Author

A. V. DiMarco

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· 3

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Assay:DNA methylation· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

J. V. Alvarez· 3 shared N. M. G. Garcia· 2 shared A. Walens· 1 shared B. A. Hanks· 1 shared B. J. McKinney· 1 shared B. McKinney· 1 shared B. R. Kroger· 1 shared F. Wu· 1 shared

Activity by Year

2019-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 22 mutual co-author links

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3 shared papersCancer Biology

J. V. Alvarez

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Author profile →

3 papers

Recent·Most cited

APOBEC3 activity promotes the survival and evolution of drug-tolerant persister cells during acquired resistance to EGFR inhibitors in lung cancer

N. M. G. Garcia, J. N. Becerra, B. J. McKinney, A. V. DiMarco, F. Wu, M. Fitzgibbon, J. V. Alvarez

This study shows APOBEC3 activity supports drug-tolerant persister cells in EGFR inhibitor-resistant lung cancer by promoting transdifferentiation and mutation acquisition.

bioRxiv · Jul 2, 2023 · PreprintCancer Biology

APOBEC mutagenesis inhibits breast cancer growth through induction of a T cell-mediated antitumor immune response

A. V. DiMarco, X. Qin, S. Van Alsten, B. McKinney, N. M. G. Garcia, J. Force, B. A. Hanks, M. A. Troester, K. Owzar, J. Xie, J. V. Alvarez

This study shows that APOBEC mutagenesis in breast cancer promotes T cell-mediated antitumor immunity, leading to tumor growth inhibition and sensitivity to checkpoint inhibitors.

bioRxiv · Feb 13, 2021Cancer Biology

CCL5 promotes breast cancer recurrence through macrophage recruitment in residual tumors

A. Walens, A. V. DiMarco, R. Lupo, B. R. Kroger, J. S. Damrauer, J. V. Alvarez

This study identifies CCL5 as a factor promoting breast cancer recurrence by recruiting macrophages in residual tumors following Her2 downregulation.

bioRxiv · Apr 11, 2019Cancer Biology