Author

Srabani Sahu

Albert Einstein College of MedicineORCID 0009-0002-3667-3592Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Cancer Biology· 1 Immunology· 1

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 2 Research Focus:cell type annotation· 2 Approach:deep learning· 2 Organism:human· 2 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Approach:experimental assay· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

Amit VermaiD· 2 shared Adila IzgutdinaiD· 1 shared Aishwarya Kulkarni· 1 shared Akul Naik· 1 shared Amrik S. KangiD· 1 shared Antonio ValeriiD· 1 shared Ariel Fromowitz· 1 shared Arun P. WiitaiD· 1 shared

Activity by Year

2024-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 31 mutual co-author links

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2 shared papersImmunology

Amit VermaORCID

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2 papers

Recent·Most cited

Affinity-matured CD72-targeting Nanobody CAR T-cells Enhance Elimination of Antigen-Low B-cell Malignancies

Adila Izgutdina, Tasfia Rashid, William C. Temple, Sarah Aminov, Bonell Patiño-Escobar, Sujata B. Walunj, Huimin Geng, Hiroyuki Takamatsu, Daniel Gil-Alós, Amrik S. Kang, Emilio Ramos, Szu‐Ying Chen, Haley Johnson, Matthew A. Nix, Akul Naik, , Arun P. Wiita

This study shows that affinity-matured CD72-targeting nanobody CAR T-cells improve in vitro efficacy against CD72-low tumors but show limited in vivo benefit, while CD72 expression remains stable after CD19 resistance in B-cell malignancies.

Journal for ImmunoTherapy of Cancer · Dec 1, 2025Peer-reviewedImmunology

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

Meenakshi Venkatasubramanian, Leya Schwartz, Nandini Ramachandra, Joshua Bennett, Krithika R. Subramanian, Xiaoting Chen, Shanisha Gordon-Mitchell, Ariel Fromowitz, Kith Pradhan, David Shechter, Srabani Sahu, Diane Heiser, Peggy Scherle, Kashish Chetal, Aishwarya Kulkarni, , 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.

bioRxiv · Feb 4, 2024Cancer Biology