WHAT MAKES A TUMOR SWITCH FROM DORMANT TO MALIGNANCY
Cancer constantly
wages war on the human body. Battles are won, lost or sometimes end in a
stalemate. In pancreatic cancer, this stalemate -- known as tumor dormancy --
can last up to 25 years before becoming aggressively malignant, a phenomena
that is poorly understood.
A new computational
model developed in the laboratory of Salvatore Torquato, a Professor of
Chemistry at Princeton University, may help illuminate the conditions
surrounding tumor dormancy and the switch to a malignant state. Published today
inPLOS ONE, the so-called cellular automaton model simulated various
scenarios of tumor growth leading to tumor suppression, dormancy or
proliferation.
"The power of the
model is that it lets people to test medically realistic scenarios,"
Torquato said. In future collaborations, these scenarios could be engineered in
laboratory experiments and the observed outcomes could be used to calibrate the
model.
For each scenario, a
set of rules is imposed on the virtual cell population. Rules are possible
interactions, such as neighboring cell death or immune system suppression, that
dictate cell division through probabilities derived from past experimental
data. Once the researchers programmed the rules, they watched as the simulated
competition unfolded between the tumor and the environmental factors that may
suppress its growth.
"We were very
surprised to observe this phenomena where the tumor all of a sudden began to
rapidly divide," said Duyu Chen, graduate student in the Torquato lab and
lead author on the article. This was the first time that the emergent switch
behavior, which has been observed clinically, occurred spontaneously in a
model, Chen said.
The researchers
evaluated a number of factors that could affect tumor cell growth including
phenotypic changes, mechanical properties and the rate and strength of
suppression factors such as the immune system. One of the model's findings was
the likely suppression of tumors in harsh environments, characterized by high
density and pressure.
The research team also
predicted that if the number of actively dividing cells within the
proliferative rim reached a certain critical level, the tumor was very likely
to begin rapidly growing. This result could provide insight into early cancer
treatment, Chen said.
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