Cornell researchers eliminated more residual melanoma cells in mice by stimulating an immune response after tumors became resistant to targeted cancer drugs, suggesting that the timing and sequence of therapies could improve treatment.
The findings, published Aug. 5 in the journal Cancer Research, could help researchers determine when immunotherapy may be most effective against cancer cells that remain after an initial therapy shrinks a tumor.
Oncogene-targeted therapies block mutated cancer-causing proteins and can initially shrink tumors. As cancer cells die, immune cells called macrophages secrete proteins that recruit T cells and natural killer cells to attack the cancer, but that response weakens when tumors become resistant.
Researchers gave mice with transplanted melanoma cells the same type of targeted drugs prescribed to people. The tumors initially shrank but left residual cells that resisted further treatment.
The team then used a compound developed at Purdue University to activate macrophages and keep them recruiting cancer-killing immune cells. The approach eliminated many more residual melanoma cells, although it did not completely cure the mice.
Andrew C. White, an associate professor in Cornell's College of Veterinary Medicine and the study's senior author, said tracking tumors at multiple points could help identify when immunotherapy is most likely to clear remaining cells.
The compound used in the study is a research tool, not a treatment ready for patients. Researchers said the results point toward developing a functional drug that could be given after a cancer becomes resistant to targeted therapy.
Chia-Hsin Hsu, a doctoral student in White's lab, was the study's first author. The work was funded by Cornell and the National Institutes of Health.
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