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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State: Public
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
Institution
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
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.
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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