  Primary tumors infrequently lead to demise of cancer patients; instead,
mortality and a significant degree of morbidity result from the growth of
secondary tumors in distant organs (metastasis). It is well-known that
malignant tumors induce the formation of a lymphatic and a blood vascular
network around themselves. A similar but far less studied process occurs in
relation to the nervous system and is referred to as \emph{neoneurogenesis}; in
fact, recent studies have demonstrated that tumors initiate their own
innervation. However, the relationship between tumor progression and the
nervous system is still poorly understood. This process is most likely
regulated by a multitude of factors in the tumor-nerve microenvironment and it
is therefore important to study the interactions between the nervous system and
tumor cells through mathematical/computational modelling: this may reveal the
most significant factors of the plethora of interacting elements regulating
neoneurogenesis. The present work is a first attempt to model the
neurobiological aspect of cancer development through a (simple) system of
differential equations. The model confirms the experimental observations that a
tumor is able to promote nerve formation/elongation around itself, and that
high levels of nerve growth factor (NGF) and axon guidance molecules (AGMs) are
recorded in the presence of a tumor. Our results also reflect the observation
that high stress levels (represented by higher norepinephrine release by
sympathetic nerves) contribute to tumor development and spread, indicating a
mutually beneficial relationship between tumor cells and neurons. The model
predictions suggest novel therapeutic strategies, aimed at blocking the stress
effects on tumor growth and dissemination.
