Reaction-Difusion Model of Early Carcinogenesis:The Effects of Influx of Mutated Cells

Abstract

In this paper we explore a new model of field carcinogenesis, inspired by lungcancer precursor lesions, which includes dynamics of a spatially distributed population ofpre-cancerous cells c(t, x), constantly supplied by an influx μ of mutated normal cells. Cellproliferation is controlled by growth factor molecules bound to cells, b(t, x). Free growthfactor molecules g(t, x) are produced by precancerous cells and may diffuse before they becomebound to other cells. The purpose of modelling is to investigate the existence of solutions,which correspond to formation of multiple spatially isolated lesions of pre-cancerous cellsor, mathematically, to stable spike solutions. These multiple lesions are consistent with thefield theory of carcinogenesis. In a previous model published by these authors, the influxof mutated cells was equal to zero, μ = 0, which corresponded to a single pre-malignantcolony of cells. In that model, stable patterns appeared only if some of the growth factorwas supplied from outside, arguably, a biologically tenuous hypothesis. In the present model,when μ > 0, that hypothesis is no more required, which makes this model more realistic.We present a range of results, both mathematical and computational, which taken togetherallow understanding the dynamics of this model. The equilibrium solutions in the currentmodel result from the balance between new premalignant colonies being initiated and theold ones dying out.