Lineage Plasticity in Cancer: How Tumors Change Identity and Resist Therapy
Lineage plasticity allows cancer cells to reprogram their identity and adopt new cellular states, enabling them to resist therapies that target specific pathways. This biological flexibility suggests that tumor evolution is driven by epigenetic changes rather than just new mutations.
Why it matters
Understanding this mechanism is critical for developing more effective cancer treatments that can overcome therapy-induced resistance.
Cancer is not always biologically fixed. As tumors evolve, some cancer cells can change their identity, adopt new cellular states, and become less dependent on the pathways that originally defined them.
This process, known as lineage plasticity in cancer, is emerging as an important explanation for why some tumors behave differently over time and why treatment resistance can develop even without a new dominant mutation. Instead of simply becoming stronger versions of the same cancer, some tumor cells can reprogram themselves and take on a different biological state.
Understanding how cancer cells change identity is opening a new way of thinking about tumor evolution, treatment resistance, and the limits of therapies that target a single pathway. It also raises an important question: how much of cancer resistance is driven not by new mutations, but by the ability of tumor cells to become something different?
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