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

The leukemic fusion gene <i>AML1-MDS1-EVI1</i> suppresses <i>CEBPA</i> in acute myeloid leukemia by activation of <i>Calreticulin</i>

23 Aug 2004

Abstract excerpt

The leukemic fusion gene AML1-MDS1-EVI1 (AME) encodes a chimeric transcription factor that results from the t(3,21)(q26;q22) translocation seen in patients with acute myeloid leukemia, with therapy-related myelodysplastic syndrome, or with chronic myeloid leukemia in blast crisis. The myeloid transcription factor CEBPA is crucial for normal granulopoiesis. Here, we found that conditional expression of AME...

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 Chronic Myeloid Leukemia Treatments
Share to Protein Degradation and Inhibitors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 15326310
DOI: 10.1073/pnas.0404731101

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The leukemic fusion gene <i>AML1-MDS1-EVI1</i> suppresses <i>CEBPA</i> in acute myeloid leukemia by activation of <i>Calreticulin</i>PMID 15326310Read ↗

CBFB-SMMHC is correlated with increased calreticulin expression and suppresses the granulocytic differentiation factor CEBPA in AML with inv(16)Semantic proximity Read ↗

C/EBPα overrides epigenetic reprogramming by oncogenic transcription factors in acute myeloid leukemia.Semantic proximity Read ↗

A regulatory element in the 3'-untranslated region of CEBPA is associated with myeloid/NK/T-cell leukemia.Semantic proximity Read ↗

A novel EVI1 gene family, MEL1, lacking a PR domain (MEL1S) is expressed mainly in t(1;3)(p36;q21)-positive AML and blocks G-CSF–induced myeloid differentiationSemantic proximity Read ↗

Core binding factor fusion downregulation of ADAR2 RNA editing contributes to AML leukemogenesisSemantic proximity Read ↗

Pharmacological targeting of the Wdr5-MLL interaction in C/EBPα N-terminal leukemia.Semantic proximity Read ↗

Repression of RUNX1 Activity by EVI1: A New Role of EVI1 in LeukemogenesisSemantic proximity Read ↗

The tumour-suppressive miR-29a/b1 cluster is regulated by CEBPA and blocked in human AMLSemantic proximity Read ↗

The retinoic acid receptor co-factor NRIP1 is uniquely upregulated and represents a therapeutic target in acute myeloid leukemia with chromosome 3q rearrangementsSemantic proximity Read ↗

ETO, fusion partner in t(8;21) acute myeloid leukemia, represses transcription by interaction with the human N-CoR/mSin3/HDAC1 complexSemantic proximity Read ↗

CCAAT-enhancer binding protein delta functions as a tumor suppressor gene in acute myeloid leukemiaSemantic proximity Read ↗

Gain‐of‐Function Effects of N‐Terminal CEBPA Mutations in Acute Myeloid LeukemiaSemantic proximity Read ↗

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