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Cancer cells can enter a bear-like dormant state to escape chemotherapy



According to a new study, cancer cells will hibernate like winter bears when threatened like chemotherapy. This is obviously a strategy used by certain animals (although they have long been lost in humans) to avoid resource shortages. Survive in the period of time.

Knowing exactly how cancer evades and undergoes drug treatment is an important part of trying to overcome cancer forever, which is why understanding this hibernation behavior may play a key role in future research. In the years after treatment, the cancer usually recurs after remaining dormant or apparently disappearing.

Preclinical studies on human colorectal cancer cells show that they can slow down to enter a low-maintenance, “drug resistance persistence”

; (DTP) state, which will help explain the reasons for treatment failure and tumor recurrence.

Catherine O’Brien, a researcher and surgeon from the Princess Margaret Cancer Center in Canada, said: “The tumor behaves like a complete organism, able to enter a state of slow division, saving energy to help it survive.”

“There are examples of animals entering a reversible and slowly dividing state to withstand harsh environments. It seems that cancer cells have cleverly chosen the same state in order to survive.”

The researchers collected human colorectal cancer cells in a petri dish and exposed them to chemotherapy. They observed that when chemotherapy drugs are present, the colorectal cancer cells enter the same dormant state in a coordinated manner. Cells stop expanding, which means they need little nutrition to sustain life.

These observations are also “suitable for a mathematical model in which all cancer cells, not small subgroups, have the equivalent ability to become DTP”, indicating that these survival strategies can be seen in all cancer cells.

The researchers also used xenografts of colorectal cancer cells in different groups of mice. Once the mice developed tumors of a certain size, the researchers treated the mice with standard chemotherapy. Scientists observed negligible tumor growth in mice that received treatment within eight weeks. After treatment stopped, the tumor began to grow again.

After the regeneration period, the cancer cells removed from the tumor were transplanted into different mice and treated again. The regenerated cells are still sensitive to treatment, and their growth stops and starts in the same way. This finding is consistent with cancer cells entering the DTP state.

This DTP state is similar to the dormant state, called embryonic diapause, and mouse embryos fall as an emergency survival mode. Embryonic diapause allows many animals (including mice) to effectively suspend embryonic development until environmental conditions are more favorable.

Here, cancer cells have been found to have similar effects. Another link between DTP status and embryonic diapause is their reliance on a biological mechanism called autophagy, in which cells essentially feed themselves to find what they need. Autophagy is a natural way to remove waste from the body, but in this case, cancer is using autophagy to maintain life.

Aaron Schimmer, an oncologist at the Princess Margaret Cancer Center, said: “We never really knew that cancer cells are like hibernating bears.” “This study also tells us how to target these sleeping bears. So that they don’t hibernate and wake up, then come back unexpectedly.”

“I think this will become an important cause of resistance and will explain something that we didn’t understand well before.”

By targeting and inhibiting the autophagy process, researchers are able to break the hibernation (or DTP) state and kill cancer cells through chemotherapy. This may be a way to solve cancer tumors that are resistant to conventional treatments in the future.

Scientists already know several other ways that cancer can hide in the body, so this new study adds more and more evidence of how to absorb cancer cells that are most resistant to current drugs and methods.

O’Brien said: “This provides us with a unique opportunity for treatment.” “We need to target cancer cells when they are in this slow cycle, vulnerable state, and then get the genetic mutations that drive resistance.

“This is a new way of thinking about resistance to chemotherapy and how to overcome it.”

The research has been published in cell.


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