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Researchers pinpoint central tumor cells that fuel lung cancer growth
(MENAFN) Scientists from China and the United States have identified a rare and highly flexible group of tumor cells that plays a critical role in driving the progression of lung cancer, according to research findings released this week.
The study outlines a new therapeutic approach aimed at cancers that are difficult to eliminate and tend to return after treatment. Researchers explain that one major reason cancer survives therapy is its ability to adapt, with tumor cells shifting between different states to withstand drug attacks and later regenerate.
To observe this process in real time, the research team engineered lung cancer mouse models with a sophisticated genetic monitoring system. This system effectively embedded "trackable chips" and "precision clearance switches" into tumor cells, allowing scientists to follow their behavior and selectively remove them.
Using this method, the researchers identified what they call a "high-plasticity cell state" (HPCS). These cells function as a "central traffic hub" within tumors, guiding cancer cells toward various growth pathways while also enabling them to revert to a highly adaptable form when needed.
Experiments showed that removing HPCS cells at early stages stopped tumors from becoming malignant. In more advanced cases, targeting these cells significantly slowed tumor expansion.
The elimination of HPCS cells also lowered resistance to chemotherapy and targeted cancer drugs.
When this strategy was combined with existing cancer treatments, tumors in the models were almost entirely eradicated. The findings suggest that focusing on this highly adaptable tumor cell state could open a powerful new avenue for treating not only lung cancer but potentially a wide range of cancers as well.
The study outlines a new therapeutic approach aimed at cancers that are difficult to eliminate and tend to return after treatment. Researchers explain that one major reason cancer survives therapy is its ability to adapt, with tumor cells shifting between different states to withstand drug attacks and later regenerate.
To observe this process in real time, the research team engineered lung cancer mouse models with a sophisticated genetic monitoring system. This system effectively embedded "trackable chips" and "precision clearance switches" into tumor cells, allowing scientists to follow their behavior and selectively remove them.
Using this method, the researchers identified what they call a "high-plasticity cell state" (HPCS). These cells function as a "central traffic hub" within tumors, guiding cancer cells toward various growth pathways while also enabling them to revert to a highly adaptable form when needed.
Experiments showed that removing HPCS cells at early stages stopped tumors from becoming malignant. In more advanced cases, targeting these cells significantly slowed tumor expansion.
The elimination of HPCS cells also lowered resistance to chemotherapy and targeted cancer drugs.
When this strategy was combined with existing cancer treatments, tumors in the models were almost entirely eradicated. The findings suggest that focusing on this highly adaptable tumor cell state could open a powerful new avenue for treating not only lung cancer but potentially a wide range of cancers as well.
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