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Editorial
. 2022 Jul-Dec;19(7-12):283-287.
doi: 10.1080/14789450.2023.2176757. Epub 2023 Feb 10.

Oncoproteomic profiling of AML: moving beyond genomics

Affiliations
Editorial

Oncoproteomic profiling of AML: moving beyond genomics

Sunil K Joshi et al. Expert Rev Proteomics. 2022 Jul-Dec.
No abstract available

Keywords: AML; FLT3 inhibitor; drug resistance; leukemia; oncoproteomics; phosphoproteomics; proteogenomics.

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Conflict of interest statement

B.J.Druker potential competing interests – Scientific advisory board: Adela Bio, Aileron Therapeutics, Therapy Architects/ALLCRON (inactive), Cepheid, Celgene, DNA SEQ, Nemucore Medical Innovations, Novartis, RUNX1 Research Program, Vivid Biosciences (inactive); scientific advisory board & Stock: Aptose Biosciences, Blueprint Medicines, Enliven Therapeutics, Iterion Therapeutics, GRAIL, Recludix Pharma; Board of Directors & Stock: Amgen, Vincerx Pharma; Board of Directors: Burroughs Wellcome Fund, CureOne; Joint Steering Committee: Beat AML LLS; Advisory Committee: Multicancer Early Detection Consortium; Founder: VB Therapeutics; Sponsored Research Agreement: Enliven Therapeutics, Recludix Pharma; Clinical Trial Funding: Novartis, Astra-Zeneca; Royalties from Patent 6958335 (Novartis exclusive license) and OHSU and Dana-Farber Cancer Institute (one Merck exclusive license, one CytoImage, Inc. exclusive license, and one Sun Pharma Advanced Research Company non-exclusive license); US Patents 4326534, 6958335, 7416873, 7592142, 10473667, 10664967, 11049247.

C.E.Tognon potential competing interests – scientific advisory board: Notable Labs. Sponsored research: Notable Labs. Consultant: St. Jude’s Children’s Hospital.

The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

Figures

Figure 1.
Figure 1.. Proteomics & phosphoproteomics can unveil the dynamic nature of AML.
a. An integrative approach that combined genomic, metabolomic, phosphoproteomic, proteomic analyses with small-molecule inhibitor and genome-wide CRISPR screens revealed a stepwise process for FLT3 inhibitor resistance. This discovery dataset led to the creation of a targeted proteomics panel that was used to investigate FLT3 inhibitor resistance in a subset of ex vivo serial patient samples. Our cell culture model recapitulated the underlying biology of patients resistant to FLT3 inhibitors. b. The integration and aggregation of the amassing - omics data with ex vivo small-molecule inhibitor screening holds the potential to individualize clinical management for patients with cancer.

References

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    1. de Boer B, Prick J, Pruis MG, et al. Prospective isolation and characterization of genetically and functionally distinct AML subclones. Cancer Cell. 2018;34(4):674–689. e8. - PubMed

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