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

Pro‐inflammatory cytokines favor the emergence of ETV6‐RUNX1‐positive pre‐leukemic cells in a model of mesenchymal niche

2 Mar 2020

Abstract excerpt

Summary ETV6‐RUNX1 (E/R) fusion gene, arising in utero from translocation t(12;21)(p13:q22), is the most frequent alteration in childhood acute lymphoblastic leukemia (ALL). However, E/R is insufficient to cause overt leukemia since it generates a clinically silent pre‐leukemic clone which persists in the bone marrow but fails to out‐compete normal progenitors. Conversely, pre‐leukemic cells show increased...

Read the complete abstract on PubMed

Topics

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

Share to Acute Lymphoblastic Leukemia research
Share to Acute Myeloid Leukemia Research
Share to Hematopoietic Stem Cell Transplantation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 32118299
DOI: 10.1111/bjh.16523

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Pro‐inflammatory cytokines favor the emergence of ETV6‐RUNX1‐positive pre‐leukemic cells in a model of mesenchymal nichePMID 32118299Read ↗

Pathogenesis of ETV6/RUNX1-positive childhood acute lymphoblastic leukemia and mechanisms underlying its relapseSemantic proximity Read ↗

A Human IPS Model Implicates Embryonic B-Myeloid Fate Restriction as Developmental Susceptibility to B Acute Lymphoblastic Leukemia-Associated ETV6-RUNX1Semantic proximity Read ↗

The Leukemia-Specific Fusion Gene ETV6/RUNX1 Perturbs Distinct Key Biological Functions Primarily by Gene RepressionSemantic proximity Read ↗

The Second Oncogenic Hit Determines the Cell Fate of ETV6-RUNX1 Positive LeukemiaSemantic proximity Read ↗

The TEL-AML1 leukemia fusion gene dysregulates the TGF-β pathway in early B lineage progenitor cellsSemantic proximity Read ↗

Leukemic stem cells hijack lineage inappropriate signalling pathways to promote their growthSemantic proximity Read ↗

Leukemic stem cells activate lineage inappropriate signalling pathways to promote their growth.Semantic proximity Read ↗

Infection Exposure Promotes ETV6-RUNX1 Precursor B-cell Leukemia via Impaired H3K4 DemethylasesSemantic proximity Read ↗

Germline ETV6 mutation promotes inflammation and disrupts lymphoid development of early hematopoietic progenitors.Semantic proximity Read ↗

<i>Etv6/Runx1</i> Fusion Gene Abrogation Decreases The Oncogenic Potencial Of Tumour Cells In A Preclinical Model Of Acute Lymphoblastic LeukaemiaSemantic proximity Read ↗

Distinct Stromal Cell Populations Define the B-cell Acute Lymphoblastic Leukemia MicroenvironmentSemantic proximity Read ↗

Modeling first-hit functions of the t(12;21) TEL-AML1 translocation in mice.Semantic proximity Read ↗

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