Author

A. Conway

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 Cell Biology· 1

Signature Assays, Organisms & Methods

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Approach:genetic perturbation / CRISPR· 3 Organism:human· 3 Research Focus:drug response / drug discovery· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell type annotation· 1

Frequent Co-Authors

K. Stegmaier· 2 shared A. L. Robichaud· 1 shared A. Letai· 1 shared A. Puissant· 1 shared A. Robichaud· 1 shared A. Su· 1 shared A. Villegas· 1 shared B. Adane· 1 shared

Activity by Year

2020-2023 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 20 mutual co-author links

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2 shared papersCancer Biology

K. Stegmaier

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Author profile →

3 papers

Recent·Most cited

A Serum- and Feeder-Free System to Generate CD4 and Regulatory T Cells from Human iPSCs

H. Fong, M. Mendel, J. Jascur, L. Najmi, K. Kim, G. Lew, S. Garimalla, S. Schock, J. Hu, A. Villegas, A. Conway, J. D. Fontenot, S. Zompi

This paper describes a serum- and feeder-free method to generate CD4 and regulatory T cells from human iPSCs, enabling scalable production for therapeutic applications.

bioRxiv · Jul 1, 2023Cell Biology

An in vivo CRISPR screening platform for prioritizing therapeutic targets in AML

S. Lin, C. Larrue, B. K. A. Seong, N. V. Dharia, M. Kuljanin, C. Wechsler, G. Kugener, A. Robichaud, A. Conway, T. N. Mashaka, S. Mouche, B. Adane, J. Ryan, J. D. Mancias, S. T. Younger, , K. Stegmaier

This study identifies novel therapeutic targets for AML using an in vivo CRISPR screening platform, revealing SLC5A3 as a metabolic vulnerability and MARCH5 as an apoptosis regulator.

bioRxiv · Dec 28, 2020Cancer Biology

Targeting serine hydroxymethyltransferases 1 and 2 for T-cell acute lymphoblastic leukemia therapy.

Y. Pikman, N. Ocasio-Martinez, G. Alexe, S. Kitara, F. F. Diehl, A. L. Robichaud, A. Conway, A. Su, J. Qi, G. Roti, C. A. Lewis, A. Puissant, M. G. Vander Heiden, K. Stegmaier

This study identifies SHMT1 and SHMT2 as therapeutic targets in T-ALL by showing their inhibition impairs leukemia progression and is effective despite methotrexate resistance.

bioRxiv · Feb 6, 2020Cancer Biology