Author

R. Newcomb

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

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Cancer Biology· 4

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Research Focus:cancer & tumor microenvironment· 4 Approach:experimental assay· 4 Organism:mouse· 4 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Assay:metabolomics· 1 Assay:proteomics· 1

Frequent Co-Authors

J. V. Alvarez· 4 shared R. Lupo· 3 shared D. B. Fox· 2 shared N. W. Mabe· 2 shared A. Walens· 1 shared B. A. Vilona· 1 shared C.-C. LIN· 1 shared E. Dean· 1 shared

Activity by Year

2019-2021 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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4 shared papersCancer Biology

J. V. Alvarez

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4 papers

Recent·Most cited

Context-dependent effects of whole-genome duplication during mammary tumor recurrence

R. Newcomb, E. Dean, J. V. Alvarez

This study investigates the context-dependent effects of whole-genome duplication in mammary tumors, finding that WGD slows recurrence but promotes primary tumor growth.

bioRxiv · May 3, 2021Cancer Biology

Adaptation and Selection Shape Clonal Evolution During Residual Disease and Recurrence

A. Walens, J. Lin, J. S. Damrauer, R. Lupo, R. Newcomb, D. B. Fox, N. W. Mabe, J. Gresham, T. De Buysscher, H. Kelkar, P. Mieczkowski, K. Owzar, J. V. Alvarez

This study tracks clonal evolution in residual breast cancer tumors and finds that recurrence can arise through distinct evolutionary paths with different clonal compositions and drug sensitivities.

bioRxiv · Apr 22, 2020Cancer Biology

G9a Promotes Breast Cancer Recurrence Through Repression of a Pro-inflammatory Program

N. W. Mabe, S. E. Wolery, R. Newcomb, R. C. Meingasner, B. A. Vilona, C.-C. LIN, R. Lupo, J.-T. A. Chi, J. V. Alvarez

This study shows that G9a promotes breast cancer recurrence by repressing pro-inflammatory genes, leading to necroptosis when inhibited.

bioRxiv · Jan 9, 2020Cancer Biology

NRF2-dependent metabolic reprogramming is required for tumor recurrence following oncogene inhibition

D. B. Fox, R. Lupo, L. C. Noteware, R. Newcomb, J. Liu, J. W. Locasale, M. D. Hirschey, J. V. Alvarez

This study identifies NRF2-driven metabolic reprogramming as essential for breast cancer recurrence after oncogene inhibition and shows it can be targeted with glutaminase inhibitors.

bioRxiv · Jan 8, 2019 · PreprintCancer Biology