Chromosomes in Ewing's sarcoma. I. An evaluation of 85 cases and remarkable consistency of t(11;22)(q24;q12)

Turc‐Carel, Claude; Aurias, Alain; Mugneret, Francine; Lizard, Sarab; Sidaner, I; Völk, Christian; Thiery, Jean Paul; Olschwang, Sylviane; Philip, I; Berger, M; Philip, Thierry; Lenoir, Gilbert; Mazabraud, A

doi:10.1016/0165-4608(88)90285-3

Cited by 459 publications

(192 citation statements)

References 26 publications

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“…This chromosomal region is rarely altered in Ewing tumors (Turc-Carel et al, 1988). However, we identi®ed homozygous p15/p16 loss in approximately one third of cases.…”

Section: Discussionmentioning

confidence: 75%

Among genes involved in the RB dependent cell cycle regulatory cascade, the p16 tumor suppressor gene is frequently lost in the Ewing family of tumors

et al. 1997

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The pRB cell cycle regulatory cascade is frequently perturbed in neoplasia by overexpression of a component of the pRB-phosphorylating cyclin D1/CDK4 complex or by inactivation of pRB or the CDK4 inhibitors p16 and p15. We investigated the status and expression of p16, p15, CCND1, CDK4 and RB genes in the Ewing family of tumors. P16 loss was observed in 8 of 27 tumors (30%) and in 12 of 23 (52%) tumor cell lines from unrelated patients. There were no discrepancies in the p16 status between primary tumors and the corresponding cell lines and between cell lines established from consecutive tumor samples. p15 was codeleted in most cases but p15 mRNA was absent also in cell lines retaining the gene. In addition, posttranscriptional p16 inactivation was observed in two cases. Although no evidence for CDK4 or CCND1 ampli®cation was obtained, expression of these genes varied considerably in the cell lines in a case speci®c manner. In wild-type p16 cell lines, pRB expression was lost in one case. Our data indicate that, despite the absence of cytogenetically detectable 9p21 chromosomal aberrations, p16 deletions constitute the most frequent secondary molecular aberration in Ewing tumors so far. These results are discussed in the context of the stage of disease and the clinical outcome of the patients. The potential prognostic impact of these ®ndings remains to be further evaluated.

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“…This chromosomal region is rarely altered in Ewing tumors (Turc-Carel et al, 1988). However, we identi®ed homozygous p15/p16 loss in approximately one third of cases.…”

Section: Discussionmentioning

confidence: 75%

Among genes involved in the RB dependent cell cycle regulatory cascade, the p16 tumor suppressor gene is frequently lost in the Ewing family of tumors

et al. 1997

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“…It has been suggested that 14q24.3-q32.33 may also represent a critical chromosome region that is lost not only in meningioma tumors (3,41), but also in Ewing's sarcoma (42) and in leiomyosarcoma (43). In this sense, specific deletions of 14q22-24 and 14q32, where the AKT (44), ELK-2 (45; a member of the ETS family of oncogenes), and TC1-1 (46; another oncogene) genes are located, appear to be of particular relevance.…”

Section: Discussionmentioning

confidence: 99%

Incidence of numerical chromosome aberrations in meningioma tumors as revealed by fluorescence in situ hybridization using 10 chromosome‐specific probes

