The IL13RA2-HAS2 axis as therapeutic co-targets in DIPG

Already funded by the Matthew “Iron Matt” Larson Foundation

Diffuse intrinsic pontine glioma (DIPG) is a fatal childhood brain cancer afflicting approximately 350 new patients in the US per year. Most DIPG patients survive less than 1 year. Chemotherapy, radiation, and many newly explored drugs are nearly ineffective. Our research group started a clinical trial for a drug called panobinostat as a promising treatment for DIPG. However, while panobinostat will likely help extend life, cures for DIPG are needed.

We looked at gene activity in 28 DIPG samples and found two genes highly active in DIPG tumor cells and absent in normal cells: IL13RA2 and HAS2. IL13RA2 and HAS2 have both been shown to cause tumor cell growth in brain cancer. HAS2 also modifies the environment around cancer cells, making cancer cells have an easier time growing and thus the tumor grows faster.
Recently, published studies have suggested that HAS2 and IL13RA2 being highly expressed at the same time can control a process that turns normal cells into “stem-like” cells. “Stem-like” cells replicate quickly and can move around easily, and are thought to be a cause of extremely dangerous cancers, such as DIPG.

We hypothesize that HAS2 and IL13RA2 turn DIPG cells into “stem-like” cells that grow quickly and invade into the cancer-promoting environment caused by HAS2. We will perform experiments in petri dishes to confirm our hypothesis. We will also test a HAS2 + IL13RA2 targeting combination treatment in mice with human DIPG to determine if HAS2 and IL13RA2 treatment can be an effective cure for DIPG.

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