Author

S. Meshinchi

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· 7

Signature Assays, Organisms & Methods

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Organism:human· 6 Approach:experimental assay· 5 Assay:bulk RNA-seq· 4 Approach:statistical model· 4 Research Focus:cancer & tumor microenvironment· 3 Assay:ChIP-seq· 3 Research Focus:differential expression· 3 Assay:whole-genome sequencing· 3

Frequent Co-Authors

D. S. Gerhard· 3 shared A. S. Gamis· 2 shared E. A. Kolb· 2 shared J. F. Sarthy· 2 shared J. L. Smith· 2 shared J. M. Guidry Auvil· 2 shared J. Zhang· 2 shared M. A. Smith· 2 shared

Activity by Year

2017-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 28 mutual co-author links

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3 shared papersCancer Biology

D. S. Gerhard

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7 papers

Recent·Most cited

KMT2A oncoproteins induce epigenetic resistance to targeted therapies

D. H. Janssens, M. Duran, D. J. Otto, W. Wu, Y. Xu, D. Kirkey, C. G. Mullighan, J. S. Yi, S. Meshinchi, J. F. Sarthy, K. Ahmad, S. Henikoff

This study shows KMT2A oncoproteins drive lineage-switching and epigenetic resistance in leukemia by dynamically binding chromatin and persisting as ENL-marked lesions despite therapy.

bioRxiv · Dec 29, 2023 · PreprintCancer Biology

Chromatin Profiling of CBFA2T3-GLIS2 AMLs Identifies Key Transcription Factor Dependencies and BRG1 Inhibition as a Novel Therapeutic Strategy

S. Kaonis, J. L. Smith, N. Katiyar, M. Merrill, T. Hylkema, S. Namciu, Q. Le, E. Babaeva, T. Ikeda, S. M. Morris, E. Girard, S. Furuyama, R. Ries, I. Bernstein, S. Meshinchi, , J. F. Sarthy

This study identifies BRG1 inhibition as a therapeutic strategy for CBFA2T3-GLIS2 AML by analyzing chromatin profiles and CRISPR dependencies.

bioRxiv · Aug 30, 2023 · PreprintCancer Biology

Integrative genomics identifies lncRNA regulatory networks across 1,044 pediatric leukemias and extra-cranial solid tumors

A. Modi, G. Lopez, K. L. Conkrite, C. Su, T. C. Leung, S. Ramanan, E. Manduchi, M. E. Johnson, D. Cheung, S. Gadd, J. Zhang, M. A. Smith, J. M. Guidry Auvil, D. S. Gerhard, S. Meshinchi, , S. J. Diskin

The paper identifies lncRNA regulatory networks in pediatric cancers using integrated genomics data from 1,044 samples, revealing their roles in proliferation, metabolism, and DNA damage.

bioRxiv · Dec 10, 2020 · PreprintCancer Biology

A JAK/STAT-Mediated Inflammatory Signaling Cascade Drives Oncogenesis In AF10-Rearranged AML

B. Chen, A. Deshpande, K. O. Barbosa, M. Kleppe, X. Lei, N. Yeddula, A. Rosa Campos, R. Wechsler-Reya, A. Bagchi, S. Meshinchi, C. J. Eaves, I. Jeremias, T. Haferlach, D. Frank, Z. Ronai, , A. Deshpande

This study identifies JAK1 as a therapeutic target in AF10-rearranged AML by showing its role in JAK/STAT-mediated inflammatory signaling and oncogenesis.

bioRxiv · Aug 31, 2020Cancer Biology

Myeloid Lineage Enhancers Drive Oncogene Synergy in CEBPA/CSF3R Mutant Acute Myeloid Leukemia

T. P. Braun, M. Okhovat, C. Coblentz, S. A. Carratt, A. Foley, Z. Schonrock, K. Nevonen, B. Davis, B. Garcia, D. LaTocha, B. R. Weeder, M. R. Grzadkowski, J. C. Estabrook, H. G. Manning, K. Watanabe-Smith, , J. E. Maxson

The paper identifies mutation synergy between CSF3R and CEBPA in AML, showing their interaction at myeloid lineage enhancers and the requirement of CEBPA mutations as an initial event.

bioRxiv · May 15, 2019Cancer Biology

Genetic mechanisms of primary chemotherapy resistance in pediatric acute myeloid leukemia: A report from the TARGET initiative

N. McNeer, J. Philip, H. Geiger, R. Ries, V.-P. Lavallee, M. Walsh, M. Shah, K. Arora, A.-K. Emde, N. Robine, T. A. Alonzo, E. A. Kolb, A. S. Gamis, M. Smith, D. S. Gerhard, , A. Kentsis

The paper identifies genetic mechanisms of primary chemotherapy resistance in pediatric AML through whole-genome and transcriptome sequencing of treatment-failure cases.

bioRxiv · Nov 26, 2018Cancer Biology

Comprehensive characterization of pediatric AML reveals diverse fusion oncoproteins and age-specific mutational interactions

H. Bolouri, J. E. Farrar, T. J. Triche, R. E. Ries, E. L. Lim, T. A. Alonzo, Y. Ma, R. Moore, A. Mungall, M. A. Marra, J. Zhang, X. Ma, Y. Liu, Y. Liu, J. M. Guidry Auvil, , S. Meshinchi

This study characterizes the molecular landscape of pediatric AML, identifying age-specific mutations and fusion oncoproteins that differ from adult AML.

bioRxiv · Oct 10, 2017Cancer Biology