Genegoggle is unveiling the chromatin physical properties (3D DNA folding) of cells derived from diffuse intrinsic pontine gliomas (DIPG). The current work is oriented to finding DNA-DNA contacts that can be used as cell type markers to characterise DIPG cells and as drug delivery targets. Michał Marzęcki, Chief Technical Officer, declared that “this is another crucial milestone confirming the rightness of our solution and increasing our value proposition”.
Also Read: Fluence Launches SPYDR 2h, Enabling Commercial Cannabis Cultivators to Produce Higher Crop Yields
One of the hallmarks of DIPG is a mutation in histone H3.3 that leads to the change of the amino acid lysine to methionine (K27M), which influences epigenetic processes. Genegoggle has successfully identified dozens of DNA-DNA contacts (aka DNA loops) exclusive to DIPG cells carrying the K27M mutation and changes in the H3K27me3 profile when compared with normal cells. By using cutting-edge epigenetic technology, many of these DNA loops have been linked to differential gene expression and differential chromatin accessibility.
“These results inform us about several histone modification profiles to describe chromatin states of DIPG cells better, that will allow us to identify novel characteristics and clinical targets,” said Jakub Mieczkowski, PhD, and Chief Executive Officer. The data was obtained during the Illumina Accelerator partnership and in collaboration with Prof. Jacek Majewski from McGill University. When asked about Genegoggle‘s future, Chief Business Officer Marcin Kruczyk, PhD, said, “we believe that we are strongly positioned for the next round of fundraising to take this journey forward”.
About diffuse intrinsic pontine glioma (DIPG)
Diffuse intrinsic pontine glioma is the most common type of paediatric brain-stem cancer. The median survival for children with DIPG is less than one year from diagnosis, and little improvement in survival has been achieved in decades. The current diagnostic method is MRI examination (magnetic resonance imaging) and usually takes place when the symptoms are advanced. A genetic hallmark of DIPG is a mutation in the gene H3F3A that encodes histone H3.3.