Author

K. L. Abbott

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· 7 Cell Biology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 7 Organism:human· 6 Research Focus:cell type annotation· 4 Assay:bulk RNA-seq· 3 Research Focus:differential expression· 3 Research Focus:cancer & tumor microenvironment· 2 Research Focus:cell signaling & trafficking· 2 Research Focus:development & morphogenesis· 2

Frequent Co-Authors

M. G. Vander Heiden· 5 shared B. T. Do· 3 shared C. A. Lewis· 3 shared T. Kunchok· 3 shared A. Ali· 2 shared A. M. Darnell· 2 shared A. Muir· 2 shared C. B. Clish· 2 shared

Activity by Year

2020-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 38 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

5 shared papersCancer Biology

M. G. Vander Heiden

Mutual co-authors in cluster

Author profile →

8 papers

Recent·Most cited

Metabolite profiling of human renal cell carcinoma reveals tissue-origin dominance in nutrient availability

K. L. Abbott, A. Ali, B. I. Reinfeld, A. A. I. Deik, S. Subudhi, M. D. Landis, R. A. Hongo, K. L. Young, T. Kunchok, C. S. Nabel, K. D. Crowder, J. R. Kent, M. L. L. Madariaga, R. K. Jain, K. E. Beckermann, , M. G. Vander Heiden

This study profiles metabolites in renal cell carcinoma tissue and fluid to show that nutrient availability is more influenced by tissue-specific factors than tumor-driven changes.

bioRxiv · Dec 24, 2023Cancer Biology

Screening in serum-derived medium reveals differential response to compounds targeting metabolism

K. L. Abbott, A. Ali, D. Casalena, B. T. Do, R. Ferreira, J. H. Cheah, C. K. Soule, A. Deik, T. Kunchok, D. R. Schmidt, S. Renner, S. E. Honeder, M. Wu, S. H. Chan, T. Tseyang, , M. G. Vander Heiden

The paper screens compounds targeting metabolism in serum-derived medium to identify differential responses in cancer cells, aiming to improve drug response prediction.

bioRxiv · Feb 25, 2023Cancer Biology

Myristoylated Neuronal Calcium Sensor-1 captures the ciliary vesicle at distal appendages

T. Kanie, R. Ng, K. L. Abbott, O. Pongs, P. K. Jackson

This study identifies NCS1 as a key protein recruited by CEP89 to the distal appendage, facilitating ciliary vesicle capture and cilium formation.

bioRxiv · Jan 6, 2023Cell Biology

Cancer tissue of origin constrains the growth and metabolism of metastases

S. Sivanand, Y. Gultekin, P. Winter, S. Y. Vermeulen, K. Tchourine, K. L. Abbott, L. V. Danai, F. Gourgue, B. T. Do, K. Crowder, T. Kunchok, A. N. Lau, A. M. Darnell, A. Jefferson, S. Morita, , M. G. Vander Heiden

This study shows that cancer tissue-of-origin influences the metabolism and growth preferences of both primary and metastatic tumors.

bioRxiv · Aug 17, 2022Cancer Biology

Nucleotide depletion promotes cell fate transitions by inducing DNA replication stress

B. T. Do, P. P. Hsu, S. Y. Vermeulen, Z. Wang, T. Hirz, K. L. Abbott, N. Aziz, J. M. Replogle, S. Bjelosevic, J. Paolino, S. Nelson, S. Block, A. M. Darnell, R. Ferreira, H. Zhang, , M. G. Vander Heiden

The paper shows that nucleotide depletion and DNA replication stress drive cell fate transitions in hematopoietic systems by activating lineage-specific maturation genes.

bioRxiv · Aug 16, 2022Cancer Biology

Leukemia-intrinsic determinants of CAR-T response revealed by iterative in vivo genome-wide CRISPR screening.

A. Ramos, C. E. Koch, Y. Liu, R. D. Hellinger, T. Kyung, K. L. Abbott, J. Froese, D. Goulet, K. S. Gordon, R. C. Larson, J. G. Doench, A. Regev, M. G. Vander Heiden, M. V. Maus, M. E. Birnbaum, M. Hemann

This study identifies leukemia-intrinsic resistance mechanisms to CAR-T therapy through in vivo CRISPR screening in a murine B-ALL model, revealing IFNγ/JAK/STAT and antigen processing pathways as key mediators.

bioRxiv · Feb 15, 2022 · PreprintCancer Biology

Cancer cells depend on environmental lipids for proliferation when electron acceptors are limited

Z. Li, B. W. Ji, P. D. Dixit, E. C. Lien, K. Tchourine, A. M. Hosios, K. L. Abbott, A. M. Westermark, E. F. Gorodetsky, L. B. Sullivan, M. Vander Heiden, D. Vitkup

This study shows that cancer cells rely on environmental lipids for proliferation under conditions of limited electron acceptors, such as hypoxia or mitochondrial inhibition.

bioRxiv · Jun 8, 2020Cancer Biology

Combined Proteomic and Genetic Interaction Mapping Reveals New RAS Effector Pathways and Susceptibilities

M. R. Kelly, K. Kostyrko, K. Han, N. Mooney, E. E. Jeng, K. L. Abbott, D. M. Gwinn, E. A. Sweet-Cordero, M. C. Bassik, P. K. Jackson

The paper identifies new RAS effector pathways and synthetic lethal interactions in lung adenocarcinoma using proteomic and genetic screening.

bioRxiv · Apr 20, 2020Cancer Biology