Author

M. Majidi

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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Research Focus:cancer & tumor microenvironment· 3 Approach:experimental assay· 3 Organism:human· 3 Assay:bulk RNA-seq· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Research Focus:gene regulatory network inference· 1 Assay:proteomics· 1

Frequent Co-Authors

I. M. MERAZ· 3 shared J. A. Roth· 3 shared E. J. Shpall· 2 shared F. Haderk· 2 shared F. Meng· 2 shared J. W. Riess· 2 shared J. Wang· 2 shared L. Gao· 2 shared

Activity by Year

2021-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersCancer Biology

I. M. MERAZ

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Author profile →

3 papers

Recent·Most cited

NPRL2 gene therapy induces effective antitumor immunity in KRAS/STK11 mutant anti-PD1 resistant metastatic non-small cell lung cancer (NSCLC) in a humanized mouse model

I. M. MERAZ, M. Majidi, R. Song, F. Meng, L. Gao, Q. Wang, J. Wang, E. J. Shpall, J. A. Roth

This study shows NPRL2 gene therapy reduces lung metastases in KRAS/STK11 mutant NSCLC in humanized mice by enhancing immune cell infiltration and reducing T cell inhibitory signals.

bioRxiv · Mar 26, 2024Cancer Biology

3-Phosphoinositide-dependent kinase 1 drives acquired resistance to osimertinib

I. M. Meraz, M. Majidi, B. Fang, F. Meng, L. Gao, R. Shao, R. Song, F. Li, M. J. Ha, Q. Wang, J. Wang, E. J. Shpall, S. Y. Jung, F. Haderk, P. Gui, , J. A. Roth

This study identifies PDK1 as a driver of osimertinib resistance in NSCLC, showing its inhibition sensitizes resistant cells and correlates with disease progression.

bioRxiv · Dec 10, 2021Cancer Biology

A focal adhesion kinase-YAP signaling axis drives drug tolerant persister cells and residual disease in lung cancer

F. Haderk, C. Fernandez-Mendez, L. Cech, J. Yu, I. M. Meraz, V. Olivas, D. Barbosa Rabago, D. L. Kerr, C. Gomez, D. V. Allegakoen, J. Guan, K. N. Shah, K. A. Herrington, O. M. Gbenedio, S. Nanjo, , T. G. Bivona

This study identifies a FAK-YAP signaling axis that drives drug-tolerant persister cells and residual disease in lung cancer, showing that inhibiting this axis improves tumor response to targeted therapies.

bioRxiv · Oct 23, 2021Cancer Biology