Author

D. T. Starczynowski

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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Assay:bulk RNA-seq· 3 Organism:human· 3 Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:chromatin & epigenetic regulation· 1 Assay:CITE-seq· 1

Frequent Co-Authors

A. Verma· 2 shared K. Pradhan· 2 shared L. Schwartz· 2 shared S. Gordon-Mitchell· 2 shared A. Fromowitz· 1 shared A. Kulkarni· 1 shared A. Pellagatti· 1 shared A. Shastri· 1 shared

Activity by Year

2022-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 37 mutual co-author links

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2 shared papersCancer Biology

A. Verma

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Author profile →

3 papers

Recent·Most cited

Broad de-regulated U2AF1 splicing is prognostic and augments leukemic transformation via protein arginine methyltransferase activation

M. Venkatasubramanian, L. Schwartz, N. Ramachandra, J. Bennett, K. R. Subramanian, S. Gordon-Mitchell, A. Fromowitz, K. Pradhan, D. Shechter, S. Sahu, D. Heiser, P. Scherle, X. Chen, C. Chetal, A. Kulkarni, , N. G. Salomonis

The paper identifies a splicing mechanism in AML independent of mutations, showing it drives poor prognosis and can be targeted with PRMT5 inhibition.

bioRxiv · Feb 4, 2024Cancer Biology

Chronic inflammation suppresses del(5q)-like MDS HSCs via p53

T. Muto, C. Walker, K. Choi, M. Niederkorn, C. Ishikawa, M. Varney, K. Hueneman, D. T. Starczynowski

This study shows chronic inflammation impairs del(5q)-like MDS HSPCs by activating p53, leading to reduced quiescence and disease severity, which may drive p53 mutations in myeloid malignancies.

bioRxiv · Jun 22, 2022 · PreprintCancer Biology

Activation of targetable inflammatory immune signaling is seen in Myelodysplastic Syndromes with SF3B1 mutations

G. Choudhary, A. Pellagatti, B. Agianian, M. Smith, T. D. Bhagat, S. Gordon-Mitchell, S. Pandey, N. Shah, S. Aluri, L. Schwartz, V. Steeples, R. Booher, M. Ramachandra, M. Samson, M. Carbajal, , A. Verma

This study identifies a longer, oncogenic IRAK4 isoform caused by SF3B1 mutations in MDS/AML, which is targetable by IRAK4 inhibition.

bioRxiv · Mar 9, 2022Cancer Biology