MYB rearrangements and over-expression in T-cell acute lymphoblastic leukemia.

doi:10.1002/gcc.22943

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

Community

Back to search

Article

MYB rearrangements and over-expression in T-cell acute lymphoblastic leukemia.

Genes, chromosomes & cancer - 1 Jul 2021

Bardelli Valentina, Arniani Silvia, Pierini Valentina, Pierini Tiziana, Di Giacomo Danika, Gorello Paolo, Moretti Martina, Pellanera Fabrizia, Elia Loredana, Vitale Antonella, Storlazzi Clelia Tiziana, Tolomeo Doron, Mastrodicasa Elena, Caniglia Maurizio, Chiaretti Sabina, Ruggeri Loredana, Roti Giovanni, Schwab Claire, Harrison Christine J, Almeida André, Pieters Tim, Van Vlierberghe Pieter, Mecucci Cristina, La Starza Roberta

Abstract excerpt

We investigated MYB rearrangements (MYB-R) and the levels of MYB expression, in 331 pediatric and adult patients with T-cell acute lymphoblastic leukemia (T-ALL). MYB-R were detected in 17 cases and consisted of MYB tandem duplication (tdup) (= 14) or T cell receptor beta locus (TRB)-MYB (= 3). As previously reported, TRB-MYB was found only in children (1.6%) while MYB tdup occurred in both age groups, although...

Read the complete abstract on PubMed

Topics

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

Share to Down-Regulation

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to F-Box-WD Repeat-Containing Protein 7

Share to Gene Duplication

Share to Homeodomain Proteins

Share to Precursor T-Cell Lymphoblastic Leukemia-Lymphoma

Share to Proto-Oncogene Proteins c-myb

Share to Receptor, Notch1

Share to Thyroid Nuclear Factor 1

Source

Open in PubMed

Identifiers

PMID: 33611795
DOI: 10.1002/gcc.22943

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

MYB rearrangements and over-expression in T-cell acute lymphoblastic leukemia.PMID 33611795Read ↗

Duplication of the MYB oncogene in T cell acute lymphoblastic leukemia.Semantic proximity Read ↗

The C-MYB locus is involved in chromosomal translocation and genomic duplications in human T-cell acute leukemia (T-ALL), the translocation defining a new T-ALL subtype in very young childrenSemantic proximity Read ↗

TAL1 activation in T-cell acute lymphoblastic leukemia: a novel oncogenic 3' neo-enhancer.Semantic proximity Read ↗

Reactivation of a TAL1 progenitor cell enhancer region by non-coding somatic variants in T-lineage acute lymphoblastic leukemiaSemantic proximity Read ↗

MYB oncoproteins: emerging players and potential therapeutic targets in human cancerSemantic proximity Read ↗

Characterization of a pediatric T-cell acute lymphoblastic leukemia patient with simultaneous LYL1 and LMO2 rearrangementsSemantic proximity Read ↗

Genetic rearrangements in relation to immunophenotype and outcome in T-cell acute lymphoblastic leukaemia.Semantic proximity Read ↗

TCRB gene rearrangements in childhood and adult precursor-B-ALL: frequency, applicability as MRD-PCR target, and stability between diagnosis and relapseSemantic proximity Read ↗

Expression of A-myb, but not c-myb and B-myb, is restricted to Burkitt's lymphoma, sIg+ B-acute lymphoblastic leukemia, and a subset of chronic lymphocytic leukemias.Semantic proximity Read ↗

Myb drives B-cell neoplasms and myeloid malignancies in vivoSemantic proximity Read ↗

Suppression of super-enhancer-driven TAL1 expression by KLF4 in T-cell acute lymphoblastic leukemiaSemantic proximity Read ↗

Regulation of MYB by distal enhancer elements in human myeloid leukemiaSemantic proximity Read ↗

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