Characterizing NSD3 Amplification in Lung Cancer

SGC Open Notebook Project to Characterize the HMTase NSD3 Exp020 Objective: NSD3 (WHSC1L1) is amplified in ~5% of Non-Small Cell Lung Cancer patients( cBioPortal : Cerami et al. Cancer Discov. 2012 and Gao et al. Sci. Signal. 2013). However, the implications of this event on the formation and progression of the disease are unclear. While NSD3 may be a driver of lung cancer, it is also plausible that this locus is simply amplified at a higher frequency in the context of cancer-associated genomic instability. To dive deeper into this question I will use The Cancer Genome Atlas (TCGA) lung cancer data-sets to look for associations between NSD3 amplification and mutational status as well as gene expression profiles. This data has been generated by the TCGA Research Network: http://cancergenome.nih.gov/. I hypothesize that if NSD3 amplification is a driving force in a subset of lung tumors, these samples will share similar gene expression profiles and exhibit higher expression levels of NSD3. Here, I am using FirebrowserR (Deng M., et al. Database. 2017 - PMID:28062517), an R client for Broad Institute’s Firehose Web API, which allows TCGA data processed by the Firehose Pipeline to be directly imported into R for analysis.Funding Acknowledgment: The SGC is a registered charity (number 1097737) that receives funds from AbbVie, Bayer Pharma AG, Boehringer Ingelheim, Canada Foundation for Innovation, Eshelman Institute for Innovation, Genome Canada through Ontario Genomics Institute [OGI-055], Innovative Medicines Initiative (EU/EFPIA) [ULTRA-DD grant no. 115766], Janssen, Merck KGaA, Darmstadt, Germany, MSD, Novartis Pharma AG, Ontario Ministry of Research, Innovation and Science (MRIS), Pfizer, São Paulo Research Foundation-FAPESP, Takeda, and Wellcome