Every tumor cell in the mass carries the same driver mutation — the alteration next-generation sequencing found in the patient's biopsy. A targeted drug built for that exact mutation cuts through the tumor fast; the same drug against the wrong mutation barely slows it down. Immunotherapy doesn't care which mutation is driving the tumor at all — instead it rides on tumor mutation burden (TMB): a tumor riddled with mutations presents more neoantigens for the immune system to recognize, so a high-TMB tumor responds well and a low-TMB one barely responds. Chemotherapy is the blunt fallback: mutation-agnostic, always mildly effective, never a knockout.
dN/dt = r·N·(1 − N/K) − k·N
k = k_targeted · dose if therapy mutation == tumor mutation
k = k_immuno · (TMB/40) · dose if therapy = immunotherapy
k = k_chemo · dose if therapy = chemotherapy (mutation-agnostic)
- Tumor driver mutation — the actionable alteration found on molecular profiling (EGFR, HER2 or BRAF V600E); only a targeted drug built for this exact mutation gets the high kill-rate bonus.
- Therapy — targeted (mutation-specific), immunotherapy (TMB-dependent) or chemotherapy (weak but universal); switch it mid-run to see the response curve change shape immediately.
- Tumor mutation burden — mutations per megabase found in the tumor's sequencing panel; only matters for immunotherapy, where a higher burden means more neoantigens for T-cells to target.
- Dose intensity — scales whichever kill rate is currently active; the tumor's own logistic growth rate keeps pushing back regardless of therapy.
Real-world relevance: this mismatch between a targeted drug and the wrong mutation is exactly why molecular tumor boards sequence a biopsy before choosing therapy — giving erlotinib to an EGFR-negative tumor, or pembrolizumab to a tumor with a rock-bottom TMB, wastes the treatment window a patient doesn't have.