Author

Soledad A. Camolotto

Huntsman Cancer Institute

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· 2

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:differential expression· 1 Research Focus:gene regulatory network inference· 1 Approach:genetic perturbation / CRISPR· 1

Frequent Co-Authors

Eric L. SnyderiD· 2 shared Anna K. Waters· 1 shared Benjamin T. SpikeiD· 1 shared Gabriela Fort· 1 shared Headtlove Essel DadzieiD· 1 shared Henry Arnold· 1 shared Katherine GillisiD· 1 shared Kayla T. O’TooleiD· 1 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersCancer Biology

Eric L. SnyderORCID

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2 papers

Recent·Most cited

HNF4α controls growth, identity and response to KRAS inhibition of invasive mucinous adenocarcinoma of the lung

Headtlove Essel Dadzie, Yangsook Song Green, Soledad A. Camolotto, Matthew Gumbleton, Yutaka Maeda, Benjamin T. Spike, Eric L. Snyder

bioRxiv · Jun 6, 2025 · PreprintCancer Biology

Opposing lineage specifiers induce a pro-tumor hybrid-identity state in lung adenocarcinoma

Gabriela Fort, Henry Arnold, Soledad A. Camolotto, Kayla T. O’Toole, Rushmeen Tariq, Anna K. Waters, Katherine Gillis, Eric L. Snyder

This study identifies HNF4 as a driver of hybrid-identity states in KRAS-driven lung adenocarcinoma, showing that opposing lineage specifiers promote tumor progression and affect therapy response.

bioRxiv · Dec 2, 2024 · PreprintCancer Biology