Author

B. R. Paolella

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

Signature Assays, Organisms & Methods

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Organism:human· 4 Approach:experimental assay· 3 Research Focus:cancer & tumor microenvironment· 2 Assay:CRISPR screen· 2 Research Focus:differential expression· 2 Research Focus:drug response / drug discovery· 2 Research Focus:gene regulatory network inference· 2 Approach:statistical model· 2

Frequent Co-Authors

F. Vazquez· 3 shared J. M. McFarland· 3 shared T. R. Golub· 3 shared A. Tsherniak· 2 shared A. Warren· 2 shared D. E. Root· 2 shared J. M. Krill-Burger· 2 shared J. S. Boehm· 2 shared

Activity by Year

2019-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 43 mutual co-author links

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3 shared papersCancer Biology

F. Vazquez

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4 papers

Recent·Most cited

Partial gene suppression improves identification of cancer vulnerabilities when CRISPR-Cas9 knockout is pan-lethal

J. M. Krill-Burger, J. M. Dempster, A. A. Borah, B. R. Paolella, D. E. Root, T. R. Golub, J. S. Boehm, W. Hahn, J. M. McFarland, F. Vazquez, A. Tsherniak

This study compares CRISPR-Cas9 and RNAi screens to identify cancer vulnerabilities, finding that RNAi better detects pan-dependencies while CRISPR identifies more dependencies overall.

bioRxiv · Mar 2, 2022Cancer Biology

Phosphate dysregulation via the XPR1:KIDINS220 protein complex is a therapeutic vulnerability in ovarian cancer

D. P. Bondeson, B. R. Paolella, A. Asfaw, M. Rothberg, T. Skipper, C. Langan, A. Gonzalez, L. Surface, K. Ito, M. Kazachkova, W. N. Colgan, A. Warren, J. Dempster, J. M. Krill-Burger, M. Ericcson, , T. R. Golub

The paper identifies XPR1 and KIDINS220 as therapeutic targets in ovarian cancer by showing their role in phosphate dysregulation leading to cell death.

bioRxiv · Oct 16, 2020Cancer Biology

Multiplexed single-cell profiling of post-perturbation transcriptional responses to define cancer vulnerabilities and therapeutic mechanism of action

J. M. McFarland, B. R. Paolella, A. Warren, K. Geiger-Schuller, T. Shibue, M. Rothberg, O. Kuksenko, A. Jones, E. Chambers, D. Dionne, S. Bender, B. M. Wolpin, M. Ghandi, I. Tirosh, O. Rozenblatt-Rosen, , A. Tsherniak

The paper introduces MIX-Seq, a method for multiplexed single-cell transcriptional profiling of cancer cell responses to perturbations, revealing drug mechanisms and predicting cell viability.

bioRxiv · Dec 8, 2019Cancer Biology

Loss of heterozygosity of essential genes represents a widespread class of potential cancer vulnerabilities

C. A. Nichols, W. J. Gibson, M. S. Brown, J. A. Kosmicki, J. P. Busanovich, H. Wei, L. M. Urbanski, N. Curimjee, A. C. Berger, G. F. Gao, A. D. Cherniack, S. Dhe-Paganon, B. R. Paolella, R. Beroukhim

The paper identifies LOH of essential genes as a class of non-driver cancer vulnerabilities by showing allele-specific inactivation can selectively kill cancer cells.

bioRxiv · Jan 29, 2019Cancer Biology