WUHAN, Jan. 25 — Scientists have pinpointed a group of remarkably adaptable tumor cells that appear to orchestrate lung cancer’s progression, fueling its ability to diversify and resist treatment. It’s a bit like discovering the conductor of a chaotic orchestra, and potentially silencing it.
Unmasking the ‘Hub’ That Drives Lung Cancer’s Spread
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New research identifies a key cell state responsible for tumor growth and treatment resistance.
- A “high-plasticity cell state” (HPCS) acts as a central hub within lung tumors.
- Eliminating HPCS cells can prevent tumors from becoming malignant in early stages.
- Targeting HPCS cells significantly slows cancer growth and overcomes drug resistance.
- The findings suggest a common mechanism for cancer plasticity applicable to multiple cancer types.
Why is lung cancer so notoriously difficult to treat? A major reason, researchers say, is that cancer cells are masters of disguise, constantly shifting their form to evade drugs. Now, a collaborative effort between scientists in China and the United States has revealed a crucial piece of this puzzle.
A New Way to Track Cancer’s Adaptability
To understand how these cellular shifts occur, the team—led by researchers from China’s Huazhong Agricultural University and the Memorial Sloan Kettering Cancer Center in New York—developed a novel genetic reporting system. Think of it as installing “trackable chips” and “precision clearance switches” within tumor cells in mouse models of lung cancer, allowing them to monitor changes in real-time.
This innovative approach allowed them to identify a “high-plasticity cell state” (HPCS). These HPCS cells aren’t just passively changing; they function as a “central traffic hub,” directing cells along different growth pathways and even enabling other cells to revert to this adaptable state, according to the study published this week in the journal Nature.
A: These cells act as a central hub, distributing cells into different growth paths and allowing other cells to revert to an adaptable state, driving tumor diversity and resistance to therapies.
The implications are significant. Researchers demonstrated that eliminating HPCS cells in early-stage tumors could prevent them from becoming malignant. In established tumors, targeting these cells dramatically slowed cancer growth.
Combining Approaches for Maximum Impact
Perhaps most promisingly, removing HPCS cells suppressed resistance to both chemotherapy and targeted drugs. When combined with standard treatments, this approach nearly eliminated tumors in the mouse models. “A major reason cancers are difficult to treat and often recur is that tumor cells can switch between different states to survive attacks from drugs,” explained Yan Yan, a corresponding author of the paper.
The researchers believe this discovery points to a common mechanism driving cellular plasticity across various cancers. Targeting this central “hub” state could offer a broadly applicable strategy for improving cancer treatment outcomes.
