14 DAY TRIAL // Investigators announce the discovery of a gene that contributes to the spread of small cell lung cancer, a highly-aggressive form of lung cancer that makes up for about 15 percent of all cases. The team says that the finding may lead to the development of new therapies against the condition.
Oncologists have been searching for ways of addressing the most aggressive forms of cancer for many years, but thus far their efforts have largely failed. Regardless if it affects the lung, the liver, or the brain, the most deadly cancers move with extreme speed.
Recently, experts at the Massachusetts Institute of Technology (MIT) decided to take on a huge endeavor, which they hoped would reveal the genetic underpinning of SCLC. In the end, their hunch proved to be accurate, and the gene was identified.
In order to find it, the team had to look through hundreds of genetic mutations, using a research method called whole-genome profiling. It was determined that the gene Nuclear Factor I/B (NFIB) is responsible for allowing the invasive cancer to develop with ease.
The investigation turned out to be correct both in humans and mouse models, that researchers had engineered to precise specifications. The lab rodents did not express the two key tumor-suppressor genes, p53 and Rb.
In mice that lacked this defense mechanism, investigators learned that SCLC progressed very fast, leading to death in a short period of time. In humans, 95 percent of all patients who develop this condition die within 5 years.
Without the tumor suppressors, NFIB was found to be over-expressed in both humans and mice. This provides investigators with a new target for future therapies, says Alison Dooley, PhD.
She works in the lab of MIT David H. Koch Institute for Integrative Cancer Research director Tyler Jacks, and is the lead author of a new paper describing the findings. The work is published in the July 15 issue of the journal Genes and Development.
The expert says that this is the first study ever to link NFIB with the development of cancer. The role this gene plays in the body is not yet understood, but experts suspect it has something to do with the development of lung cells.
“The question, always, with mouse models is whether they can tell you anything about a human disease. Some tell you something, but in others, there may be only a similarity in behavior, and the genetic changes are nothing like what is seen in humans,” says Barry Nelkin.
The expert, who is a professor of oncology at the Johns Hopkins University School of Medicine, was not a part of the new investigation.