Rajees Varghese
A5047990683- Cancer Genomics and Diagnostics
- Pancreatic and Hepatic Oncology Research
- Bioinformatics and Genomic Networks
- Phagocytosis and Immune Regulation
- RNA modifications and cancer
- Metabolomics and Mass Spectrometry Studies
- RNA Research and Splicing
- Lung Cancer Treatments and Mutations
- Computational Drug Discovery Methods
- Single-cell and spatial transcriptomics
- Cancer Cells and Metastasis
Washington University in St. Louis
2018-2022
James S. McDonnell Foundation
2021-2022
For the past decade, cancer genomic studies have focused on mutations leading to splice-site disruption, overlooking those having splice-creating potential. Here, we applied a bioinformatic tool, MiSplice, for large-scale discovery of splice-site-creating (SCMs) across 8,656 TCGA tumors. We report 1,964 originally mis-annotated clear evidence creating alternative splice junctions. TP53 and GATA3 26 18 SCMs, respectively, ATRX has 5 from lower-grade gliomas. Mutations in 11 genes, including...
Pancreatic ductal adenocarcinoma is a lethal disease with limited treatment options and poor survival. We studied 83 spatial samples from 31 patients (11 treatment-naïve 20 treated) using single-cell/nucleus RNA sequencing, bulk-proteogenomics, transcriptomics cellular imaging. Subpopulations of tumor cells exhibited signatures proliferation, KRAS signaling, cell stress epithelial-to-mesenchymal transition. Mapping mutations copy number events distinguished populations normal transitional...
Although large-scale, next-generation sequencing (NGS) studies of cancers hold promise for enabling precision oncology, challenges remain in integrating NGS with clinically validated biomarkers. To overcome such challenges, we utilized the Database Evidence Precision Oncology (DEPO) to link druggability genomic, transcriptomic, and proteomic Using a pan-cancer cohort 6570 tumors, identified tumors potentially druggable biomarkers consisting drug-associated mutations, mRNA expression...
SUMMARY Pancreatic Ductal Adenocarcinoma (PDAC) is a lethal disease with limited treatment options and poor survival. We studied 73 samples from 21 patients (7 treatment-naïve 14 treated neoadjuvant regimens), analyzing distinct spatial units performing bulk proteogenomics, single cell sequencing, cellular imaging. Spatial drivers, including mutant KRAS , SMAD4 GNAQ, were associated differential phosphosignaling metabolic responses compared to wild type. Single subtyping discovered 12 of...
Abstract Cancer development is an incremental process. Mutations that initiate clonal hematopoiesis often arise in individuals many years before disease symptoms are apparent. We discovered blood somatic mutations 8,612 germline samples The Genome Atlas, drawing fundamental distinctions between these events and variants. In a preliminary scan of 5,949 samples, 13,345 blood-specific were identified, preferentially distributed across 26 genes, including ones frequently mutated hematologic...