Mathematical model of phenotypic plasticity predicts interconversion is a drug target for neuroblastoma.

In a three-population ordinary-differential-equation model of neuroblastoma, five of 64 interconversion patterns reduce the target population, with N-suppressing plus S inhibition most consistently stable during treatment.

• Why it matters: Interconversion among noradrenergic, mesenchymal-like, and intermediate states is linked to treatment resistance and relapse, but which inhibitor–transition patterns work best is unclear.
• What they did: The model uses three coupled ODEs with logistic growth, interconversion, and drug-induced death, then applies stability and multi-stage or cyclic scheduling across all 64 interconversion patterns.
• The result: N targeting is more effective at higher interconversion rates, while S targeting is more effective at lower rates; N-suppressing with an S inhibitor, then S-suppressing with an N inhibitor, yields more reliable remission.

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