Identification of EWS/FLI-1 transcripts in giant-cell tumor of bone

Scotlandi, Katia; Chano, Tokuhiro; Benini, Stefania; Serra, Massimo; Manara, Maria Cristina; Cerisano, Vanessa; Picci, Piero; Baldini, Nicola

doi:10.1002/1097-0215(20000801)87:3<328::aid-ijc4>3.0.co;2-1

Cited by 22 publications

(21 citation statements)

References 39 publications

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“…Afterwards, CD99-suppressed colonies started to grow normally and to spread-out consistent with the loss of RNAi-suppression. These results may be considered in context with previous reports on homotypic aggregation and impaired cellular migration of hematopoietic and ESFT cells when CD99 was ligated to antibody (Bernard et al, 1995;Scotlandi et al, 2000;Schenkel et al, 2002).…”

Section: Cd99 Suppresses Kcmf1supporting

confidence: 85%

“…In hematopoietic cells, CD99 ligation has been implicated in induction of homotypic aggregation, cell adhesion, migration (Bernard et al, 1995;Hahn et al, 1997;Schenkel et al, 2002), upregulation of TCR expression , vesicular transport of MHC molecules (Sohn et al, 2001), and costimulation to induce a Th1-type cytokine production (Waclavicek et al, 1998). In immature thymocytes and ESFT cells, CD99 antibodies induce massive apoptosis (Bernard et al, 1997;Sohn et al, 1998) as well as caspase-independent cell death (Cerisano et al, 2004) and increase sensitivity to chemotherapeutic agents (Scotlandi et al, 2000). Recent studies have provided fragmentary information about the involvement of protein kinases in CD99 triggering of intracellular signal-transduction (Hahn et al, 2000;Kasinrerk et al, 2000).…”

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confidence: 99%

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Suppression of KCMF1 by constitutive high CD99 expression is involved in the migratory ability of Ewing's sarcoma cells

et al. 2005

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High CD99 expression levels and rearrangements of the EWS gene with ETS transcription factor genes characterize the Ewing's sarcoma family of tumors (ESFT). CD99 is a cell surface glycoprotein whose engagement has been implicated in cell proliferation as well as upregulation and transport of several transmembrane proteins in hematopoietic cells. In ESFT, antibody ligation of CD99 induces fast homotypic cell aggregation and cell death although its functional role in these processes remains largely unknown. Here, using an RNAi approach, we studied for the first time the consequences of modulated CD99 expression in six different ESFT cell lines, representing the most frequent variant forms of EWS gene rearrangement. CD99 suppression resulted in growth inhibition and reduced migration of ESFT cells. Among genes whose expression changes in response to CD99 modulation, the potassium-channel modulatory factor KCMF1 was consistently upregulated. In a series of 22 primary ESFT, KCMF1 expression levels inversely correlated with CD99 abundancy. Cells forced to express ectopic KCMF1 showed a similar reduction in migratory ability as CD99 silenced ESFT cells. Our results suggest that in ESFT, high CD99 expression levels contribute to the malignant properties of ESFT by promoting growth and migration of tumor cells and identify KCMF1 as a potential metastasis suppressor gene downregulated by high constitutive CD99 expression in ESFT.

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Section: Cd99 Suppresses Kcmf1supporting

confidence: 85%

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confidence: 99%

Suppression of KCMF1 by constitutive high CD99 expression is involved in the migratory ability of Ewing's sarcoma cells

et al. 2005

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“…2 The notion that the pathogenesis of GCT is different from that of other bone tumors was recently challenged by a report claiming that fusion of the EWS and FLI1 genes, a molecular genetic event caused by the translocation t(11;22)(q24;q12) and a characteristic feature of the Ewing family of tumors, could be detected also in a large subset (13 of 15 analyzed cases) of GCT. 4 Although the chimeric EWS/FLI1 transcript was expressed at very low levels, requiring the use of highly sensitive, nested reverse transcriptase polymerase chain reaction (RT-PCR) analysis, the detected fusion transcripts were of the same type as previously described for Ewing tumors. Based on these findings, it was argued that EWS/ FLI1-positive tumor cell populations may influence the clinical behavior of GCT.…”

