Researchers at the Herbert Irving Comprehensive Cancer Center (HICCC) have made an important discovery about why some prostate cancer treatments stop working.
Their findings, published in the journal Nature, may help doctors find new ways to treat patients whose cancer has become resistant to the latest drugs.
Prostate cancer is one of the most common cancers in men. Over the years, researchers have developed new drugs to block hormones like testosterone that fuel cancer growth. These drugs, called androgen receptor inhibitors, are now standard treatment.
But in many patients, the cancer finds a way to escape the effects of the treatment. It does this by changing into a different form, known as neuroendocrine prostate cancer, which does not respond to hormone therapy.
Dr. Michael Shen at HICCC has studied this problem for years. He focuses on something called “lineage plasticity,” which is when cancer cells change their identity. Instead of acting like normal prostate cancer cells, they start behaving like a completely different type of cell. This shape-shifting ability helps them survive treatment.
Shen’s lab discovered that this change isn’t caused by permanent mutations in the DNA. Instead, the cells make what are called epigenetic changes—altering how their genes are turned on and off. To learn more, Shen teamed up with Dr. Chao Lu, an expert in how these changes happen.
Lu’s lab discovered that a specific chemical change to proteins called histones plays a key role. Histones help control which genes are active in a cell.
Lu had already been studying one particular pathway involving a protein called NSD2, which changes histones. It turns out that this same protein is heavily involved in helping prostate cancer cells change into the drug-resistant form.
For years, scientists thought NSD2 could not be targeted with drugs. But recently, the company Novartis created small molecules that could block NSD2.
Shen and Lu tested one of these new drugs in lab-grown cell clusters and in animals. They found that blocking NSD2 helped push the cancer cells back into their original form—one that can be treated with hormone therapy again.
Even though the drug alone didn’t kill the cancer, combining it with hormone therapy made both treatments work better. One drug weakened the cells, while the other made them sensitive to hormone treatment again.
This is the first time scientists have shown that a common type of drug resistance in prostate cancer can be reversed, not just avoided. That’s a big deal. It means that instead of switching treatments, doctors might someday use a drug to “reset” the cancer, making old treatments work again.
Even more exciting, the same process of shape-shifting happens in other cancers too. The team is already studying if blocking NSD2 could help in lung cancer as well.
This discovery opens up a new way to treat drug-resistant cancers, offering fresh hope to patients who have run out of options.
If you care about prostate cancer, please read studies about a natural ally against prostate cancer, and supplements and keto diet can boost immunotherapy for prostate cancer.
For more health information, please see recent studies about how to harness the power of anti-cancer foods and supplements, and low-fat diet may help stop cancer growth.
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