A. Kentsis

Overcoming clinical resistance to EZH2 inhibition using rational epigenetic combination therapy

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

Epigenetic mechanisms controlling human leukemia stem cells and therapy resistance

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

Childhood cancer mutagenesis caused by a domesticated DNA transposase

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

Quantitative Cell Proteomic Atlas: Pathway-scale targeted mass spectrometry for high-resolution functional profiling of cell signaling

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.

Discovery of protein modifications using high resolution differential mass spectrometry proteomics

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.

Convergent organization of aberrant MYB complex controls oncogenic gene expression in acute myeloid leukemia

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.

A cancer-associated missense mutation in PP2A-Aα increases centrosome clustering during mitosis

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

Prohibitin is a prognostic marker of relapse and therapeutic target to block chemotherapy resistance in Wilms tumor

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

Genetic mechanisms of primary chemotherapy resistance in pediatric acute myeloid leukemia: A report from the TARGET initiative

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

Acute myeloid/T-lymphoblastic leukemia (AMTL): A distinct category of acute leukemias with common pathogenesis in need of improved therapy

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

Peptidomimetic blockade of MYB in acute myeloid leukemia

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.

Therapeutic targeting of PGBD5-induced DNA repair dependency in pediatric solid tumors

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.

Human PGBD5 DNA transposase promotes site-specific oncogenic mutations in rhabdoid tumors

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

MEF2C phosphorylation is required for chemotherapy resistance in acute myeloid leukemia

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.