Author

M. Bere

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· 2

Signature Assays, Organisms & Methods

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Approach:experimental assay· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:chromatin & epigenetic regulation· 1 Research Focus:host-pathogen & immune response· 1 Organism:human· 1

Frequent Co-Authors

J. Calvo· 2 shared J. Krais· 2 shared K. Cong· 2 shared M. Peng· 2 shared N. J. Panzarino· 2 shared N. Johnson· 2 shared S. Cantor· 2 shared S. Nayak· 2 shared

Activity by Year

2019-2019 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 44 mutual co-author links

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2 shared papersCancer Biology

J. Calvo

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2 papers

Recent·Most cited

PARPi synthetic lethality derives from replication-associated single-stranded DNA gaps

K. Cong, A. N. Kousholt, M. Peng, N. J. Panzarino, W. T. C. Lee, S. Nayak, J. Krais, J. Calvo, M. Bere, E. Rothenberg, N. Johnson, J. Jonkers, S. Cantor

This study shows PARPi sensitivity in BRCA-deficient cells arises from replication-associated ssDNA gaps, not replication speed.

bioRxiv · Sep 25, 2019Cancer Biology

Replication gaps underlie BRCA-deficiency and therapy response

N. J. Panzarino, J. Krais, M. Peng, M. Mosqueda, S. Nayak, S. Bond, J. Calvo, K. Cong, M. Doshi, M. Bere, J. Ou, B. Deng, L. J. Zhu, N. Johnson, S. Cantor

This study challenges the existing model of BRCA-deficiency hypersensitivity to chemotherapy by proposing that ssDNA replication gaps, rather than DNA double strand breaks or stalled forks, underlie the therapeutic response.

bioRxiv · Sep 25, 2019Cancer Biology