Author

A. Sayad

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 Immunology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:drug response / drug discovery· 2 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1

Frequent Co-Authors

B. G. Neel· 2 shared A. Dhabaria· 1 shared A. Heguy· 1 shared A. J. Gehring· 1 shared A. Khodadadi-Jamayran· 1 shared A. Nixon· 1 shared A. S. Mer· 1 shared A. Singh· 1 shared

Activity by Year

2017-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 36 mutual co-author links

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2 shared papersCancer Biology

B. G. Neel

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

B Cells Promote T Cell Immunosenescence and Mammalian Aging Parameters

S. Khan, M. Chakraborty, F. Wu, N. Chen, T. Wang, Y. T. Chan, A. Sayad, J.-D. S. Vasquez, M. Kotlyar, K. Nguyen, Y. Huang, F. J. Alibhai, M. Woo, R.-K. Li, M. Husain, , D. A. Winer

The paper identifies B cells as drivers of T cell immunosenescence and aging, showing that targeting B cells with CD20 antibodies can reverse age-related T cell dysfunction.

bioRxiv · Sep 12, 2023 · PreprintImmunology

Ontogeny and Vulnerabilities of Drug-Tolerant Persisters in HER2+ Breast Cancer

C. A. Chang, J. Jen, S. Jiang, A. Sayad, A. S. Mer, K. R. Brown, A. Nixon, A. Dhabaria, K. H. Tang, D. Venet, C. Sotiriou, J. Deng, K.-k. Wong, S. Adams, P. Meyn, , B. G. Neel

This study identifies drug-tolerant persisters (DTPs) in HER2+ breast cancer and reveals their origins and vulnerabilities to TKI resistance.

bioRxiv · Aug 28, 2020Cancer Biology

SHP2 Is Required for BCR-ABL1-Induced Hematologic Neoplasms

S. Gu, A. Sayad, G. Chan, W. Yang, Z. Lu, C. Virtanen, R. A. Van Etten, B. G. Neel

This study shows SHP2 is essential for BCR-ABL1-induced hematologic cancers, affecting proliferation and signaling pathways in pre-B cells.

bioRxiv · Jun 30, 2017Cancer Biology