Author

T. S. Lawrence

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

Click to filter author papers

Cancer Biology· 3

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 3 Organism:human· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Assay:proteomics· 2 Research Focus:metabolism & bioenergetics· 1 Organism:mouse· 1 Assay:spatial transcriptomics· 1

Frequent Co-Authors

A. Ahsan· 1 shared A. de Carvalho· 1 shared A. J. Scott· 1 shared A. L. Elaimy· 1 shared A. Lin· 1 shared A. Obrien· 1 shared A. Rao· 1 shared A. Rehemtulla· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 18 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

1 shared paperCancer Biology

A. Ahsan

Author profile →

3 papers

Recent·Most cited

GTP signaling links metabolism, DNA repair, and responses to genotoxic stress

W. Zhou, Z. Zhao, A. Lin, J. Yang, J. Xu, K. Wilder-Romans, A. Yang, J. Li, S. Solanki, J. Speth, N. Walker, A. J. Scott, A. U. Kothari, Y. Yao, E. R. Peterson, , D. R. Wahl

This study identifies a GTP-mediated signaling pathway linking metabolism to DNA repair and resistance to genotoxic stress in glioblastoma and non-malignant cells.

bioRxiv · Apr 12, 2023Cancer Biology

Subclonal evolution and expansion of THY1-positive cells is associated with recurrence in glioblastoma

W. N. Al-Holou, H. Wang, V. Ravikumar, M. Oneka, R. Verhaak, H. Kim, D. Pratt, S. Camelo-Piragua, C. Speers, D. Wahl, S. Shankar, T. Hollon, O. Sagher, J. Heth, K. Muraszko, , A. Rehemtulla

This paper identifies THY1-positive, mesenchymal/stem-like cells as drivers of glioblastoma recurrence and shows that targeting TGFβ signaling can restore sensitivity to therapy.

bioRxiv · Sep 10, 2021Cancer Biology

Mutant EGFR is a preferred SMURF2 substrate of ubiquitination: role in enhanced receptor stability and TKI sensitivity

P. Ray, K. Raghunathan, A. Ahsan, U. S. Allam, S. Shukla, V. Basrur, S. Veatch, T. S. Lawrence, M. K. Nyati, D. Ray

This paper identifies SMURF2-mediated ubiquitination of EGFR mutants as a mechanism enhancing receptor stability and TKI sensitivity.

bioRxiv · Apr 2, 2020 · PreprintCancer Biology