Array CGH analysis of nodal t-cell lymphomas: identification of genomic alterations specific to angioimmunoblastic and unspecified subtypes, and correlation with gene expression signature [234]

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Version: author
Serval ID
serval:BIB_388F01572035
Type
Inproceedings: an article in a conference proceedings.
Publication sub-type
Abstract (Abstract): shot summary in a article that contain essentials elements presented during a scientific conference, lecture or from a poster.
Collection
Publications
Title
Array CGH analysis of nodal t-cell lymphomas: identification of genomic alterations specific to angioimmunoblastic and unspecified subtypes, and correlation with gene expression signature [234]
Title of the conference
10th International Conference on Malignant Lymphoma
Author(s)
De Leval L., De Reynies A., Rickman D., Huang Y., Thomas E., Berger F., Molina T., Xerri L., Gisselbrecht C., Bastard C., Gaulard P.
Address
Lugano, Switzerland, 2008, June, 4-7
ISBN
0923-7534
ISSN-L
0923-7534
Publication state
Published
Issued date
2008
Volume
19
Series
Annals of Oncology
Pages
iv154
Language
english
Abstract
Genetic alterations underlying angioimmunoblastic and unspecified peripheral T-cell
lymphomas (AITL and PTCL-u) are largely unknown.
Seventeen AITL and 16 PTCL-u previously characterized by gene expression
profiling, were analyzed by CGH on DNA microarrays comprising 4434 BAC clones
with a resolution of about 600 KB.
Chromosomal imbalances were identified in all cases. On average, more genomic
alterations were detected in PTCL-u than in AITL (p=0,09). PTCL-U cases had a mean
of 302 aberrations (range, 55 to 892). Gains (n=668, 43 to 1810) were more
frequent than losses (n=149, 3 to 1439). AITL cases also had more gains (n=520, 68 to
903) than losses (n=45, 13 to 1019). The most frequent recurrent gains, present in 50%
of all cases, were observed at 1p36, 2q37, 4p16, 5p15, 6p12, 7p11;q36, 8q24, 9q34,
11p15, 11q13, 16p13; p33; q24, 17q12; q25, 19p13, 19q13; q33-q34, 20q11, 22q12,
Xp11, Xq28. The only recurrent losses present in >50% of cases were at 1p21 and
Yp11.3-q11.2. The comparison of the genomic profiles of AITL and PTCL-u identified
112 genomic alterations significantly associated with either type (Fisher test, p <0,05).
Several gains (at 1q, 5q, 6p, 7p, 12q, 13q, 17q) and losses at 14q were specifically
associated with PTCL-u while gains at 10q and 15q and losses at 16p were associated
with AITL. The coordinate analysis of the transcriptomic and CGH data identified 123
genes differentially expressed in PTCL-u and AITL mapping to genomic regions
differentially altered (p<0,02). Among these were 24 genes belonging to the molecular
signature of these entities.
In conclusion: all nodal PTCL analyzed harbor genomic imbalances (gains>losses), of
which many are common to AITL and PTCL-u; the pattern of genomic aberrations
differs between the two groups, with certain aberrations being overrepresented in
PTCL-u, and only a few specific for AITL; coordinate appraisal of transcriptomic and
genomic data highlights correlations between genomic imbalances and gene
expression signatures.
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