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

AML1/RUNX1 point mutation possibly promotes leukemic transformation in myeloproliferative neoplasms

22 Oct 2009

Abstract excerpt

Myeloproliferative neoplasms (MPNs) are clonal hematopoietic stem cell disorders characterized by proliferation of one or more myeloid cell lineages. Some patients exhibit leukemic transformation (LT) by unknown mechanisms, and chemotherapy may increase the risk of LT. To clarify the molecular mechanisms of LT, gene alterations involved in LT from patients in the chronic phase (CP) of MPNs were identified. Among...

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 Myeloproliferative Neoplasms: Diagnosis and Treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 19850737
DOI: 10.1182/blood-2009-06-223982

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

AML1/RUNX1 point mutation possibly promotes leukemic transformation in myeloproliferative neoplasmsPMID 19850737Read ↗

The Clinical, Molecular, and Mechanistic Basis of RUNX1 Mutations Identified in Hematological Malignancies.Semantic proximity Read ↗

Point mutations in the RUNX1/AML1 gene: another actor in RUNX leukemia.Semantic proximity Read ↗

New mechanisms of AML1 gene alteration in hematological malignancies.Semantic proximity Read ↗

Molecular pathways mediating MDS/AML with focus on AML1/RUNX1 point mutations.Semantic proximity Read ↗

MN1 overexpression induces acute myeloid leukemia in mice and predicts ATRA resistance in patients with AMLSemantic proximity Read ↗

Mutation analysis of JAK2V617F, FLT3-ITD, NPM1, and DNMT3A in Chinese patients with myeloproliferative neoplasms.Semantic proximity Read ↗

Biological Activities of RUNX1 Mutants Predict Secondary Acute Leukemia Transformation from Chronic Myelomonocytic Leukemia and Myelodysplastic Syndromes.Semantic proximity Read ↗

RUNX1/AML1 mutant collaborates with BMI1 overexpression in the development of human and murine myelodysplastic syndromes.Semantic proximity Read ↗

M0 AML, clinical and biologic features of the disease, including AML1 gene mutations: a report of 59 cases by the Groupe Francais d'Hematologie Cellulaire (GFHC) and the Groupe Francais de Cytogenetique Hematologique (GFCH)Semantic proximity Read ↗

RUNX1 DNA-binding mutations and RUNX1-PRDM16 cryptic fusions in BCR-ABL+ leukemias are frequently associated with secondary trisomy 21 and may contribute to clonal evolution and imatinib resistance.Semantic proximity Read ↗

RUNX1 mutations are frequent in chronic myelomonocytic leukemia and mutations at the C-terminal region might predict acute myeloid leukemia transformation.Semantic proximity Read ↗

Functional features of RUNX1 mutants in acute transformation of chronic myeloid leukemia and their contribution to inducing murine full-blown leukemia.Semantic proximity Read ↗

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