Our laboratory investigates the molecular underpinnings of pediatric malignancies with a focus on acute myeloid leukemia (AML) and Ewing sarcoma. Through advanced single-cell genomics and functional studies, we aim to identify novel therapeutic targets and understand disease mechanisms to improve outcomes for children with cancer.
Using cutting-edge multimodal single-cell approaches, we characterized distinct transcriptional programs regulated by EWS::FLI1 fusions in Ewing sarcoma, revealing critical insights into tumor cell plasticity and therapeutic vulnerabilities.
Waltner OG et al. (In Press) bioRxiv PMID: 40667384
With our collaborators, we identified cancer-associated fibroblast-like tumor cells that actively remodel the Ewing sarcoma tumor microenvironment, providing new understanding of how these tumors interact with their surroundings.
Wrenn ED et al. (2023) Clin Cancer Res 29(24): 5140-5154 PMID: 37471463
This work demonstrated how EWS::FLI1 and HOXD13 cooperatively control tumor cell plasticity in Ewing sarcoma, identifying key regulatory networks that maintain the malignant phenotype.
Apfelbaum AA et al. (2022) Clin Cancer Res 28(20): 4466-4478 PMID: 35653119
With our collaborators, we developed a preclinical model of CBFA2T3-GLIS2 acute megakaryoblastic leukemia and identified FOLR1 as a promising CAR T cell target, opening new therapeutic avenues for this aggressive pediatric malignancy.
Le Q et al. (2024) J Clin Invest 134(16) PMID: 39145456
With our collaborators, we outline a comprehensive molecular characterization of NUP98 fusions revealed distinct clinical and biological features, improving risk stratification for children with this AML subtype.
Bertrums EJM et al. (2023) Haematologica 108(8): 2044-2058 PMID: 36815378
With our collaborators, we identified and characterized cryptic ALK fusions in monosomy 7 AML, demonstrating their functional consequences and establishing them as targetable vulnerabilities with available ALK inhibitors.
Manselle MK et al. (2023) Pediatr Blood Cancer 70(4): e30180 PMID: 36720638
Our collaborators show an integrated analysis of stem cell signatures and cytomolecular features provides improved risk determination in pediatric AML, helping to personalize treatment strategies.
Huang BJ et al. (2022) Nat Commun 13(1): 5487 PMID: 36123353
Our collaborators demonstrate that CBFB-MYH11 fusion transcripts distinguish AML cases with distinct molecular landscapes and clinical outcomes, refining prognostic capabilities.
Huang BJ et al. (2021) Blood Adv 5(23): 4963-4968 PMID: 34547772
This work is conducted in collaboration with the Meshinchi Lab, Lawlor Lab, and the Children's Oncology Group
Furlan Lab1241 Eastlake Ave E, Seattle, WA
furlan_lab@fredhutch.org