Chemotherapy Dosing & Tumor Resistance Simulator

Therapy Controls

Chemotherapy dose intensity 1.00×

Dosing interval 14 d

Concurrent radiation therapy

Simulation speed 8 d/s

Live Readouts

Tumor burden

0.5%

Days elapsed

0 d

Resistant fraction

1.0%

Cycles given

Chemo-sensitive cells Drug-resistant clone

How it works

Tumor growth follows the Gompertz law — fast while small, saturating as it approaches a carrying capacity K (the vasculature/space limit):

dN/dt = r · N · ln(K / N)

The population is split into a chemo-sensitive clone and a small drug-resistant clone, each growing with its own rate (resistance carries a small fitness cost, so r_res < r):

dN_s/dt = r     · N_s · ln(K / N_total)
dN_r/dt = r_res · N_r · ln(K / N_total)

Every dosing cycle applies instantaneous log-kill (Skipper's model) — a fixed fraction of cells dies per dose, not a fixed number, and the resistant clone survives far better:

N_s → N_s · e^(−k_s · dose)
N_r → N_r · e^(−k_r · dose),   k_r ≪ k_s

A slow mutation term nudges a trickle of sensitive cells into the resistant pool every cycle (clonal evolution). Because the resistant clone is barely touched by chemo, repeated cycles act as an evolutionary filter: the sensitive population collapses while the resistant one is left to regrow into the space it vacates — exactly the mechanism behind acquired chemoresistance and relapse.

Radiation therapy kills both clones by an independent, non-cross-resistant mechanism (DNA double-strand breaks rather than the chemo drug's target), so enabling it alongside chemo suppresses the resistant clone too — mirroring why concurrent chemoradiation is standard of care for many solid tumors.

Tumor cell population — 1.0% of lethal burden

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