Scientists have identified a biological change that may help explain why some prostate cancers become much more aggressive and spread to other parts of the body.
The discovery could eventually help doctors identify high-risk patients earlier and develop more targeted treatments.
The research was led by Lukas Kenner and colleagues at the Medical University of Vienna, also known as MedUni Vienna. Their findings were published in the scientific journal Molecular Cancer.
Prostate cancer is one of the most common cancers in men. It begins when cells in the prostate, a small gland below the bladder, start growing in an uncontrolled way.
Many prostate cancers grow slowly and remain inside the prostate for years. When the disease is found at this stage, treatments such as surgery or radiation can often be very effective.
The situation becomes much more serious when cancer cells leave the prostate and spread to other organs. This is known as metastatic prostate cancer, and it is much harder to cure.
Researchers have therefore been trying to understand what makes some prostate tumors stay relatively contained while others become aggressive. The new study points to an important protein called KMT2C.
KMT2C helps control how genes are used inside cells. Although the DNA code contains thousands of genes, cells need systems that decide which genes should be active and which should remain quiet.
In healthy cells, KMT2C is part of this control system. It helps maintain normal patterns of gene activity and prevents cells from behaving in ways that could encourage uncontrolled growth.
But KMT2C can become damaged by mutations. The researchers found that when the protein loses its normal function, an important brake on cancer growth may disappear.
One major consequence involves MYC, a gene that has long been linked to cancer. MYC helps regulate cell growth and division, but when it becomes too active, cells can multiply rapidly and behave more aggressively.
The study suggests that loss of normal KMT2C activity allows MYC to become more active. This creates conditions that can encourage prostate cancer cells to grow, survive and potentially spread.
This connection could help explain why KMT2C mutations are often found in more advanced cancers. Instead of being a harmless genetic change that appears as cancer progresses, the mutation may actively contribute to making the disease more dangerous.
The discovery may also have implications for diagnosis. If future studies confirm that KMT2C changes reliably predict aggressive disease, doctors might eventually be able to use genetic testing to identify patients who need closer monitoring or earlier treatment.
One possibility raised by the research is detecting cancer-related genetic material in blood. Such tests, sometimes called liquid biopsies, look for pieces of DNA released by tumors into the bloodstream.
A blood test would potentially be less invasive than repeatedly taking tissue samples from the prostate. However, more research is needed before KMT2C testing could be used routinely to predict whether an individual patient’s cancer will spread.
The findings also point toward a possible treatment strategy. Because loss of KMT2C appears to increase MYC activity, medicines designed to block MYC or the pathways it controls may be useful against some aggressive prostate cancers.
Researchers have spent years trying to target MYC because it plays a role in many cancers. New approaches aimed at interfering with MYC activity are being investigated, but they are not yet a standard treatment for metastatic prostate cancer.
The new study could help scientists identify which patients might be most likely to benefit from such treatments. A tumor carrying particular KMT2C changes could potentially become a marker used to guide more personalized therapy.
Still, the findings are at an early stage. Understanding a molecular pathway in laboratory research does not automatically mean that a blood test or new treatment will work safely and effectively in patients.
Further studies will need to confirm how accurately KMT2C mutations predict prostate cancer progression. Clinical research will also be needed to determine whether targeting MYC improves survival or slows the disease in patients whose tumors have these changes.
The study is important because it provides a clearer biological link between a genetic change and aggressive prostate cancer. Rather than treating every prostate tumor as equally dangerous, research like this may eventually help doctors distinguish cancers that can be carefully monitored from those that need rapid treatment.
For now, KMT2C is best viewed as a promising research target rather than an established clinical test. If the findings are confirmed, however, the KMT2C-MYC connection could give doctors another way to understand, predict and eventually fight metastatic prostate cancer.
Copyright © 2026 Knowridge Science Report. All rights reserved.
