Author

A. V. Kossenkov

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cancer Biology· 2 Cell Biology· 1

Signature Assays, Organisms & Methods

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Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Organism:human· 2 Organism:mouse· 2 Approach:statistical model· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Assay:ChIP-seq· 1

Frequent Co-Authors

A. Bertotti· 1 shared A. C. O'Farrell· 1 shared A. L. Welm· 1 shared A. Lafferty· 1 shared A. N. Guterres· 1 shared A. R. Goldman· 1 shared A. Srivastava· 1 shared B. Davis-Dusenbery· 1 shared

Activity by Year

2019-2021 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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1 shared paperCancer Biology

A. Bertotti

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Selective abrogation of S6K2 maps lipid homeostasis as a survival vulnerability in MAPKi-resistant NRASmut melanoma

B. Lipchick, A. N. Guterres, H.-Y. Chen, D. M. Zundell, S. Del Aguila, P. I. Reyes-Uribe, S. Basu, X. Yin, A. V. Kossenkov, Y. Lu, G. B. Mills, Q. Liu, A. R. Goldman, M. E. Murphy, D. W. Speicher, J. Villanueva

This study identifies S6K2 as a vulnerability in MAPK inhibitor-resistant NRAS-mutant melanoma, showing its abrogation disrupts lipid homeostasis and triggers cell death.

bioRxiv · Apr 7, 2021 · PreprintCancer Biology

DOT1L modulates the senescence-associated secretory phenotype through epigenetic regulation of IL1A

K. E. Leon, R. Buj, E. Lesko, E. S. Dahl, C.-W. Chen, Y. Imamura Kawasawa, A. V. Kossenkov, R. P. Hobbs, K. M. Aird

This study shows that DOT1L regulates the senescence-associated secretory phenotype (SASP) through epigenetic control of IL1A expression in oncogene-induced senescence.

bioRxiv · Aug 21, 2020Cell Biology

Conservation of copy number profiles during engraftment and passaging of patient-derived cancer xenografts

X. Y. Woo, J. Giordano, A. Srivastava, Z.-M. Zhao, M. W. Lloyd, R. de Bruijn, Y.-S. Suh, R. Patidar, L. Chen, S. Scherer, M. Bailey, C.-H. Yang, E. Cortes-Sanchez, Y. Xi, J. Wang, , B. E Welm

This study shows that copy number profiles are conserved in patient-derived xenografts (PDXs) through engraftment and passaging, indicating minimal impact from the mouse host on tumor evolution.

bioRxiv · Dec 3, 2019Cancer Biology