Author

Kith Pradhan

Albert Einstein College of MedicineORCID 0000-0001-7089-1652Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 2 Neuroscience· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 2 Research Focus:differential expression· 2 Organism:mouse· 2 Approach:statistical model· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Approach:deep learning· 1 Approach:experimental assay· 1

Frequent Co-Authors

Shanisha Gordon-MitchelliD· 2 shared Abdullah KhasawnehiD· 1 shared Aditi ShastriiD· 1 shared Aishwarya Kulkarni· 1 shared Amit K. VermaiD· 1 shared Amit VermaiD· 1 shared Anna SkwarskaiD· 1 shared Ariel Fromowitz· 1 shared

Activity by Year

2024-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersCancer Biology

Shanisha Gordon-MitchellORCID

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3 papers

Recent·Most cited

NeurosciencebioRxivPreprintAug 4, 2026

Genetic and stochastic basis of phenotypic discordance in 16p11.2 mouse model deletion

Julián Taranda, Jana Velı́šková, Sukalp Muzumdar…·Pavel Osten

This study identifies two distinct subgroups of 16p11.2 deletion mice with different seizure susceptibility, circuit activity, brain structure, and gene expression profiles.

DOI 10.64898/2026.07.29.741187

mousebulk RNA-seq

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Cancer BiologyLeukemiaPeer-reviewedFeb 17, 2026

A STAT3 Degrader Demonstrates Pre-clinical Efficacy in Venetoclax resistant Acute Myeloid Leukemia

Samarpana Chakraborty, Claudia Morganti, Kimberly S. Zaldana…·Aditi Shastri

This paper shows that targeting STAT3 with a degrader can overcome Venetoclax resistance in AML by reducing MCL1 and improving mitochondrial function.

14 citationstop 1%

mouseproteomics

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Cancer BiologybioRxivFeb 4, 2024

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

Meenakshi Venkatasubramanian, Leya Schwartz, Nandini Ramachandra…·Nathan Salomonis

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

DOI 10.1126/scitranslmed.adr1471

humanbulk RNA-seq

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