Author

M. P. Carroll

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· 5

Signature Assays, Organisms & Methods

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Approach:experimental assay· 5 Organism:human· 4 Research Focus:cancer & tumor microenvironment· 3 Research Focus:cell type annotation· 3 Research Focus:clustering· 2 Research Focus:differential expression· 2 Approach:statistical model· 2 Assay:bulk RNA-seq· 1

Frequent Co-Authors

I. S. Csete· 2 shared L. A. Miles· 2 shared R. L. Bowman· 2 shared R. L. Levine· 2 shared S. E. Meyer· 2 shared A. A. Moverley· 1 shared A. Apffel· 1 shared A. D. Goldberg· 1 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 26 mutual co-author links

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2 shared papersCancer Biology

I. S. Csete

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5 papers

Recent·Most cited

A mitochondrial surveillance mechanism activated by SRSF2 mutations in hematologic malignancies

X. Liu, S. A. Devadiga, R. F. Stanley, R. Moroow, K. Janssen, M. Quesnel-Vallieres, O. Pomp, A. A. Moverley, C. Li, N. Skuli, M. P. Carroll, J. Huang, D. C. Wallace, K. W. Lynch, O. Abdel-Wahab, P. S. Klein

This study shows that SRSF2 mutations disrupt mitochondrial mRNA splicing, impair complex I function, and increase mitophagy through a PINK1 splicing mechanism, identifying mitophagy as a therapeutic target in MDS and AML.

bioRxiv · Jun 25, 2023 · PreprintCancer Biology

Clonal evolution mediates Menin-inhibitor resistance in KMT2A-rearranged leukemias.

L. Mahdavi, H. Goodrow, F. Alikarami, A. Lenard, S. S. Riedel, C. Libbrecht, I. Bowser, S. K. Tasian, C. Falkenstein, B. Manning, S. Skuli, M. P. Carroll, G. Wertheim, S. Cai, G. McGeehan, , K. M. Bernt

This study shows that Menin-inhibitor resistance in KMT2A-rearranged leukemias arises through clonal evolution, with resistance developing without prior exposure to the inhibitor.

bioRxiv · Mar 16, 2023Cancer Biology

Modeling clonal evolution and oncogenic dependency in vivo in the context of hematopoietic transformation

R. L. Bowman, A. Dunbar, T. Mishra, W. Xiao, M. R. Waarts, I. Fernandez Maestre, S. E. Eisman, L. Cai, S. F. Cai, P. Sanchez Vela, S. Mowla, A. R. Martinez Benitez, Y. Park, I. S. Csete, A. Krishnan, , R. L. Levine

This study models clonal evolution and oncogenic dependency in hematopoietic transformation using reversible mutagenesis and allelic frameworks.

bioRxiv · May 18, 2022 · PreprintCancer Biology

BCOR and BCORL1 mutations disrupt PRC1.1 repressive function in leukemia by unlinking the RING-PCGF1 enzymatic core from target genes

E. J. Schaefer, W. C. Wang, C. A. Meyer, P. Cejas, M. D. Gearhart, E. R. Adelman, I. Fares, A. Apffel, K. Lim, Y. Xie, C. J. Gibson, M. Schenone, H. M. Murdock, E. S. Wang, L. P. Gondek, , R. C. Lindsley

This study shows BCOR and BCORL1 mutations disrupt PRC1.1 function in leukemia by separating its enzymatic core from chromatin targets, leading to treatment resistance.

bioRxiv · Mar 8, 2021 · PreprintCancer Biology

Single cell mutational profiling delineates clonal trajectories in myeloid malignancies

L. A. Miles, R. L. Bowman, T. R. Merlinsky, I. S. Csete, A. Ooi, R. Durruthy-Durruthy, M. Bowman, C. Famulare, M. A. Patel, P. Mendez, C. Ainali, M. Manivannan, S. Sahu, A. D. Goldberg, K. Bolton, , R. L. Levine

This study uses single-cell mutational profiling to analyze clonal trajectories in myeloid malignancies, revealing patterns of mutation acquisition and clonal complexity.

bioRxiv · Feb 7, 2020 · PreprintCancer Biology