Author

N. J. Rossiter

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

Biology Disciplines

Click to filter author papers

Cancer Biology· 4 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Organism:human· 5 Approach:experimental assay· 4 Research Focus:drug response / drug discovery· 3 Assay:bulk RNA-seq· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Approach:genetic perturbation / CRISPR· 1

Frequent Co-Authors

Y. M. Shah· 3 shared C. A. Lyssiotis· 2 shared J. A. Paulo· 2 shared J. D. Mancias· 2 shared J. R. Cantor· 2 shared M. Shin· 2 shared P. Morlacchi· 2 shared Y. Zhang· 2 shared

Activity by Year

2020-2024 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 32 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

3 shared papersCancer Biology

Y. M. Shah

Mutual co-authors in cluster

Author profile →

5 papers

Recent·Most cited

Recharacterization of RSL3 reveals that the selenoproteome is a druggable target in colorectal cancer

S. L. DeAngelo, L. Zhao, S. Dziechciarz, M. Shin, S. Solanki, A. Balia, M. O. El-Derany, C. Castillo, Y. Qin, N. K. Das, H. N. Bell, J. A. Paulo, Y. Zhang, N. J. Rossiter, E. C. McCulla, , Y. M. Shah

This study recharacterizes RSL3 as a broad selenoprotein inhibitor, showing its potential as a therapeutic target for colorectal cancer by inducing ferroptosis.

bioRxiv · Mar 29, 2024 · PreprintCancer Biology

Targeting PIKfyve-driven lipid homeostasis as a metabolic vulnerability in pancreatic cancer

C. Cheng, J. Hu, R. Mannan, R. Bhattacharyya, N. J. Rossiter, B. Magnuson, J. P. Wisniewski, Y. Zheng, L. Xiao, C. Li, D. Awad, T. He, Y. Bao, Y. Zhang, X. Cao, , A. M. Chinnaiyan

This study identifies PIKfyve as a targetable vulnerability in pancreatic cancer by showing its role in lipid metabolism and synthetic lethality with KRAS-MAPK inhibitors.

bioRxiv · Mar 18, 2024Cancer Biology

BRD4-mediated epigenetic regulation of endoplasmic reticulum-mitochondria contact sites is governed by the mitochondrial complex III

B. Chen, D. C. Stark, P. V. Jadhav, T. M. Lynn-Nguyen, B. S. Halligan, N. J. Rossiter, N. Sindoni, M. Shin, J. A. Paulo, M. Chang, I. Koo, S. Koshkin, S. Eyunni, P. Ronchi, M. T. Paulsen, , Y. M. Shah

The paper identifies fedratinib as a drug that increases endoplasmic reticulum-mitochondria contact sites by inhibiting BRD4, revealing a novel epigenetic pathway linking ERMCS to cellular metabolism.

bioRxiv · Feb 2, 2024 · PreprintCell Biology

Conditional lethality profiling reveals anticancer mechanisms of action and drug-nutrient interactions

K. M. Flickinger, K. M. Wilson, N. J. Rossiter, A. L. Hunger, T. D. Lee, M. D. Hall, J. R. Cantor

This study uses conditional lethality profiling in human plasma-like medium to identify drug mechanisms and interactions with nutrients, revealing new therapeutic strategies.

bioRxiv · Jun 4, 2023Cancer Biology

CRISPR screens in physiologic medium reveal conditionally essential genes in human cells

N. J. Rossiter, K. S. Huggler, C. H. Adelmann, H. R. Keys, R. W. Soens, D. M. Sabatini, J. R. Cantor

This study uses CRISPR screens in different media to identify conditionally essential genes in human cells, showing how medium composition affects gene essentiality.

bioRxiv · Aug 31, 2020Cancer Biology