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confidence: 89%

“…4 Although the chimeric EWS/FLI1 transcript was expressed at very low levels, requiring the use of highly sensitive, nested reverse transcriptase polymerase chain reaction (RT-PCR) analysis, the detected fusion transcripts were of the same type as previously described for Ewing tumors. Based on these findings, it was argued that EWS/ FLI1-positive tumor cell populations may influence the clinical behavior of GCT.To find out whether we could reproduce the results obtained by Scotlandi et al, 4 we subjected frozen tissue from 10 cases of GCT to single-step and nested RT-PCR analysis for the EWS/FLI1 fusion. …”

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NoEWS/FLI1 fusion transcripts in giant-cell tumors of bone

et al. 2001

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Giant-cell tumor of bone (GCT) is a locally aggressive neoplasm of unknown etiology and pathogenesis. Cytogenetically, no consistent chromosomal alterations, apart from telomeric associations involving various chromosome ends, have been described. Recently, however, it was reported that by using highly sensitive nested RT-PCR, a high proportion of GCT displays chimeric EWS/FLI1 fusion transcripts, i.e., the molecular genetic feature previously known to be strongly associated with the Ewing family of tumors. Thus, we decided to perform single-step and nested RT-PCR analyses on fresh frozen samples from 10 cases of GCT, all of which had also been subjected to cytogenetic analysis. After short-term culturing, none of the samples displayed any t Giant-cell tumor of bone (GCT) is a relatively uncommon neoplasm, usually presenting between 20 -40 years of age. It preferentially involves the ends of the long bones, may be locally aggressive, but rarely metastasizes. 1 The etiology and pathogenesis are largely unknown and, so far, no consistent genetic alterations have been detected in GCT. Of the 35 cytogenetically abnormal cases that are included in the Mitelman Database of Chromosome Aberrations in Cancer, 2 all but 2 have near diploid chromosome numbers, and the most common type of alteration is telomeric association, i.e., end-to-end fusions of 2 chromosomes, most often affecting chromosome arms 11p, 15p, 19q, 20q, and 21p. 3 In addition to the telomeric associations, detected in 20 of the 35 cases described in the literature, a few recurrent numerical alterations have been described, the most common being loss of chromosome 12, detected in 4 cases. Thus, at the cytogenetic level, GCT is different from other bone tumors, which either show characteristic patterns of chromosomal imbalances (e.g., chondrosarcoma, osteosarcoma, and chordoma) or recurrent structural rearrangements (e.g., Ewing sarcoma, aneurysmal bone cysts and chondroma). 2 The notion that the pathogenesis of GCT is different from that of other bone tumors was recently challenged by a report claiming that fusion of the EWS and FLI1 genes, a molecular genetic event caused by the translocation t(11;22)(q24;q12) and a characteristic feature of the Ewing family of tumors, could be detected also in a large subset (13 of 15 analyzed cases) of GCT. 4 Although the chimeric EWS/FLI1 transcript was expressed at very low levels, requiring the use of highly sensitive, nested reverse transcriptase polymerase chain reaction (RT-PCR) analysis, the detected fusion transcripts were of the same type as previously described for Ewing tumors. Based on these findings, it was argued that EWS/ FLI1-positive tumor cell populations may influence the clinical behavior of GCT.To find out whether we could reproduce the results obtained by Scotlandi et al., 4 we subjected frozen tissue from 10 cases of GCT to single-step and nested RT-PCR analysis for the EWS/FLI1 fusion. MATERIAL AND METHODS PatientsClinical data on the 10 patients are summarized in Table I. RNA isolation and ele...

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Leydig cell tumor after treatment for Ewing's sarcoma

Butros

Phillip

Chou

et al. 2006

Pediatric Blood & Cancer

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Leydig cell tumors account for 3% of testicular tumors and have never been reported after treatment for Ewing's sarcoma. We report the unusual occurrence of a patient who developed a Leydig cell tumor of the testis 18 years after successful treatment for Ewing's sarcoma. Additional monitoring for second malignancies may become appropriate as long-term survival continues to improve for patients with Ewing's sarcoma.

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Identification of EWS/FLI-1 transcripts in giant-cell tumor of bone

Cited by 22 publications

References 39 publications

Suppression of KCMF1 by constitutive high CD99 expression is involved in the migratory ability of Ewing's sarcoma cells

Suppression of KCMF1 by constitutive high CD99 expression is involved in the migratory ability of Ewing's sarcoma cells

NoEWS/FLI1 fusion transcripts in giant-cell tumors of bone

Leydig cell tumor after treatment for Ewing's sarcoma

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