Author

K. M. Bernt

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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Organism:human· 5 Assay:bulk RNA-seq· 3 Research Focus:cell type annotation· 3 Research Focus:drug response / drug discovery· 3 Approach:statistical model· 3 Research Focus:clustering· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2

Frequent Co-Authors

F. Alikarami· 3 shared A. Lenard· 2 shared C. Chen· 2 shared C. Libbrecht· 2 shared G. Wertheim· 2 shared H. M. Xie· 2 shared K. Tan· 2 shared S. K. Tasian· 2 shared

Activity by Year

2019-2023 · peak 2/yr

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10 top collaborators · 30 mutual co-author links

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3 shared papersCancer Biology

F. Alikarami

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5 papers

Recent·Most cited

Oncogenic RAS-Pathway Activation Drives Oncofetal Reprogramming and Creates Therapeutic Vulnerabilities in Juvenile Myelomonocytic Leukemia

M. Hartmann, M. Schoenung, J. Rajak, V. Maurer, L. Hai, K. Bauer, M. Hakobyan, S. Staeble, J. Langstein, L. Jardine, R. Roelz, S. Bohler, E. Khabirova, A.-H. Maag, D. Vonficht, , D. B. Lipka

This study identifies oncofetal reprogramming in juvenile myelomonocytic leukemia, linking RAS-pathway activation to fetal gene expression and revealing CD52 as a therapeutic target.

bioRxiv · Oct 27, 2023Cancer 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

Pharmacologic Inhibition of DYRK1A Results in MYC Hyperactivation and ERK Hyperphosphorylation rendering KMT2A-R ALL Cells Sensitive to BCL2 Inhibition

C. Hurtz, V. S. S. A. Ayyadevara, G. Wertheim, J. Chukinas, J. P. Loftus, S. J. Lee, A. Kumar, R. S. Bhansali, S. Swaminathan, H. Geng, T. Milne, X. Hua, K. M. Bernt, T. Besson, J. Shi, , S. K. Tasian

This study shows that inhibiting DYRK1A in KMT2A-R ALL cells leads to MYC upregulation and ERK hyperphosphorylation, making them sensitive to BCL2 inhibition.

bioRxiv · Oct 2, 2022 · PreprintCancer Biology

Single-cell multi-omics reveals elevated plasticity and stem-cell-like blasts relevant to the poor prognosis of KMT2A-rearranged leukemia

C. Chen, W. Yu, F. Alikarami, Q. Qiu, C.-h. Chen, J. Flournoy, P. Gao, Y. Uzun, L. Fang, Y. Yu, Q. Zhu, K. Wang, C. Libbrecht, A. Felmeister, I. Rozich, , K. Tan

This study uses single-cell multi-omics to identify lineage plasticity and stem-cell-like blasts in KMT2A-rearranged leukemia, linking these features to poor prognosis in infants.

bioRxiv · Dec 6, 2020 · PreprintCancer Biology

Epigenetic regulation of protein translation in KMT2A-rearranged AML

A. Lenard, H. M. Xie, S. S. Riedel, Z.-F. Yuan, N. Zhu, T. Neff, K. M. Bernt

This paper evaluates combinations of DOT1L and EZH2 inhibitors in KMT2A-rearranged AML, finding synergistic effects with a protein translation inhibitor but not with EZH2 inhibition.

bioRxiv · Oct 2, 2019Cancer Biology