Vasilena Gocheva, Ph.D.
Affiliations: | 2011 | Weill Cornell Medical College, New York, NY, United States |
Area:
Genetics, Cell Biology, Molecular Biology, OncologyGoogle:
"Vasilena Gocheva"Parents
Sign in to add mentorJohanna Joyce | grad student | 2011 | Weill Cornell Medical College | |
(Exploring the roles of cysteine cathepsins in the tumor microenvironment.) |
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Publications
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Damo M, Fitzgerald B, Lu Y, et al. (2020) Inducible de novo expression of neoantigens in tumor cells and mice. Nature Biotechnology |
Lau AN, Li Z, Danai LV, et al. (2020) Dissecting cell type-specific metabolism in pancreatic ductal adenocarcinoma. Elife. 9 |
Lau AN, Li Z, Danai LV, et al. (2020) Author response: Dissecting cell-type-specific metabolism in pancreatic ductal adenocarcinoma Elife |
Dayton TL, Gocheva V, Miller KM, et al. (2018) Isoform-specific deletion of PKM2 constrains tumor initiation in a mouse model of soft tissue sarcoma. Cancer & Metabolism. 6: 6 |
Gocheva V, Naba A, Bhutkar A, et al. (2017) Quantitative proteomics identify Tenascin-C as a promoter of lung cancer progression and contributor to a signature prognostic of patient survival. Proceedings of the National Academy of Sciences of the United States of America |
Muzumdar MD, Dorans KJ, Chung KM, et al. (2016) Clonal dynamics following p53 loss of heterozygosity in Kras-driven cancers. Nature Communications. 7: 12685 |
Edgington-Mitchell LE, Wartmann T, Fleming AK, et al. (2016) Legumain is Activated in Macrophages during Pancreatitis. American Journal of Physiology. Gastrointestinal and Liver Physiology. ajpgi.00047.2016 |
Prudova A, Gocheva V, Auf dem Keller U, et al. (2016) TAILS N-Terminomics and Proteomics Show Protein Degradation Dominates over Proteolytic Processing by Cathepsins in Pancreatic Tumors. Cell Reports |
Dayton TL, Gocheva V, Miller KM, et al. (2016) Germline loss of PKM2 promotes metabolic distress and hepatocellular carcinoma. Genes & Development |
Akkari L, Gocheva V, Quick ML, et al. (2016) Combined deletion of cathepsin protease family members reveals compensatory mechanisms in cancer. Genes & Development. 30: 220-32 |