Author

D. Ayeni

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· 2 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Approach:genetic perturbation / CRISPR· 1 Organism:human· 1

Frequent Co-Authors

K. Politi· 3 shared S. Levy· 3 shared C. Robles-Oteiza· 2 shared R. Homer· 2 shared A. Kuhlmann· 1 shared A. Kuhlmann-Hogan· 1 shared A. Wurtz· 1 shared B. Miller· 1 shared

Activity by Year

2018-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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3 shared papersCancer Biology

K. Politi

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

EGFR+ lung adenocarcinomas coopt alveolar macrophage metabolism and function to support EGFR signaling and growth

A. Kuhlmann-Hogan, T. Cordes, Z. Xu, K. Traina, C. Robles-Oteiza, D. Ayeni, E. M. Kwong, S. Levy, M. Nobari, G. Z. Cheng, R. J. Shaw, S. L. Leibel, C. Metallo, K. Politi, S. M. Kaech

This study shows EGFR-mutant lung adenocarcinomas exploit alveolar macrophage metabolism via GM-CSF--PPARγ signaling to support tumor growth and EGFR signaling, suggesting new therapeutic strategies combining statins and PPARγ inhibition.

bioRxiv · Apr 15, 2023 · PreprintImmunology

Genetic determinants of EGFR-Driven Lung Cancer Growth and Therapeutic Response In Vivo

G. Foggetti, C. Li, H. Cai, J. Hellyer, W.-Y. Lin, D. Ayeni, K. Hastings, J. Choi, A. Wurtz, L. Andrejka, D. Maghini, N. Rashleigh, S. Levy, R. Homer, S. Gettinger, , K. Politi

This study investigates how genetic alterations affect EGFR-driven lung cancer growth and therapy response using a mouse model and CRISPR-Cas9 editing.

Cancer Discovery · Mar 11, 2021Peer-reviewedCancer Biology

Tumor regression mediated by oncogene withdrawal or erlotinib stimulates infiltration ofinflammatory immune cells in EGFR mutant lung tumors

D. Ayeni, B. Miller, A. Kuhlmann, P.-C. Ho, C. Robles-Oteiza, M. Gaefele, S. Levy, F. de Miguel, C. Perry, T. Guan, D. Zelterman, R. Homer, Z. Liu, S. Kaech, K. Politi

The paper shows that erlotinib and oncogene withdrawal in EGFR mutant lung tumors increase infiltration of inflammatory immune cells, suggesting immunostimulatory effects of tumor regression.

bioRxiv · Jan 27, 2018Cancer Biology