Molecular delineation of the commonly deleted segment in mature B-cell lymphoid neoplasias with deletion of 7q

Hernández, Jesús M.; Schoenmakers, Eric; Cin, Paola Dal; Michaux, Lucienne; Ven, Wim J.M. Van de; Berghe, Herman Van den

doi:10.1002/(sici)1098-2264(199702)18:2<147::aid-gcc10>3.0.co;2-h

Cited by 17 publications

(4 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This region is situated between the D7S685 and D7S514 markers, which define the smallest commonly deleted region observed by Hernandez and colleagues in a previous study of a group of NHL. 33 The data reported here confirm and expand initial observations made by Sole et al 4 using cytogenetic and fluorescence in situ hybridization techniques pointing to 7q alterations as a significant cytogenetic finding in SMZL defined on the basis of splenic histology. It now appears after LOH analysis that the incidence of this genetic loss is more frequent than initially expected and that, additionally, it seems to be associated with a more aggressive course.…”

Section: Discussionsupporting

confidence: 89%

7q31-32 Allelic Loss Is a Frequent Finding in Splenic Marginal Zone Lymphoma

Mateo

Mollejo

Villuendas

et al. 1999

The American Journal of Pathology

151

View full text Add to dashboard Cite

Splenic marginal zone lymphoma (SMZL) has been recognized as an entity defined on the basis of its morphological , phenotypic , and clinical characteristic features. Nevertheless , no characteristic genetic alterations have been described to date for this entity, thus making an exact diagnosis of SMZL difficult in some cases. As initial studies showed that chromosome region 7q22-32 is deleted in some of these cases, we analyzed a larger group of SMZL and other lymphoproliferative disorders that may partially overlap with it. To better define the frequency of 7q deletion in SMZL and further identify the deleted region , polymerase chain reaction analysis of 13 microsatellite loci spanning 7q21-7q36 was performed on 20 SMZL and 26 non-SMZL tissue samples. The frequency of allelic loss in SMZL (8/20; 40%) was higher than that observed in other B-cell lymphoproliferative syndromes (2/26; 7.7%). This difference was statistically significant (P < 0.05). The most frequently deleted microsatellite was D7S487 (5/11; 45% of informative cases). Surrounding this microsatellite the smallest common deleted region of 5cM has been identified, defined between D7S685 and D7S514. By comparative multiplex polymerase chain reaction analysis , we detected a homozygous deletion in the D7S685 (7q31.

show abstract

Section: Discussionsupporting

confidence: 89%

7q31-32 Allelic Loss Is a Frequent Finding in Splenic Marginal Zone Lymphoma

Mateo

Mollejo

Villuendas

et al. 1999

The American Journal of Pathology

151

View full text Add to dashboard Cite

show abstract

“…FISH studies were carried out following well-established methods [30]. Polysomies (chromosomal gains) were defined as more than 10% of nuclei containing three or more CEP signals.…”

Section: Methodsmentioning

confidence: 99%

Molecular analysis of ex-vivo CD133+ GBM cells revealed a common invasive and angiogenic profile but different proliferative signatures among high grade gliomas

