Functional dissection of the chromosome 13q14 tumor-suppressor locus using transgenic mouse lines

Lia, Marie; Carette, Amanda; Tang, Hongyan; Shen, Qiong; Mo, Tongwei; Bhagat, Govind; Dalla‐Favera, Riccardo; Klein, Ulf

doi:10.1182/blood-2011-09-381814

Cited by 68 publications

(52 citation statements)

References 48 publications

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“…Only the DLEU7 gene was located between the MDR and the breakpoint cluster ( Figure 2B). This is particularly striking in light of a new mouse model of CLL in which codeletion of the DLEU7 homolog was shown to lead to higher disease penetrance and aggressiveness 13 and a potential role of DLEU7 found in familial CLL. 34 These major breakpoint clusters have been identified previously without further specification of these regions.…”

Section: Discussionmentioning

confidence: 99%

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High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations

Edelmann

Holzmann²,

Miller

et al. 2012

Blood

173

203

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To identify genomic alterations in chronic lymphocytic leukemia (CLL), we performed single-nucleotide polymorphismarray analysis using Affymetrix Version 6.0 on 353 samples from untreated patients entered in the CLL8 treatment trial. Based on paired-sample analysis (n ‫؍‬ 144), a mean of 1.8 copy number alterations per patient were identified; approximately 60% of patients carried no copy number alterations other than those detected by fluorescence in situ hybridization analysis. Copy-neutral loss-ofheterozygosity was detected in 6% of CLL patients and was found most frequently on 13q, 17p, and 11q. Minimally deleted regions were refined on 13q14 (deleted in 61% of patients) to the DLEU1 and DLEU2 genes, on 11q22.3 (27% of patients) to ATM, on 2p16.1-2p15 (gained in 7% of patients) to a 1.9-Mb fragment containing 9 genes, and on 8q24.

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Section: Discussionmentioning

confidence: 99%

“…11 Mice carrying a deletion of the Dleu2/miR-15a/miR-16-1 cluster develop lymphoproliferative disorders partly resembling human CLL. 12,13 Genes involved in other genomic aberrations such as trisomy 12, del(6q), trisomy 2p, trisomy 19, or trisomy 8q, are unknown.…”

Section: Introductionmentioning

confidence: 99%

High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations

Edelmann

Holzmann²,

Miller

et al. 2012

Blood

173

203

View full text Add to dashboard Cite

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“…Reproducing the MDR in mice showed that 40% of those "MDR mice" develop a "CLL-like" monoclonal CD51 lymphoproliferation [116]. Another mouse strain with specific deletion of MIR15A/16-1 show a similar CLL-like phenotype, but appear less penetrant and aggressive than the "MDR mice" [117]. This suggests that DLEU2 have specific function, beside MIR15A/16-1.…”

Section: Noncoding Alterations: Mi-rnamentioning

confidence: 99%

Chronic lymphocytic leukemia: Time to go past genomics?

2016

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Recent advances in massively parallel sequencing technologies have provided a detailed picture of the mutational landscape in CLL and underscored the vast degree of interpatient and intratumor heterogeneities. These studies have led to the characterization of novel putative driver genes and recurrently affected biological pathways, and to the modeling of CLL clonal evolution. We herein review selected aspects including recent advances in the biology of CLL and present cellular and biological processes involved in the development of CLL and potentially other mature B-cell lymphoproliferative neoplasms.

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“…Both sets of homozygous mice developed a disease reminiscent of human CLL, whilst those mice that harboured a deleted MDR had a more aggressive disease phenotype, suggesting that additional genetic components in this region contribute to the effect of the MIR15A/16-1 cluster in CLL pathogenesis. Further evidence that this is indeed the case comes from a more recent study by the same authors, in which a third mouse strain was engineered that extended the MDR to include further genes DLEU7 and RNASEH2B, representing the commonly deleted region (CDR) of CLL (Lia et al, 2012). These mice had an even more aggressive phenotype than those with either MDR or MIR15A/16-1 deletions alone, and a higher proportion of mice that developed CLL as opposed to lymphomas.…”

Section: Mir15a/16-1 Clustermentioning

confidence: 96%

MicroRNAs and lymphomagenesis: a functional review

Lawrie

2012

Br J Haematol

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SummaryThe relatively recent discovery of microRNAs (miRNAs) has exposed an extra layer of gene expression regulation that affects many physiological and pathological processes of biology. Dysregulation of miRNAs is a ubiquitous feature of cancer in general, including lymphomas. The identity of these aberrantly-expressed miRNAs has been thoroughly investigated in all but a few types of lymphomas, however their functional role in lymphomagenesis much less so. This review focuses on those miRNAs that have an experimentally confirmed functional role in the pathogenesis of the most frequent forms of lymphoma. In particular, the MIR15A/16-1 cluster, MIR21, MIR155, MIR17HG (MIR17-92 cluster), MIR34A and MIR125B, which have in vivo animal model evidence for their involvement in lymphomagenesis, are highlighted.

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Functional dissection of the chromosome 13q14 tumor-suppressor locus using transgenic mouse lines

Cited by 68 publications

References 48 publications

High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations

High-resolution genomic profiling of chronic lymphocytic leukemia reveals new recurrent genomic alterations

Chronic lymphocytic leukemia: Time to go past genomics?

MicroRNAs and lymphomagenesis: a functional review

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