Author

William J. Gibson

Broad InstituteORCID 0000-0003-3159-8175Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Organism:human· 3 Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Research Focus:cell type annotation· 1 Approach:deep learning· 1 Research Focus:differential expression· 1 Research Focus:host-pathogen & immune response· 1 Assay:proteomics· 1

Frequent Co-Authors

Maximilian CarsoniD· 3 shared Ananthan SadagopaniD· 2 shared Eriks J. ZamursiD· 2 shared Aaron R. ThorneriD· 1 shared Amanda GarzaiD· 1 shared Anurag Sodhi· 1 shared Anwesha NagiD· 1 shared Benjamin L. EbertiD· 1 shared

Activity by Year

2025-2026 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 25 mutual co-author links

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3 shared papersBiochemistry

Maximilian CarsonORCID

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

An epigenetic bifunctional that toggles between transactivation and repression

Ananthan Sadagopan, Maximilian Carson, Eriks J. Zamurs, Shanivi Srikonda, Cary N. Weiss, Michael J. Bond, Anurag Sodhi, Katherine A. Donovan, Julia K Ryan, Eric S. Fischer, Kimberly Stegmaier, Srinivas Raghavan Viswanathan, Benjamin L. Ebert, William J. Gibson

This paper identifies a bifunctional small molecule that can induce both transactivation and repression of gene expression depending on cellular context.

bioRxiv · Mar 20, 2026 · PreprintBiochemistry

Epigenetic dysregulation of metabolic programs mediates liposarcoma cell plasticity

Erica Maria Pimenta, Amanda Garza, Sabrina Yvonne Camp, Jihye Park, Samantha E. Hoffman, Laura Valderrábano, Jingxin Fu, Kevin Bi, Maximilian Carson, Julie Karam, Breanna M. Titchen, Sofia Medjahed, Melin Janardan Khandekar, Erin E. Shannon, Yun Jee Kang, , Eliezer M. Van Allen

This study identifies epigenetic dysregulation of metabolic programs in liposarcoma, linking IGF1 loss and PPARG2 deficiency to dedifferentiation and proposing IGF1R-targeted therapy.

Science Translational Medicine · Jan 21, 2026Peer-reviewedCancer Biology

p53 protein abundance is a therapeutic window across TP53 mutant cancers and is targetable with proximity inducing small molecules

Ananthan Sadagopan, Maximilian Carson, Eriks J. Zamurs, Nicholas Garaffo, Heng-Jui Chang, Stuart L. Schreiber, Matthew M. Meyerson, William J. Gibson

The paper shows that p53 protein abundance in TP53 mutant cancers can be exploited to selectively kill these cells using proximity-inducing small molecules.

Nature Chemical Biology · Nov 3, 2025Peer-reviewedBiochemistry