Health and Me

Ishita Roy

Cancer Cells Cheat Drugs, Pretends To Be Dead, To Avoid Treatment: Study

The World Health Organization (WHO) notes that in 2022, there were nearly 20 million new <span><a href="https://www.healthandme.com/health/cancer">cancer</a></span> case in the world. These have included lung, breast, and colorectal cancers. This has led to death of 9.7 million in the year. This means about 1 in 5 people could develop cancer in their lifestyle, and the number is rising significantly by 2050. 

While there are new studies, targeted cell therapies that are now opening more doors to cancer treatments, a new study by the University of California, San Diego, could be worrisome. This new study found that some cancer cells turn on their "cell death" mode during drug therapy. So, what happens is that the drug, instead of killing them, persist and regrow in some of the case. This is how drug resistance in cancer cells functions, and by targeting this cell-death programme in cancer cells, scientists could potentially stop the growth of cancer after therapy. 

The findings have been found in a peer-reviewed journal Nature Cell Biology. 

Cancer remains one of the biggest global health threats, causing nearly 10 million deaths every year. One of the hardest parts of treating cancer is that it can return, even after treatment seems successful. Doctors call this cancer relapse or recurrence. It happens when some cancer cells survive the first round of treatment and begin growing again after a period of dormancy.

Relapse rates vary by cancer type. Lung cancer, for instance, has a higher chance of returning, while breast cancer generally has lower relapse rates. Still, one problem cuts across many cancers: drug resistance. Over time, cancer cells can learn how to survive medicines designed to kill them.

<h2>A surprising discovery during treatment</h2>

In this study, researchers set out to look for early signs of drug resistance in cancer cells. They expected to find genetic changes or mutations. Instead, they found something unexpected. Some cancer cells respond to treatment by turning into what scientists call “persister cells.”

These persister cells stop growing during therapy and enter a dormant state. At first glance, this looks like success. But what happens next is more troubling. These cells activate a built-in cell death program, the same process the body uses to break down dying cells. However, the program does not finish the job.

Rather than dying, these persister cells release enzymes that help them restart growth. One key enzyme involved is DNA Fragmentation Factor B, or DFFB. Normally, DFFB helps fragment DNA in cells that are meant to die. In these cancer cells, it is activated at low levels. That is not enough to kill the cell, but enough to help it escape dormancy and start growing again.

“This flips our understanding of cancer cell death on its head,” said senior author Matthew J. Hangauer. He explained that signals meant to kill cancer cells can sometimes help them survive and regrow instead.

<h2>What this means for <span rel="noindex"><a href="https://www.healthandme.com/health/cancer">cancer</a> treatment</span></h2>

The findings offer a new way to think about drug resistance. Instead of relying on genetic mutations, cancer cells may use internal survival mechanisms to outlast treatment. This insight opens the door to new treatment strategies.

The researchers tested this idea by disabling DFFB in melanoma, lung cancer, and breast cancer models. Without the enzyme, the cancer cells stayed dormant and could not restart growth. Importantly, DFFB does not appear to be essential in normal cells, suggesting that targeting it may not cause major side effects.

As first author August F. Williams noted, focusing on these early, non-genetic survival pathways could help patients stay in remission longer and lower the risk of cancer returning.

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The World Health Organization (WHO) notes that in 2022, there were nearly 20 million new cancer case in the world. These have included lung, breast, and colorectal cancers. This has led to death of 9.7 million in the year. This means about 1 in 5 people could develop cancer in their lifestyle, and the number is rising significantly by 2050. While there are new studies, targeted cell therapies that are now opening more doors to cancer treatments, a new study by the University of California, San Diego, could be worrisome. This new study found that some cancer cells turn on their "cell death" mode during drug therapy. So, what happens is that the drug, instead of killing them, persist and regrow in some of the case. This is how drug resistance in cancer cells functions, and by targeting this cell-death programme in cancer cells, scientists could potentially stop the growth of cancer after therapy. The findings have been found in a peer-reviewed journal Nature Cell Biology. Why cancer often comes backCancer remains one of the biggest global health threats, causing nearly 10 million deaths every year. One of the hardest parts of treating cancer is that it can return, even after treatment seems successful. Doctors call this cancer relapse or recurrence. It happens when some cancer cells survive the first round of treatment and begin growing again after a period of dormancy.Relapse rates vary by cancer type. Lung cancer, for instance, has a higher chance of returning, while breast cancer generally has lower relapse rates. Still, one problem cuts across many cancers: drug resistance. Over time, cancer cells can learn how to survive medicines designed to kill them.A surprising discovery during treatmentIn this study, researchers set out to look for early signs of drug resistance in cancer cells. They expected to find genetic changes or mutations. Instead, they found something unexpected. Some cancer cells respond to treatment by turning into what scientists call “persister cells.”These persister cells stop growing during therapy and enter a dormant state. At first glance, this looks like success. But what happens next is more troubling. These cells activate a built-in cell death program, the same process the body uses to break down dying cells. However, the program does not finish the job.How cancer cells escape deathRather than dying, these persister cells release enzymes that help them restart growth. One key enzyme involved is DNA Fragmentation Factor B, or DFFB. Normally, DFFB helps fragment DNA in cells that are meant to die. In these cancer cells, it is activated at low levels. That is not enough to kill the cell, but enough to help it escape dormancy and start growing again.“This flips our understanding of cancer cell death on its head,” said senior author Matthew J. Hangauer. He explained that signals meant to kill cancer cells can sometimes help them survive and regrow instead.What this means for cancer treatmentThe findings offer a new way to think about drug resistance. Instead of relying on genetic mutations, cancer cells may use internal survival mechanisms to outlast treatment. This insight opens the door to new treatment strategies.The researchers tested this idea by disabling DFFB in melanoma, lung cancer, and breast cancer models. Without the enzyme, the cancer cells stayed dormant and could not restart growth. Importantly, DFFB does not appear to be essential in normal cells, suggesting that targeting it may not cause major side effects.As first author August F. Williams noted, focusing on these early, non-genetic survival pathways could help patients stay in remission longer and lower the risk of cancer returning.