Author

R. K. Bradley

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· 4 Cell Biology· 1

Signature Assays, Organisms & Methods

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Organism:human· 4 Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Approach:statistical model· 2 Research Focus:benchmarking· 1 Assay:bulk RNA-seq· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

J. M. B. Pineda· 2 shared A. Kentsis· 1 shared A. Pellagatti· 1 shared A. Shastri· 1 shared A. Ventura· 1 shared A. Verma· 1 shared A. Wickrema· 1 shared B. Agianian· 1 shared

Activity by Year

2020-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

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2 shared papersCancer Biology

J. M. B. Pineda

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Author profile →

5 papers

Recent·Most cited

DUX4 is a common driver of immune evasion and immunotherapy failure in metastatic cancers

J. M. B. Pineda, R. K. Bradley

This study identifies DUX4 as a common driver of immune evasion and immunotherapy failure in metastatic cancers, associated with poor prognosis and resistance to PD-L1 blockade.

bioRxiv · Jul 10, 2023Cancer 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

The origins and consequences of UPF1 variants in pancreatic adenosquamous carcinoma

J. T. Polaski, D. B. Udy, L. F. Escobar-Hoyos, G. Askan, S. D. Leach, A. Ventura, R. Kannan, R. K. Bradley

This study investigates UPF1 mutations in pancreatic adenosquamous carcinoma, finding they are likely non-pathogenic and not a common driver of the disease.

bioRxiv · Aug 14, 2020Cancer Biology

Convergent organization of aberrant MYB complex controls oncogenic gene expression in acute myeloid leukemia

S. Takao, L. Forbes, M. Uni, S. Cheng, J. M. B. Pineda, Y. Tarumoto, P. Cifani, G. Minuesa, C. Chen, M. G. Kharas, R. K. Bradley, C. R. Vakoc, R. P. Koche, A. Kentsis

This study identifies aberrant MYB complex assembly as a driver of oncogenic gene expression in AML and shows that targeting this complex can induce differentiation and apoptosis.

bioRxiv · May 5, 2020Cancer Biology

Transgenic mice expressing tunable levels of DUX4 develop characteristic facioscapulohumeral muscular dystrophy-like pathophysiology ranging in severity

T. I. Jones, G.-L. Chew, P. Barraza-Flores, S. Schreier, M. Ramirez, R. D. Wuebbles, D. J. Burkin, R. K. Bradley, P. L. Jones

This paper develops a bi-transgenic mouse model that allows controlled expression of DUX4 to study FSHD-like pathophysiology with varying severity.

Skeletal Muscle · Apr 11, 2020Peer-reviewedCell Biology