Comparative genomic hybridization detects many recurrent imbalances in central nervous system primitive neuroectodermal tumours in children

Avet-Loiseau, Hervé; Am, Venuat; Mj, Terrier-Lacombe; Lellouch‐Tubiana, Arielle; Zérah, Michel; Vassal, Gilles

doi:10.1038/sj.bjc.6690293

Cited by 58 publications

(40 citation statements)

References 21 publications

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“…Using more sophisticated and advanced techniques such as CGH to profile a panel of 27 primary MB (Reardon et al 1997) revealed frequent loss of 10q, 11, 16q, 17p, and 8p as well as recurrent gains of chromosomes 7, and 17q. These losses and gains were also confirmed by other techniques, such as G-banding, SKY and FISH (Aldosari et al 2002;Avet-Loiseau et al 1999 ;Bayani et al 2000;Eberhart et al 2002;Gilhuis et al 2000). Array CGH of 47 MB (Speicher and Carter 2005) showed gain of 17q, 7, and 1q and loss of 17p, 11p,10q and 8.…”

Section: Chromosomal Aberration and Its Corroletion To Clinicohistopasupporting

confidence: 54%

Medulloblastoma – Genetic Alterations

Manor¹,

Bodner²

2011

Molecular Targets of CNS Tumors

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Section: Chromosomal Aberration and Its Corroletion To Clinicohistopasupporting

confidence: 54%

Medulloblastoma – Genetic Alterations

Manor¹,

Bodner²

2011

Molecular Targets of CNS Tumors

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“…To compare our ®ndings with those of previous investigations, we have reviewed genetic data from six genome-wide studies covering a total of 107 medulloblastomas (Blaeker et al, 1996;Reardon et al, 1997;Avet-Loiseau et al, 1999;Nicholson et al, 1999;Gilhuis et al, 2000;von Deimling et al, 2000). The summarized results revealed that deletions of 17p (39%), 10q (35%), 8p (32%), 11p (28%), 11q (28%), and 16q (20%) are the most frequent genetic abnormalities involving loss of genetic materials.…”

Section: Discussionmentioning

confidence: 99%

“…The TP53 gene was found to be infrequently mutated in medulloblastoma, indicating that TP53 is not the target on 17p (Saylors et al, 1991). Using comparative genomic hybridization technique, several groups have demonstrated the involvement of multiple chromosomes in medulloblastoma (Avet-Loiseau et al, 1999;Gilhuis et al, 2000;Nicholson et al, 1999;Reardon et al, 1997). Of those chromosomes that show deletions, losses of chromosomes 10q and 8p are recurrent genetic alterations, with about 30% of tumors showing such abnormalities.…”

Section: Introductionmentioning

confidence: 99%

Identification of a region of homozygous deletion on 8p22–23.1 in medulloblastoma

Yin

Pang

2002

Oncogene

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To identify critical tumor suppressor loci that are associated with the development of medulloblastoma, we performed a comprehensive genome-wide allelotype analysis in a series of 12 medulloblastomas. Non-random allelic imbalances were identi®ed on chromosomes 7q (58.3%), 8p (66.7%), 16q (58.3%), 17p (58.3%) and 17q (66.7%). Comparative genomic hybridization analysis con®rmed that allelic imbalances on 8p, 16q and 17p were due to loss of genetic materials. Finer deletion mapping in an expanded series of 23 medulloblastomas localized the common deletion region on 8p to an interval of 18.14 cM on 8p22 ± 23.2. We then searched within the region of loss on 8p for loci that might contain homozygous deletion using comparative duplex PCR. An overlapping homozygous deletion region was identi®ed in a 1.8 cM interval on 8p22 ± 23.1, between markers D8S520 and D8S1130, in two medulloblastomas. This region of homozygous deletion also encompasses the 1.4 cM minimal deletion region detected on 8p in ductal carcinoma in situ of breast. In conclusion, we reported for the ®rst time a detailed deletion mapping on 8p in medulloblastoma and have identi®ed a region of homozygous deletion on 8p22 ± 23.1 that is likely to contain a critical tumor suppressor gene involved in the development of medulloblastoma.

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“…Medulloblastoma, a representative malignant brain tumor, showed frequent disruption at chromosome 3p by a deletion mapping study, suggesting a novel tumor suppressor gene in this region (Avet-Loiseau et al, 1999;Bayani et al, 2000). Recently, hypermethylation of the RASSF1A promoter region in medulloblastoma has been reported (Harada et al, 2002;Lusher et al, 2002).…”

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confidence: 99%

Epigenetic inactivation of RASSF1A candidate tumor suppressor gene at 3p21.3 in brain tumors

et al. 2003

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The human Ras association domain family 1A (RASS-F1A) gene, recently isolated from the lung and breast tumor suppressor locus 3p21.3, is highly methylated in primary lung, breast, nasopharyngeal and other tumors, and re-expression of RASSF1A suppresses the growth of several types of cancer cells. Epigenetic inactivation of RASSF1A by promoter hypermethylation is also important in the development of several human cancers. The methylation status of the promoter region of RASSF1A was analysed in primary brain tumors and glioma cell lines by methylation-specific polymerase chain reaction. In primary brain tumors, 25 of 46 (54.3%) gliomas and five of five (100%) medulloblastomas showed RASSF1A methylation. In benign tumors, only one of 10 (10%) schwannomas and two of 12 (16.7%) meningiomas showed RASSF1A methylation. The RASSF1A promoter region was methylated in all four glioma cell lines. RASSF1A was re-expressed in all methylated cell lines after treatment with the demethylating agent 5-aza-2 0 -deoxycytidine. Methylation of the promoter CpG islands of the RASSF1A may play an important role in the pathogenesis of glioma and medulloblastoma.

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Comparative genomic hybridization detects many recurrent imbalances in central nervous system primitive neuroectodermal tumours in children

Cited by 58 publications

References 21 publications

Medulloblastoma – Genetic Alterations

Medulloblastoma – Genetic Alterations

Identification of a region of homozygous deletion on 8p22–23.1 in medulloblastoma

Epigenetic inactivation of RASSF1A candidate tumor suppressor gene at 3p21.3 in brain tumors

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