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

Loss of a 7q gene,CUX1, disrupts epigenetically driven DNA repair and drives therapy-related myeloid neoplasms

27 May 2021

Abstract excerpt

Therapy-related myeloid neoplasms (t-MNs) are high-risk late effects with poorly understood pathogenesis in cancer survivors. It has been postulated that, in some cases, hematopoietic stem and progenitor cells (HSPCs) harboring mutations are selected for by cytotoxic exposures and transform. Here, we evaluate this model in the context of deficiency of CUX1, a transcription factor encoded on chromosome 7q and...

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 Epigenetics and DNA Methylation
Share to Histone Deacetylase Inhibitors Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 34473231
DOI: 10.1182/blood.2020009195

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of a 7q gene,CUX1, disrupts epigenetically driven DNA repair and drives therapy-related myeloid neoplasmsPMID 34473231Read ↗

Distinct clinical and biological implications of CUX1 in myeloid neoplasmsSemantic proximity Read ↗

Oncogenic RAS promotes leukemic transformation of CUX1-deficient cells.Semantic proximity Read ↗

The crossroads of cancer therapies and clonal hematopoiesis.Semantic proximity Read ↗

CUX1 is a haploinsufficient tumor suppressor gene on chromosome 7 frequently inactivated in acute myeloid leukemiaSemantic proximity Read ↗

Therapy-related myeloid neoplasms: when genetics and environment collide.Semantic proximity Read ↗

Mechanisms associated with t(7;12) acute myeloid leukaemia: from genetics to potential treatment targetsSemantic proximity Read ↗

Oncologic therapy shapes the fitness landscape of clonal hematopoiesisSemantic proximity Read ↗

Utx loss causes myeloid transformation.Semantic proximity Read ↗

Inactivating CUX1 mutations promote tumorigenesis.Semantic proximity Read ↗

Engineered model of t(7;12)(q36;p13) AML recapitulates patient-specific features and gene expression profilesSemantic proximity Read ↗

Engineered model of t(7;12)(q36;p13) AML recapitulates patient-specific features and gene expression profilesSemantic proximity Read ↗

p53-dependent induction of P2X7 on hematopoietic stem and progenitor cells regulates hematopoietic response to genotoxic stressSemantic proximity Read ↗

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