancer-driving proteins remain continuously active, causing abnormally strong proliferation signals inside cells. While these signals induce tumor growth, excessively strong signaling can also impose severe stress on cells and potentially trigger cell death.
Leukemia cells can grow continuously despite an unstable signaling environment.
Most existing therapies generally aim to halt tumor growth by blocking proliferation signals, but the mechanisms that allow cancer cells to maintain growth under such conditions have yet to be fully understood.
The research team said it has long studied the protein CD25, which is widely known as a receptor for the immune system signaling molecule interleukin-2 (IL-2). They found that protein CD25 can function even without binding to IL-2.
According to the study, CD25 generates inhibitory proteins inside the cell to lower proliferation signaling on its own, helping leukemia cells maintain a balanced signaling state that supports survival.
For the study, the researchers removed CD25 from leukemia cells in animal models.
The loss of CD25 significantly reduced cancer cell proliferation and self-renewal capacity. In addition, an antibody-drug conjugate therapy targeting CD25 effectively eliminated leukemia cells even in models that did not respond to existing treatments.
Source: Korea Times News
