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Scientists have pinpointed an enzyme called PTPN2 that shields a key growth-driving protein in acute myeloid leukemia (AML) cells from being destroyed. When PTPN2 is blocked, leukemia cells stop growing and begin to die. An experimental drug targeting this enzyme also slowed tumor growth in mice, offering a promising new direction for AML treatment.
Researchers at China Pharmaceutical University have identified a new vulnerability in acute myeloid leukemia (AML) cells: an enzyme called PTPN2 that acts as a bodyguard for c-MYC, a protein that fuels uncontrolled cell growth. Normally, c-MYC gets tagged for destruction, but PTPN2 removes that tag — keeping c-MYC alive and leukemia cells proliferating. When scientists dialed down PTPN2 levels in lab experiments, leukemia cells stalled in their growth cycle and started dying off.
The team also tested WS35, an experimental small-molecule inhibitor of PTPN2, in human leukemia cell lines and in mice implanted with leukemia cells. The compound reproduced the anti-tumor effects seen when PTPN2 was genetically suppressed — and slowed tumor growth in mice without significant side effects.
Key Takeaways:
Why it matters: AML remains difficult to treat, with drug resistance and toxicity limiting current options. Targeting the PTPN2–c-MYC axis offers a novel preclinical strategy to disrupt a core survival mechanism in leukemia cells, potentially complementing existing therapies like venetoclax.
