Author

M. G. Lee

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 3

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:mouse· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Assay:bulk RNA-seq· 1 Research Focus:database / resource· 1 Assay:DNA methylation· 1

Frequent Co-Authors

A. Aparicio· 1 shared A. G. Hoang· 1 shared A. K. Jain· 1 shared A. Lazar· 1 shared A. R. Pandiri· 1 shared A. Raman· 1 shared A. Shah· 1 shared B. A. Foster· 1 shared

Activity by Year

2018-2024 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

1 shared paperCancer Biology

A. Aparicio

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

A Lung Cancer Mouse Model Database

L. Cai, Y. Gao, R. J. DeBerardinis, G. Acquaah-Mensah, V. Aidinis, J. E. Beane, S. Biswal, T. Chen, C. P. Concepcion-Crisol, B. M. Gruner, D. Jia, R. Jones, J. M. Kurie, M. G. Lee, P. Lindahl, , J. D. Minna

The paper establishes a database of lung cancer mouse models to improve data comparison and translational relevance by aligning mouse mutations with human lung cancer mutations.

bioRxiv · Feb 28, 2024 · PreprintCancer Biology

KDM4A promotes the progression of neuroendocrine prostate cancer

C. S. L. Mak, M. Zhu, X. Liang, F. Wang, F. Yuan, A. G. Hoang, X. Song, P. Shepherd, D. Liang, J. Suh, B. Pradhan, J. Park, M. Zhang, E. Metzger, R. Schule, , G. Wang

This study identifies KDM4A as a key driver of neuroendocrine prostate cancer progression and shows that targeting KDM4A inhibits tumor growth in preclinical models.

bioRxiv · May 14, 2022 · PreprintCancer Biology

Enhancer Reprogramming Confers Dependence on Glycolysis and IGF signaling in KMT2D Mutant Melanoma

M. Maitituoheti, E. Keung, M. Tang, L. Yan, H. Alam, G. Han, A. Raman, C. Terranova, S. Sarkar, E. Orouji, S. Amin, S. Sharma, M. Williams, N. S. Samant, M. Dhamdhere, , K. Rai

This study identifies KMT2D as a tumor suppressor in melanoma, showing its loss leads to metabolic reprogramming toward glycolysis and dependence on IGF signaling, suggesting therapeutic targeting of these pathways.

bioRxiv · Dec 27, 2018Cancer Biology