Author

B. D. Robinson

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· 5 Pathology· 1

Signature Assays, Organisms & Methods

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Organism:human· 6 Assay:bulk RNA-seq· 3 Research Focus:cell type annotation· 3 Research Focus:differential expression· 3 Research Focus:drug response / drug discovery· 3 Approach:experimental assay· 3 Approach:statistical model· 3 Research Focus:gene regulatory network inference· 2

Frequent Co-Authors

M. Loda· 4 shared A. Sboner· 3 shared F. Khani· 3 shared C. Abate-Shen· 2 shared C. E. Barbieri· 2 shared D. Liu· 2 shared E. Davicioni· 2 shared K. Lin· 2 shared

Activity by Year

2021-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 35 mutual co-author links

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4 shared papersCancer Biology

M. Loda

Mutual co-authors in cluster

Author profile →

6 papers

Recent·Most cited

Canonical AREs are tumor suppressive regulatory elements in the prostate

M. A. Augello, X. Chen, D. Liu, K. Lin, A. Hakansson, M. Sjostrom, F. Khani, L. D. Deonarine, Y. Liu, J. Travascio-Green, J. Wu, M. Loda, F. Y. Feng, B. D. Robinson, E. Davicioni, , C. Barbieri

This study identifies canonical AREs as tumor suppressive regulatory elements in prostate cancer, showing their reactivation can induce death in AR+ cancer cells and is linked to better prognosis.

bioRxiv · Feb 23, 2024 · PreprintCancer Biology

NSD2 maintains lineage plasticity and castration-resistance in neuroendocrine prostate cancer

J. J. Li, A. Vasciaveo, D. Karagiannis, Z. Sun, X. Chen, F. Socciarelli, Z. Frankenstein, M. Zou, T. Pannellini, Y. Chen, K. Gardner, B. D. Robinson, J. de Bono, C. Abate-Shen, M. A. Rubin, , M. M. Shen

This study identifies NSD2 as a key driver of lineage plasticity and castration-resistance in neuroendocrine prostate cancer, showing its inhibition can restore sensitivity to AR inhibitors.

bioRxiv · Jul 18, 2023 · PreprintCancer Biology

Distinct mesenchymal cell states mediate prostate cancer progression

H. Pakula, M. Omar, R. Carelli, F. Pederzoli, G. N. Fanelli, T. Pannellini, L. Van Emmenis, S. Rodrigues, C. Fidalgo-Ribeiro, P. V. Nuzzo, N. J. Brady, M. Jere, C. Unkenholz, M. K. Alexanderani, F. Khani, , M. Loda

This study identifies distinct mesenchymal cell states in prostate cancer stroma that correlate with metastatic progression and develops a gene signature to predict patient outcomes.

bioRxiv · Mar 29, 2023Cancer Biology

Using Attention-based Deep Learning to Predict ERG:TMPRSS2 Fusion Status in Prostate Cancer from Whole Slide Images

M. Omar, Z. Xu, S. B. Rand, M. Mohammad, D. C. Salles, E. M. Schaeffer, B. D. Robinson, T. L. Lotan, M. Loda, L. Marchionni

This paper develops a deep learning model to predict ERG:TMPRSS2 fusion status in prostate cancer from whole slide images and identifies associated morphological features.

bioRxiv · Nov 18, 2022 · PreprintPathology

Harbingers of Aggressive Prostate Cancer: Precision Oncology Case Studies

J. Cyrta, D. Prandi, A. Arora, D. H. Hovelson, A. Sboner, A. Rodriguez, T. Fedrizzi, H. Beltran, D. R. Robinson, A. Gopalan, L. True, P. Nelson, B. D. Robinson, J. M. Mosquera, S. Tomlins, , M. Rubin

This study identifies molecular features of primary prostate cancer and their relation to metastasis using genomic and histopathological analysis.

bioRxiv · Nov 30, 2021 · PreprintCancer Biology

SPOP mutation confers sensitivity to AR-targeted therapy in prostate cancer by reshaping the androgen-driven chromatin landscape

I. Grbesa, M. A. Augello, D. Liu, D. R. McNally, C. D. Gaffney, D. Huang, K. Lin, R. Goueli, B. D. Robinson, F. Khani, L. D. Deonarine, M. Blattner, O. Elemento, E. Davicioni, A. Sboner, C. E. Barbieri

This study shows that SPOP mutations in prostate cancer alter the chromatin landscape and AR-driven transcription, making tumors more responsive to AR-targeted therapies.

bioRxiv · Apr 20, 2021 · PreprintCancer Biology