Brian J.P. Huntly

This study creates a mouse model of myeloid neoplasm with spontaneous RTK-RAS mutations, showing a premalignant phase and lineage restriction in tumors.

This study identifies Polθ as a therapeutic target in DNMT3A-mutated leukemia by showing its essential role in DNA repair and replication fork restart, and demonstrates that its inhibition enhances standard therapies.

The paper identifies epigenetic regulators of fibrotic transformation in cardiac fibroblasts using bulk and single-cell CRISPR screens and shows KAT5 inhibition reduces fibrotic responses in human fibroblasts.

The paper identifies molecular determinants for phosphotyrosine recognition in tyrosine kinases and shows their roles in tumor promotion and suppression.

This study identifies CREBBP mutations as a targetable vulnerability in B-ALL, showing that CREBBP inhibition sensitizes these cells to Venetoclax-induced ferroptosis.

This study shows MLL2 stabilizes 3D chromatin loops during pluripotent cell differentiation without requiring its enzymatic activity.

This study shows that DNMT3A R882H mutant HSCs resist inflammatory stress through delayed p53 activation, leading to clonal expansion and increased AML risk.

The paper identifies long-range gene regulatory interactions in cerebellar granule neuron progenitors using pcHi-C, ATAC-seq, and ChIP-seq, revealing co-regulation by Atoh1 and CHD7.

This paper introduces an acoustic chip for detecting rare leukemic cells at early stages using sound waves, showing distinct movement patterns between normal and abnormal cells.

This study uses CRISPR screens and Perturb-Seq to analyze 550 chromatin factors in haematopoiesis and AML, revealing lineage-specific roles and therapeutic implications.