In celebration of the meeting of the International Mesothelioma Interest Group, or iMig 2012, we at Kazan, McClain, Satterley & Greenwood funded this year’s Young Investigator Awards, as we have done at each meeting since 2008. This is the first in a series discussing the promising work of one of the recipients.
If there is one thing that defines a researcher, it is a never-ending desire to improve upon science’s current body of knowledge. When it comes to the search for a cure for malignant pleural mesothelioma (MPM), this drive usually means good news for patients.
At iMig 2012, we met Karin Schelch, a PhD candidate in molecular biology, who was kind enough to talk to us on video about her team’s research on fibroblast growth factors (FGF) and fibroblast growth factor receptors (FGFR). Both sets of these proteins may serve as targets for MPM treatments.
Defining the roles of the proteins in MPM
According to Schelch, FGF is important for the growth and survival of cells. However, it can also drive the development of several types of malignancies.
Despite this knowledge, the specific role of FGF in MPM had not always been entirely clear. This makes FGF and FGFR important topics for research because a better understanding of their biology can, in turn, lead to a better understanding of how to tackle mesothelioma.
In the laboratory, Schelch and her team conducted several experiments that included MPM cell models, normal mesothelial cells and human tissue samples. Specifically, the researchers were looking at what cells made what proteins.
Ultimately, they found that MPM cells and tumorous tissues have three abnormally active genes: FGFR1, FGF2 and FGF18. Through different experiments, the scientists discovered that stimulating the cells with FGF2 made them more invasive, and that blocking the actions of FGFR1 made the spread and survival of cancer cells more difficult.
“Our data show that blocking the fibroblast growth factors could be a new and more efficient option for mesothelioma treatment,” Schelch told us.
Furthermore, one experiment revealed that diseased cells that are resistant to cisplatin, a standard medication for MPM, are also more sensitive to FGFR1 inhibition. This is good news, considering that Schelch and her team theorize that blockage of FGFR1 could work well in combination with chemotherapy and radiation treatments.
These results were so exciting that the team presented this study at iMig 2012. And on behalf of MPM patients everywhere, we are happy to support work like this.