Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Targeting enhancer switching overcomes non-genetic drug resistance in acute myeloid leukaemia

20 Jun 2019

Abstract excerpt

Non-genetic drug resistance is increasingly recognised in various cancers. Molecular insights into this process are lacking and it is unknown whether stable non-genetic resistance can be overcome. Using single cell RNA-sequencing of paired drug naïve and resistant AML patient samples and cellular barcoding in a unique mouse model of non-genetic resistance, here we demonstrate that transcriptional plasticity...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Acute Myeloid Leukemia Research
Share to Genomics and Chromatin Dynamics
Share to Protein Degradation and Inhibitors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 31222014
DOI: 10.1038/s41467-019-10652-9

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Targeting enhancer switching overcomes non-genetic drug resistance in acute myeloid leukaemiaPMID 31222014Read ↗

Understanding the role of phenotypic switching in cancer drug resistance.Semantic proximity Read ↗

S125: NON-GENETIC RESISTANCE TO MENIN INHIBITION IN AML IS REVERSIBLE BY PERTURBATION OF KAT6ASemantic proximity Read ↗

In vivo CRISPR/Cas9 screening identifies Pbrm1 as a regulator of myeloid leukemia development in mice.Semantic proximity Read ↗

Modeling <i>IKZF1</i> lesions in B-ALL reveals distinct chemosensitivity patterns and potential therapeutic vulnerabilitiesSemantic proximity Read ↗

Targeting histone methylation to reprogram the transcriptional state that drives survival of drug-tolerant myeloid leukemia persistersSemantic proximity Read ↗

Resistance Signatures Manifested in Early Drug Response in Cancer and Across SpeciesSemantic proximity Read ↗

<i>ASXL1</i> truncating mutations drive leukemic resistance to T cell attackSemantic proximity Read ↗

Tracing the evolutionary trajectory of CDK4/6 inhibitor resistance in oestrogen receptor positive breast cancerSemantic proximity Read ↗

The AML microenvironment catalyzes a stepwise evolution to gilteritinib resistanceSemantic proximity Read ↗

Integrative multi-omics identifies AP-1 transcription factor as a targetable mediator of acquired osimertinib resistance in non-small cell lung cancer.Semantic proximity Read ↗

Sensitivity and engineered resistance of myeloid leukemia cells to BRD9 inhibition.Semantic proximity Read ↗

From modulation of cellular plasticity to potentiation of therapeutic resistance: new and emerging roles of MYB transcription factors in human malignanciesSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.