Author

J. Tamburini

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

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Cancer Biology· 6

Signature Assays, Organisms & Methods

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Assay:bulk RNA-seq· 5 Research Focus:cancer & tumor microenvironment· 5 Organism:human· 5 Research Focus:drug response / drug discovery· 4 Approach:experimental assay· 4 Research Focus:cell type annotation· 3 Research Focus:differential expression· 3 Approach:statistical model· 3

Frequent Co-Authors

J.-E. Sarry· 5 shared C. Larrue· 4 shared C. Recher· 3 shared E. Boet· 3 shared F. Vergez· 3 shared M. Sabatier· 3 shared S. Mouche· 3 shared C. Bosc· 2 shared

Activity by Year

2020-2023 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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5 shared papersCancer Biology

J.-E. Sarry

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Author profile →

6 papers

Recent·Most cited

Ferritinophagy is a Druggable Vulnerability of Quiescent Leukemic Stem Cells

C. Larrue, S. Mouche, P. Angelino, M. Sajot, R. Birsen, F. Vergez, C. Recher, V. Mansat-De Mas, Q. Gu, J. Xu, P. Tsantoulis, J.-E. Sarry, J. Tamburini

The paper identifies ferritinophagy as a therapeutic target in quiescent leukemic stem cells, showing that inhibiting NCOA4 reduces leukemia.

bioRxiv · Dec 18, 2023 · PreprintCancer Biology

SCD inhibition eradicates AML displaying high de novo fatty acid desaturation and synergizes with chemotherapy

V. Dembitz, H. Lawson, R. Burt, C. Philippe, S. C. James, S. Atkinson, J. Durko, L. M. Wang, J. Campos, A. M. Magee, K. Woodley, M. J. Austin, A. Rio-Machin, P. Casado-Izquierdo, F. Bewicke-Copley, , P. Gallipoli

SCD inhibition induces AML cell death and synergizes with chemotherapy to prolong survival in murine AML models.

bioRxiv · Aug 2, 2023Cancer Biology

C/EBPα confers dependence to fatty acid anabolic pathways and vulnerability to lipid oxidative stress in FLT3-mutant leukemia

M. Sabatier, R. Birsen, J. Tamburini, J.-E. Sarry

This study identifies C/EBPα's role in promoting lipid anabolism and vulnerability to lipid oxidative stress in FLT3-mutant AML through regulation of the FASN-SCD axis.

bioRxiv · Apr 15, 2022 · PreprintCancer 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

Mitochondrial determinants of response and resistance to venetoclax plus cytarabine duplet therapy in acute myeloid leukemia

C. Bosc, N. Gadaud, A. Bousard, M. Sabatier, G. Cognet, E. Saland, T. Farge, E. Boet, M. Gotanegre, N. Aroua, P.-L. Mouchel, C. Larrue, L. Jarrou, F. Rambow, F. Cabon, , J.-E. Sarry

This study identifies mitochondrial determinants of response and resistance to venetoclax plus cytarabine therapy in AML, showing that OxPHOS is a predictive marker and that targeting ETCI improves outcomes.

bioRxiv · Aug 17, 2020 · PreprintCancer Biology

Adrenomedullin-CALCRL Axis Controls Relapse-Initiating Drug Tolerant Acute Myeloid Leukemia Cells

C. Larrue, N. Guiraud, P.-L. Mouchel, M. Dubois, T. Farge, M. Gotanegre, C. Bosc, E. Saland, M.-L. Travers-Nicolau, M. Sabatier, N. Serhan, A. Sahal, E. Boet, S. Mouche, Q. Heydt, , J.-E. Sarry

The paper identifies the ADM-CALCRL axis as a driver of drug-tolerant AML cells that persist after chemotherapy and proposes it as a therapeutic target to prevent relapse.

bioRxiv · Aug 17, 2020Cancer Biology