Author

S. Thongjuea

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· 6 Cell Biology· 1

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Research Focus:cell type annotation· 7 Organism:human· 7 Research Focus:differential expression· 5 Approach:experimental assay· 5 Assay:scRNA-seq· 5 Approach:deep learning· 3 Assay:bulk RNA-seq· 2 Research Focus:cell-cell communication· 2

Frequent Co-Authors

B. Psaila· 4 shared A. J. Mead· 3 shared G. Wang· 3 shared J. O'Sullivan· 3 shared N. Sousos· 3 shared A. Hamblin· 2 shared A. Korshunov· 2 shared A. Rademacher· 2 shared

Activity by Year

2019-2024 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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4 shared papersCancer Biology

B. Psaila

Mutual co-authors in cluster

Author profile →

7 papers

Recent·Most cited

Cell-state plasticity drives heterogeneity in Group 3/4 medulloblastoma

P. Joshi, P. B. G. da Silva, K. Okonechnikov, T. Stelzer, I. Sarropoulos, M. Sepp, J. Nolle, M. V. Pour-Jamnani, A. Rademacher, T. Yamada, C. Schneider, J. Schmidt, L. Bianchini, P. Schaefer, K. Leiss, , L. M. Kutscher

This study identifies cell-state plasticity as a driver of heterogeneity in Group 3/4 medulloblastomas, showing that transcription factor perturbation can redirect tumor cells along different differentiation trajectories.

bioRxiv · Feb 9, 2024 · PreprintCancer Biology

Medulloblastoma oncogene aberrations are not involved in tumor initiation, but essential for disease progression and therapy resistance

K. Okonechnikov, P. Joshi, V. Koerber, A. Rademacher, M. Bortolomeazzi, J.-P. Mallm, P. B. G. da Silva, B. Statz, M. Sepp, I. Sarropoulos, T. Yamada-Saito, J. Vaillant, A. Wittmann, K. Schramm, M. Blattner-Johnson, , S. M. Pfister

The paper uses single-cell technologies to show that large-scale chromosomal aberrations drive medulloblastoma initiation, while single-gene oncogenic events like MYC contribute to progression and therapy resistance.

bioRxiv · Feb 9, 2024Cancer Biology

Chromothripsis orchestrates leukemic transformation in blast phase MPN through targetable amplification of DYRK1A

C. K. Brierley, B. H. Yip, G. Orlando, H. Goyal, S. Wen, J. Wen, M. F. Levine, M. G. Jakobsdottir, A. Rodriguez-Meira, A. Adamo, M. Bashton, A. Hamblin, S. A. Clark, J. O'Sullivan, L. Murphi, , A. J. Mead

The paper identifies chromothripsis-induced amplification of DYRK1A in blast phase MPN as a driver of aggressive disease and a potential therapeutic target.

bioRxiv · Dec 8, 2023 · PreprintCancer Biology

A pro-inflammatory stem cell niche drives myelofibrosis through a targetable galectin 1 axis

R. Li, M. Colombo, G. Wang, A. Rodriguez-Romera, J. O'Sullivan, S.-A. Clark, J. Perez Saez, Y. Meng, A. Khan, S. Wen, P. Dong, W. Zhou, N. Sousos, L. Murphy, M. Clarke, , B. Psaila

This study identifies a pro-inflammatory stem cell niche that drives myelofibrosis via galectin 1, offering a targetable pathway for therapy.

bioRxiv · Aug 5, 2023 · PreprintCancer Biology

Deciphering TP53 mutant Cancer Evolution with Single-Cell Multi-Omics

A. Rodriguez-Meira, R. Norfo, W. X. Wen, A. L. Chedeville, H. Rahman, J. OSullivan, G. Wang, E. Louka, W. Kretzschmar, A. Paterson, C. Brierley, J.-E. Martin, C. Demeule, M. Bashton, N. Sousos, , A. J. Mead

The paper uses single-cell multi-omic analysis to study TP53-mutant cancer evolution in leukaemia, identifying a role for chronic inflammation in promoting TP53 mutant clones.

bioRxiv · Mar 28, 2022 · PreprintCancer Biology

Identification and Age-dependent Increase of Platelet Biased Human Hematopoietic Stem Cells

M. Aksoz, G.-A. Gafencu, B. S. Stoilova, M. Buono, Y. Meng, N. A. Jakobsen, M. Metzner, S.-A. Clark, R. Beveridge, S. Thongjuea, P. Vyas, C. Nerlov

The paper identifies platelet-biased human hematopoietic stem cells (HSCs) and shows their proportion and transcriptional platelet priming increase with age.

bioRxiv · Jan 14, 2022 · PreprintCell Biology

Single-cell analyses reveal aberrant pathways for megakaryocyte-biased hematopoiesis in myelofibrosis and identify mutant clone-specific targets

B. Psaila, G. Wang, A. Rodriguez Meira, E. F. Heuston, R. Li, J. O'Sullivan, N. Sousos, S. Anderson, Y. Senis, O. Weinberg, M. L. Callicchio, NIH Intramural Sequencing Core, D. Iskander, D. Royston, D. Milojkovic, , A. J. Mead

The paper uses single-cell multi-omics to identify aberrant megakaryocyte pathways in myelofibrosis and discovers JAK2-mutant-specific targets for immunotherapy.

bioRxiv · May 20, 2019Cancer Biology