Author

G. Telliam

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

Signature Assays, Organisms & Methods

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Research Focus:cell type annotation· 2 Research Focus:differential expression· 2 Approach:experimental assay· 2 Organism:human· 2 Assay:bulk RNA-seq· 1 Assay:CITE-seq· 1 Research Focus:gene regulatory network inference· 1

Frequent Co-Authors

J. Imeri· 2 shared A. Bennaceur Griscelli· 1 shared A. Bennaceur-Griscelli· 1 shared A. G. Turhan· 1 shared A. TURHAN· 1 shared C. Desterke· 1 shared E. Balducci· 1 shared F. Griscelli· 1 shared

Activity by Year

2020-2023 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 27 mutual co-author links

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2 shared papersCancer Biology

J. Imeri

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Modeling Global Genomic Instability in Chronic Myeloid Leukemia (CML) using patient-derived induced pluripotent stem cells (iPSC)

G. Telliam, C. Desterke, J. Imeri, R. Mkacher, N. Oudrhiri, E. Balducci, M. Arnoux, H. Acloque, A. Bennaceur-Griscelli, A. G. Turhan

This study uses patient-derived iPSCs with in vitro mutagenesis to model genomic instability in CML, identifying aberrations linked to blast crisis progression.

Cancers · May 3, 2023Peer-reviewedCancer Biology

Evidence of Increased Hemangioblastic and Early Hematopoietic Potential in Chronic Myeloid Leukemia (CML)-derived Induced Pluripotent Stem Cells (iPSC)

G. Telliam, O. Feraud, S. Baykal, F. Griscelli, J. Imeri, T. Latsis, A. Bennaceur Griscelli, A. TURHAN

This study shows that CML-derived iPSC have expanded hemangioblast and hematopoietic progenitor potential compared to H1-ESC, with AHR signaling as a potential therapeutic target.

bioRxiv · Jun 17, 2020Cancer Biology