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Area of Science:

  • Oncology
  • Mathematical Biology
  • Evolutionary Medicine

Background:

  • Tumor cell populations can exhibit antifragility, gaining benefits from treatment-induced environmental fluctuations.
  • Treatment fluctuations may either promote or inhibit the evolution of resistance to targeted therapies.

Purpose of the Study:

  • To investigate the impact of treatment fluctuations on the evolution of tumor cell resistance.
  • To develop and validate novel treatment schedules that leverage antifragility principles to enhance therapeutic efficacy and prolong sensitivity.

Main Methods:

  • Analysis of dose-response curve convexity to predict responses to fluctuating treatments.
  • Experimental validation of continuous versus intermittent (high/low) dosing schedules in vivo.
  • Application of mathematical modeling to understand tumor evolutionary trajectories under different treatment protocols.

Main Results:

  • Dose response was identified as a convex (fragile) function, while resistance onset rate was concave (antifragile).
  • Uneven dosing protocols were predicted to be outperformed by continuous protocols for convex dose responses.
  • Fluctuating treatment schedules, even without altering cumulative dose, were shown to alter tumor evolutionary trajectories.

Conclusions:

  • Tumor cell antifragility is a critical factor in treatment response and resistance evolution.
  • Alternative, switching treatment protocols (evolutionary antifragile therapy) can be designed to limit resistance evolution.
  • Leveraging treatment fluctuations offers a promising strategy to maximize response and maintain prolonged sensitivity to targeted therapies.