Tumor growth and progression result from complex controls that appear
to be facilitated by the growth factors (GFs) which emerge from the tu
mor and find responsive targets both within the tumor and in the surro
unding host. For example, basic fibroblast growth factor (bFGF) and va
scular endothelial growth factor (VEGF) are both angiogenic signals wh
ich appear to emerge from upregulated genetic messages in the prolifer
ating rim of a solid tumor in response to tumor-wide hypoxia. If these
signals are generated in response to unfavorable environmental condit
ions, i.e. a tumor-wide decrease in oxygen tension, then the tumor may
be playing a role in manipulating its own environment, Two questions
are raised in this paper: (1) How does the host respond to such signal
s? (2) Is there a linkage between the host's response and the ultimate
growth of the tumor? To answer these questions, we have idealized the
se adaptive signals within a mathematical model of tumor growth. The h
ost response is characterized by a function which represents the host'
s carrying capacity for the tumor, If the function is constant, then e
nvironmental control is strictly limited to tumor shape and mitogenic
signal processing, However, if we assume that the response of the loca
l stroma to these signals is an increase in the host's ability to supp
ort an ever larger tumor, then the model describes a positive feedback
controller, In this paper, we summarize our previous results and ask
the question: What form of host response is reasonable, and how will i
t affect ultimate tumor growth? We examine some specific candidate res
ponse functions, and analyze them for system stability, In this model,
unstable states correspond to 'infinite' tumor growth, We will also d
iscuss countervailing negative feedback signals and their roles in mai
ntaining tumor stability.