The SCC team shared news about the next phase of their research and introduced a new team member who will help with computational modeling for developing new cancer-treating drugs.
Background
Childhood cancer cases rise every year, yet only a few drugs to combat them have been approved for medical use. Finding drug candidates that can target cancer cells is a lengthy process that takes research teams years to complete with the limited equipment they have access to. The Smash Childhood Cancer project teamed up with the World Community Grid to quicken the rate of clinical testing by using computational donations from thousands of volunteers across the world. To date, WCG volunteers have donated over 48,000 CPU years to childhood cancer research and have been instrumental in researching various types of tumors and sarcomas.
New team member!
We’re excited to welcome Nikita Rozanov as the newest member of the SCC research team.
As a recent graduate from Oregon State University with a Bachelor of Science in Chemical Engineering, he worked as a software engineer at Intel and Amazon. His interest eventually migrated towards molecular research using computer-modeled simulations and began working as a visiting researcher at Johns Hopkins University. There, he developed molecular dynamics simulations to predict how nanoparticles interact with proteins.
For the WCG SCC project, Nikita’s expertise in creating computer simulations of proteins and molecules will help in the search for new cancer-treating drugs.
FLI1 research
The SCC team has selected a new target protein – FLI1 – a member of the ETS transcription factor family that controls cell proliferation, differentiation and survival. Fusion of FL1 gene and EWSR1 is frequently present in cases of Ewing Sarcoma and other cancers1. EWSR1 encodes for an RNA-binding protein (EWS), and when EWS is fused to FLI1 the latter becomes constantly activated (instead of finely regulated) creating the molecular environment for tumor formation. The EWS-FLI1 fusion protein has been thought to inhibit p53 and/or activate NOTCH signaling, accelerating sarcoma progression. Useful FLI1 inhibitors need to specifically target this fusion protein but not other related ones to avoid inadvertent side effects2.
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WCG team
References:
- Elzi DJ, Song M, Houghton PJ, Chen Y, Shiio Y. The role of FLI-1-EWS, a fusion gene reciprocal to EWS-FLI-1, in Ewing sarcoma. Genes Cancer. 2015 Nov;6(11-12):452-61. doi: 10.18632/genesandcancer.86. PMID: 26807198; PMCID: PMC4701224.
- Li, Y et al. “The ets transcription factor Fli-1 in development, cancer and disease.” Oncogene vol. 34,16 (2015): 2022-31. doi:10.1038/onc.2014.162.