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Tumors appear when the cells get rid of their stresses and begin to multiply uncontrollably. But the speed with which a tumor grows depends not only on the speed with which cancer cells can divide, according to a new study.
In looking at brain tumors in mice, researchers at the University of Washington School of Medicine in St. Louis found that immune cells that should defend the body against the disease may sometimes be prompted to provide help and help. comfort to the tumor cells. The researchers found that the more tumors that can recruit immune cells, the faster the tumor grows.
The results, published on May 29 in the journal Neuro-Oncology, suggest that targeting immune system cells could potentially slow the growth of brain tumors in people with the genetic disease neurofibromatosis type 1 (NF1).
It is no longer just the tumor cell. This is also what happens in the tumor environment that drives the growth of brain cancer. This gives us another way to attack these tumors beyond a simple destruction of cancer cells, namely the interruption of communication between tumor cells and cells of the immune system. "
Lead author David H. Gutmann, MD, Ph.D., professor of neurology of the Donald O. Schnuck family and director of the Neurofibromatosis Center at the University of Washington
While people with NF1 usually consult a doctor for birthmarks on their skin, they also run an increased risk of developing tumors. One of the most common tumors in children is a low grade brain tumor called optic glioma, which affects the optic nerve that connects the brain and the eye. Some of these tumors can cause vision loss.
Unfortunately, NF1 is a notoriously variable disease. Doctors can not predict the types of tumors that a person will develop, how fast these tumors will develop or what types of medical conditions the tumors will cause, which prevents doctors from deciding when a tumor needs to be treated. chemotherapy and when it is safe to just watch and wait.
To better understand why some tumors grow faster than others, first author Xiaofan Guo, MD, a graduate student at Gutmann's research lab, created five strains of mice with different genetic changes in the NF1 gene and elsewhere in the genome of the mouse.
The five strains varied greatly in development and tumor growth. Mice belonging to three of the strains developed tumors from the age of about 3 months, with tumors of a mouse strain growing particularly rapidly. Members of the fourth strain did not develop tumors until about 6 months of age, and only a quarter of the fifth strain mice developed brain tumors on the optic nerve.
When the researchers isolated the tumor cells from the mice and grew them in a dish, they found a small difference in tumor cell growth. The growth rates and other properties of the cancer cells were very similar, regardless of the mutation of the tumor cells.
The correlation with overall tumor proliferation in mice was the presence of two types of immune cells – microglia and T cells – in tumors. Guo and Yuan Pan, PhD, a former postdoctoral researcher, have discovered that the tumor cells themselves release proteins from the immune system that attract immune cells to the tumor.
"Cells that should be part of the brain's defense against tumors are now part of the process of making and growing a tumor," said Gutmann, also a professor of genetics, neurological surgery and pediatrics.
Researchers are now trying to leverage this relationship between tumor cells and immune system cells to find new ways to treat brain tumors in people with NF1. One strategy is to slow down tumor growth by preventing microglia or T cells from providing support to cancer cells. However, a more ambitious strategy is to reprogram T cells to no longer promote the growth of tumor cells.
"The idea is to use T cells as Trojan horses," Gutmann said. "These are ongoing experiments: we are trying to change the T cells so that when they enter the brain, instead of promoting the tumor, they close it."
Source:
University of Washington School of Medicine
Journal reference:
Gutmann, D.H. et al. (2019) Genetic and genomic alterations differentially dictate the growth of low-grade gliomas through the recruitment of chemokines specific to T-cell cancer stem cells and microglia. Neuro-Oncology. dx.doi.org/10.1093/neuonc/noz080.
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