Author

J. V. Alvarez

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· 8

Signature Assays, Organisms & Methods

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Approach:experimental assay· 7 Research Focus:cancer & tumor microenvironment· 6 Organism:mouse· 6 Assay:bulk RNA-seq· 3 Approach:statistical model· 3 Research Focus:cell type annotation· 2 Research Focus:gene regulatory network inference· 2 Organism:human· 2

Frequent Co-Authors

R. Lupo· 4 shared R. Newcomb· 4 shared A. V. DiMarco· 3 shared D. B. Fox· 3 shared A. Walens· 2 shared J. S. Damrauer· 2 shared K. Owzar· 2 shared N. M. G. Garcia· 2 shared

Activity by Year

2019-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 30 mutual co-author links

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4 shared papersCancer Biology

R. Lupo

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Author profile →

8 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

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

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

Epithelial-to-mesenchymal transition activates Bcat1 expression to promote recurrent tumor growth

D. B. Fox, J. V. Alvarez

This study shows that Bcat1 expression is upregulated by EMT in breast cancer cells and correlates with EMT gene signatures, suggesting BCAT1 inhibition could target tumor recurrence.

bioRxiv · Dec 8, 2020 · PreprintCancer 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

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

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