Ravindra Majeti

This paper develops an HLA-A2-specific antibody that effectively reduces GVHD in a mouse model with minimal dose.

The paper identifies and isolates human AML leukemia stem cells using single-cell multi-omics and establishes a prognostic gene signature for clinical relevance.

The paper uses patient-derived organoids to study TAM responses to CD47 checkpoint blockade, revealing a conversion to an immunosuppressive SPP1+ phenotype in clear cell renal cell carcinoma.

This study develops lipid nanoparticles (LNPs) for spleen-targeted RNA delivery without altering charge, showing improved splenic accumulation and distinct transcriptomic effects compared to conventional LNPs.

The paper analyzes DNA methylation stochasticity in AML subtypes, identifying high-entropy subtypes and linking methylation entropy to transcriptional variability and leukemogenesis.

This study shows DNMT3AR882H mutations are not required for maintaining AML but are linked to higher leukemia stem cell frequency.

This study identifies new functionally and molecularly distinct multipotent progenitors in adult human hematopoiesis using multiomic single cell analyses and functional assays.

This study identifies ASXL1 truncating mutations as a driver of leukemic resistance to T cell attack and proposes EZH2 inhibition as a therapeutic strategy to overcome this resistance.

The paper identifies ZMAT3 and CDKN1A as key hubs in the p53 tumor suppression network through integrative multiomic analyses in a mouse model.

This study replaces the HBA1 gene with HBB in β-thalassemia-derived HSPCs using CRISPR, normalizing globin ratios and restoring functional hemoglobin.

The paper introduces TRACE-Seq, a method to track clonal reconstitution of gene-targeted human hematopoietic stem cells using barcoded AAV6 donor templates in immunodeficient mice.

This paper develops a single-cell multi-omic framework to identify malignant regulatory signatures in mixed phenotype acute leukemia by analyzing transcriptomic and epigenetic data.

EMBLEM uses mitochondrial DNA mutations in ATAC-seq data to track cell lineage with high sensitivity and specificity in acute myeloid leukemia.

The paper uses single-cell chromatin accessibility to map the continuous regulatory variation in human hematopoietic differentiation and identifies epigenomic heterogeneity within cell populations.