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Kirkey, D.

Publications and source records attributed to Kirkey, D..

2 recordsLinked to original sources

Cross-Species Morphology Learning Enables Nucleic Acid-Independent Detection of Live Mutant Blood Cells

In both neonates and adults, the presence of malignancy-associated mutations in peripheral blood (PB) correlates with an elevated risk of future neoplastic transformation, with certain mutations, such as KMT2A rearrangements, exhibiting near-complete penetrance. If feasible, pre-malignant screening could enable early intervention and even disease prevention. However, nucleic acid sequencing- and hybridization-based mutation detection have limited cost-efficiency, constraining their use in screening. Here, we introduce a computer vision platform that can identify mutant cells in fresh PB samples that carry KMT2A-MLLT3 (a frequent mutation in pediatric and adult leukemias and detectable in newborn blood samples) or JAK2V617F (a frequent mutation in myeloproliferative neoplasms and clonal hematopoiesis). This is achieved by high-throughput single-cell imaging and mutation detection by machine learning (ML)-powered morphology recognition. The ML models were developed by cross-species learning of conserved features between mutant cells from mouse genetic models and from human samples, enabling a cost-effective approach for detecting mutations in live blood cells. This platform holds promise for pre-malignant screening in asymptomatic neonates and adults with KMT2A-MLLT3 or JAK2V617Fmutation and is potentially generalizable to the detection other malignancy-associate mutations. Our platform provides a novel single-cell morphological data modality that complements existing single-cell genomics.

pathology↗

KMT2A oncoproteins induce epigenetic resistance to targeted therapies

Chromosomal translocations involving the Lysine-Methyl-Transferase-2A (KMT2A) locus generate potent oncogenic fusion proteins (oncoproteins) that disrupt regulation of developmental gene expression. By profiling the oncoprotein-target sites of 36 broadly representative KMT2A-rearranged leukemia samples, including three samples that underwent a lymphoid-to-myeloid lineage-switching event in response to therapy, we find the genomic enrichment of the oncoprotein is highly variable between samples and subject to dynamic regulation. At high levels of expression, the oncoproteins preferentially activate either an acute lymphoblastic leukemia (ALL) program, enriched for pro-B-cell genes, or an acute myeloid leukemia (AML) program, enriched for hematopoietic-stem-cell genes. The fusion-partner-specific-binding patterns over these gene sets are highly correlated with the prevalence of each mutation in ALL versus AML. In lineage-switching samples the oncoprotein levels are reduced and the oncoproteins preferentially activate granulocyte-monocyte progenitor (GMP) genes. In a sample that lineage switched during treatment with the menin inhibitor revumenib, the oncoprotein and menin are reduced to undetectable levels, but ENL, a transcriptional cofactor of the oncoprotein, persists on numerous oncoprotein-target loci, including genes in the GMP-like lineage-switching program. We propose KMT2A oncoproteins promote lineage-switching events through dynamic chromatin binding and can induce epigenetic lesions, marked by ENL, that support resistance to targeted therapies.

cancer biology↗