Mathematical model is the most powerful tool to elucidate cancer growth and evolution, but over the years it still has defects. Although there are some models having been developed to capture tumor space, these models often can not study genetic alterations. While non-space model can more accurately describe the evolution of tumors, it can not clarify their three-dimensional structure.
Now researchers from Harvard University, Edinburgh University and Johns Hopkins University collaborated to develop a first solid tumor model that may reflect the three-dimensional shape and genetic evolution. The new model explains that the cancer usually has a surprising number of genetic mutations, causing and driving mutation to spread to the entire tumor and evolve resistance mechanisms. The study was published on the Nature.
Professor Martin Nowak, Harvard University, mentioned that, in the past, we are mainly used non-spatial model to study the evolution of cancers, but these models can not describe the spatial characteristics of solid tumors. Now, however, for the first first time we can do that.
He also said that the new model provides important insights about the partial migration of cancer cells. Cell migration makes cancer grow rapidly, which makes cancer homogeneous and therefore those cancer cells share the same group of mutation. As a result it led to a rapid evolution of drug resistance. He also thought the metastases was caused by local migration.”
In this new study, scientists describe a model for tumor evolution which shows how short-range dispersal and cell turnover can be responsible for rapid cell mixing inside the tumor. They show that “even a small selective advantage of a single cell within a large tumor allows the descendants of that cell to replace the precursor mass in a clinically relevant time frame.” They also demonstrate that the same mechanisms can account for the rapid onset of resistance to chemotherapy.
Their model not only provides insights into spatial and temporal aspects of tumour growth, but also suggests that targeting short-range cellular migratory activity could have marked effects on tumour growth rates.
Source: A spatial model predicts that dispersal and cell turnover limit intratumour heterogeneity, Nature.