et al. 2002

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Objective: Although information on the cytogenetic characteristics of meningioma tumors has accumulated progressively over the past few decades, information on the genetic heterogeneity of meningiomas is still scanty. The aim of the present study was to analyze by interphase fluorescence in situ hybridization (FISH) the incidence of numerical abnormalities for chromosomes 1, 9, 10, 11, 14, 15, 17, 22, X, and Y in a group of 70 consecutive meningioma tumors. Another goal was to establish the potential associations among the altered chromosomes, as a way to assess both intertumoral and intratumoral heterogeneity. Methods: For the purpose of the study, 70 patients diagnosed with meningioma were analyzed. Interphase FISH for the detection of numerical abnormalities for chromosomes 1, 9, 10, 11, 14, 15, 17, 22, X, and Y was applied to fresh tumor samples from each of the patients studied. Results: The overall incidence of numerical abnormalities was 76%. Chromosome Y in males and chromosome 22 in the whole series were the most common abnormalities (46% and 61%, respectively). Despite the finding that monosomy of chromosome 22/22q -deletions are the most frequent individual abnormality (53%), we have observed that chromosome gains are significantly more common than chromosome losses (60% versus 40%). Chromosome gains corresponded to abnormalities of chromosomes 1 (27%), 9 (25%), 10 (23%), 11 (22%), 14 (33%), 15 (22%), 17 (23%), and X in females (35%) and males (23%) whereas chromosome losses apart from chromosome 22 frequently involved chromosomes 14 (19%), X in males (23%), and Y in males (32%). Although an association was found among most gained chromosomes on one side and chromosome losses on the other side, different association patterns were observed. Furthermore, in the latter group, monosomy 22/22q -was associated with monosomy X in females and monosomy 14/14q -was associated with nulisomy Y in males. In addition, chromosome losses usually involved a large proportion of the tumor cells whereas chromosome gains were restricted to small tumor cell clones, including tetraploid cells. Conclusions: Our results show that meningiomas are genetically heterogeneous tumors that display different patterns of numerical chromosome changes, as assessed by interphase FISH. Cytometry (Clin. Cytometry) 50:153-159, 2002.

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“…Loss of chromosome 14 has been described in meningioma (Katsuyama et al, 1986;Al Saadi et al, 1987), neuroblastoma (Suzuki et al, 1989), Ewing's Sarcoma (Turc-Carel et al, 1988) and Leiomyosarcoma (Boghosian et al, 1989). Furthermore, the description of chromosomal translocations that involve the same cytogenetic band on chromosome 14 suggest that a common genetic locus might be involved in the pathway towards tumorigenesis (Katsuyama et al, 1986;Al Saadi et al, 1987;Seizinger et al, 1987) as well as in other solid tumors such as neuroblastoma (Suzuki et al, 1989;Srivatsan et al, 1991), breast tumors (Gebhart et al, 1986;Bello and Rey, 1989), ovarian tumors (Atkin et al, 1990), astrocytoma (Bigner et al, 1986), retinoblastoma (Chaum et al, 1984) and malignant melanoma (Pedersen and Wang, 1989).…”

Section: Discussionmentioning

confidence: 99%

Frequent loss of chromosome 14 in atypical and malignant meningioma: identification of a putative `tumor progression' locus

et al. 1997

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Formation of meningiomas has been associated with the loss of genetic material on chromosome 22. To approach the additional chromosomal events that underlie progression of these tumors to malignancy, we have examined several other chromosomal regions for loss of heterozygosity (LOH) in these tumors. Fifty-eight tumors, comprising 43 benign meningiomas, 11 atypical meningiomas and four malignant meningiomas, were examined. While the loss of chromosome 22 was seen in approximately half of all these tumors, regardless of their malignancy, the most frequent chromosomal losses observed in the malignant and atypical tumors were on the long arm of chromosome 14. Thirty-nine tumors were informative for at least one of the three markers on chromosome 14 that we tested. Of these, 7/14 malignant and atypical tumors showed LOH in contrast to only 1/ 25 benign tumors. Other loci that showed LOH in malignant tumors, although at a much lower frequency, were on chromosomes 17p and 1p. The high frequency of LOH for loci on chromosome 14q in atypical and malignant tumors suggests the presence of a tumor progression gene at this locus. In one of the malignant meningiomas heterozygosity was lost at D14S13 and D14S16 but retained at the proximal marker D14S43 as well as the more distal marker D14S23. This suggests that an interstitial deletion occurred in this tumor which should be useful for further re®ning the position of the putative tumor progression locus.

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Chromosomes in Ewing's sarcoma. I. An evaluation of 85 cases and remarkable consistency of t(11;22)(q24;q12)

Cited by 459 publications

References 26 publications

Among genes involved in the RB dependent cell cycle regulatory cascade, the p16 tumor suppressor gene is frequently lost in the Ewing family of tumors

Among genes involved in the RB dependent cell cycle regulatory cascade, the p16 tumor suppressor gene is frequently lost in the Ewing family of tumors

Incidence of numerical chromosome aberrations in meningioma tumors as revealed by fluorescence in situ hybridization using 10 chromosome‐specific probes

Frequent loss of chromosome 14 in atypical and malignant meningioma: identification of a putative `tumor progression' locus

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