Hernández

Pérez-Caro²,

Gómez-Moreta

et al. 2010

BMC Cancer

View full text Add to dashboard Cite

BackgroundGliomas are the most common type of primary brain tumours, and in this group glioblastomas (GBMs) are the higher-grade gliomas with fast progression and unfortunate prognosis. Two major aspects of glioma biology that contributes to its awful prognosis are the formation of new blood vessels through the process of angiogenesis and the invasion of glioma cells. Despite of advances, two-year survival for GBM patients with optimal therapy is less than 30%. Even in those patients with low-grade gliomas, that imply a moderately good prognosis, treatment is almost never curative. Recent studies have demonstrated the existence of a small fraction of glioma cells with characteristics of neural stem cells which are able to grow in vitro forming neurospheres and that can be isolated in vivo using surface markers such as CD133. The aim of this study was to define the molecular signature of GBM cells expressing CD133 in comparison with non expressing CD133 cells. This molecular classification could lead to the finding of new potential therapeutic targets for the rationale treatment of high grade GBM.MethodsEight fresh, primary and non cultured GBMs were used in order to study the gene expression signatures from its CD133 positive and negative populations isolated by FACS-sorting. Dataset was generated with Affymetrix U133 Plus 2 arrays and analysed using the software of the Affymetrix Expression Console. In addition, genomic analysis of these tumours was carried out by CGH arrays, FISH studies and MLPA;ResultsGene expression analysis of CD133+ vs. CD133- cell population from each tumour showed that CD133+ cells presented common characteristics in all glioblastoma samples (up-regulation of genes involved in angiogenesis, permeability and down-regulation of genes implicated in cell assembly, neural cell organization and neurological disorders). Furthermore, unsupervised clustering of gene expression led us to distinguish between two groups of samples: those discriminated by tumour location and, the most importantly, the group discriminated by their proliferative potential;ConclusionsPrimary glioblastomas could be sub-classified according to the properties of their CD133+ cells. The molecular characterization of these potential stem cell populations could be critical to find new therapeutic targets and to develop an effective therapy for these tumours with very dismal prognosis.

show abstract

“…We have previously found 7q abnormalities to be the most common cytogenetic abnormality in SLVL, occurring in 26% of cases (Oscier et al, 1996). Most of the abnormalities comprise deletions involving bands 7q22 and/or 7q32 (O t et al, 1995;Hernandez et al, 1997a;Dascalescu et al, 1999), or translocations between 7q21 or q22 and other partner chromosomes (Oscier et al, 1996). Occasional cases show more distal deletions of 7q34 ± q36 (Hernandez et al, 1997b).…”

Section: Introductionmentioning

confidence: 97%

Dysregulation of cyclin dependent kinase 6 expression in splenic marginal zone lymphoma through chromosome 7q translocations

et al. 1999

Oncogene

130

View full text Add to dashboard Cite

The increased or inappropriate expression of genes with oncogenic properties through speci®c chromosome translocations is an important event in the pathogenesis of Bcell lymphoproliferative diseases. Recent studies have found deletions or translocations of chromosome 7q to be the most common cytogenetic abnormality observed in SLVL, a leukemic variant of SMZL, with the q21 ± q22 region being most frequently a ected. In three patients with translocations between chromosomes 2 and 7, the cloning of the breakpoints at 7q21 revealed that each was located within a small region of DNA 3.6 kb upstream of the transcription start site of cyclin dependent kinase 6 (CDK6). In each case the translocation event was consistent with aberrant VJ recombination between the immunoglobulin light chain region (Ig kappa) on chromosome 2p12 and DNA sequences at 7q21, resembling the heptamer recombination site. The t(7;21) breakpoint in an additional patient with splenic marginal zone lymphoma (SMZL), resided 66 kb telomeric to the t(2;7) breakpoints juxtaposing CDK6 to an uncharacterized transcript. In two of the SLVL patient samples, the CDK6 protein was found to be markedly over expressed. These results suggest that dysregulation of CDK6 gene expression contributes to the pathogenesis of SLVL and SMZL.

show abstract

Molecular delineation of the commonly deleted segment in mature B-cell lymphoid neoplasias with deletion of 7q

Cited by 17 publications

References 11 publications

7q31-32 Allelic Loss Is a Frequent Finding in Splenic Marginal Zone Lymphoma

7q31-32 Allelic Loss Is a Frequent Finding in Splenic Marginal Zone Lymphoma

Molecular analysis of ex-vivo CD133+ GBM cells revealed a common invasive and angiogenic profile but different proliferative signatures among high grade gliomas

Dysregulation of cyclin dependent kinase 6 expression in splenic marginal zone lymphoma through chromosome 7q translocations

Contact Info

Product

Resources

About