A. Kentsis

This study identifies mechanisms of resistance to EZH2 inhibition in SMARCB1-deficient cancers and proposes combination therapies to overcome resistance.

This study identifies a quiescent label-retaining cell population in human AML that drives disease and therapy resistance through epigenetic mechanisms.

This study identifies PGBD5 as a primary mutator in medulloblastoma by showing it drives somatic DNA rearrangements in cerebellar progenitor cells.

The paper introduces QCPA, a targeted mass spectrometry framework for quantifying signaling pathway activities by measuring post-translational modifications and protein abundance in human cells.

This paper introduces SAMPEI, a spectral alignment method for detecting protein modifications using high-resolution mass spectrometry, demonstrating its effectiveness in identifying sub-stoichiometric modifications in mouse macrophages.

This study identifies aberrant MYB complex assembly as a driver of oncogenic gene expression in AML and shows that targeting this complex can induce differentiation and apoptosis.

This study shows that a cancer-associated mutation in PP2A-Aα enhances centrosome clustering during mitosis after whole-genome doubling, improving cell survival.

This study identifies prohibitin as a urine biomarker for Wilms tumor relapse and shows it promotes chemotherapy resistance by disrupting mitochondrial apoptosis.

The paper identifies genetic mechanisms of primary chemotherapy resistance in pediatric AML through whole-genome and transcriptome sequencing of treatment-failure cases.

This paper identifies a new leukemia subtype, AMTL, with shared myeloid and T-cell features, common mutations, and potential for improved therapy.

This study develops a peptidomimetic inhibitor, MYBMIM, that blocks MYB:CBP/P300 complex assembly in AML cells, leading to apoptosis and reduced tumor growth in mice.

This study identifies PGBD5 as a therapeutic target in pediatric solid tumors, showing that inhibiting DNA repair pathways with AZD6738 sensitizes these tumors to apoptosis.

This study identifies PGBD5 as an oncogenic DNA transposase in rhabdoid tumors, causing site-specific genomic rearrangements through PSS sequences and end-joining repair.

This study identifies MEF2C phosphorylation as a marker of chemotherapy resistance in AML and shows that inhibiting this phosphorylation can overcome resistance in MEF2C-activated cells.