Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-8-18
pubmed:abstractText
The TAL1 gene is disrupted by translocation or deletion (tal(d)) in up to 30% of T-cell acute lymphoblastic leukaemia (T-ALL), leading to aberrant transcriptional activation, as a SIL-TAL1 fused transcript in tal(d). It has been suggested that TAL1 transcription occurs in approximately 50% of a T-ALLs without apparent rearrangement. SIL-TAL1 was positive in 15/60 (25%) of T-ALL, whereas wild-type TAL1 transcripts were detected in all 13 SIL-TAL1 and in 19/43 (44%) T-ALL without SIL-TAL1. To investigate the cellular origin of TAL1 we exploited the fact that GATA1 and TAL1 are co-ordinately expressed in non-lymphoid haemopoietic cells, whereas only the latter is found in T-ALL. GATA1 was detected in 10/23 (43%) TAL1-negative T-ALLs but in 17/19 (89%) 'unexplained' TAL1-positive cases, suggesting a common non-lymphoid cellular origin. Immunocytochemical analysis with a TAL1-specific monoclonal antibody showed nuclear expression in the blasts of 10/34 (29%) cases, including 8/10 SIL-TAL1+ and two RT-PCR TAL1+, SIL-TAL1- cases. In the remaining cases TAL1 expression was restricted to a minor population (< 5%) of larger, strongly TAL1-positive cells which comprised erythroid cells, CD34+ CD3- precursors and an unidentified TAL1+ CD45- population which morphologically resembled monocytes/macrophages. We therefore suggest that appropriate diagnostic evaluation of T-ALL should include molecular detection of SIL-TAL1 transcripts and in situ immunocytochemical detection of TAL1 protein expression by leukaemic blasts. This approach will enable accurate analysis of the prognostic significance of TAL1 deregulation in T-ALL.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0007-1048
pubmed:author
pubmed:issnType
Print
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
449-57
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9695959-Adolescent, pubmed-meshheading:9695959-Adult, pubmed-meshheading:9695959-Basic Helix-Loop-Helix Transcription Factors, pubmed-meshheading:9695959-Blotting, Southern, pubmed-meshheading:9695959-Child, pubmed-meshheading:9695959-Child, Preschool, pubmed-meshheading:9695959-DNA-Binding Proteins, pubmed-meshheading:9695959-Erythroid-Specific DNA-Binding Factors, pubmed-meshheading:9695959-GATA1 Transcription Factor, pubmed-meshheading:9695959-Gene Rearrangement, T-Lymphocyte, pubmed-meshheading:9695959-Humans, pubmed-meshheading:9695959-Immunohistochemistry, pubmed-meshheading:9695959-Infant, pubmed-meshheading:9695959-Infant, Newborn, pubmed-meshheading:9695959-Leukemia-Lymphoma, Adult T-Cell, pubmed-meshheading:9695959-Polymerase Chain Reaction, pubmed-meshheading:9695959-Proto-Oncogene Proteins, pubmed-meshheading:9695959-RNA, Messenger, pubmed-meshheading:9695959-Transcription Factors
pubmed:year
1998
pubmed:articleTitle
TAL1 expression does not occur in the majority of T-ALL blasts.
pubmed:affiliation
CNRS URA 1461 and Department of Haematology, CHU Necker-Enfants Malades and Université Paris V, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't