Cytogenetic and pathologic aspects of Ewing's sarcoma and neuroectodermal tumors

Stephenson, Christine F.; Bridge, Julia A.; Sandberg, Avery A.

doi:10.1016/0046-8177(92)90295-e

Cited by 77 publications

(30 citation statements)

References 67 publications

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“…Monosomy for 6q has been previously reported in melanoma, glioma and ovarian adenocarcinoma 11 and rearrangements of chromosome #2, #3, #5, #6 and #7 were also previously reported as a frequent secondary change in ES. 24 Thus, the chromosome abnormalities correlated again with the previous reports. The secondary changes observed reflect the high degree of malignancy in this tumor.…”

Section: Ewing Sarcomasupporting

confidence: 80%

“…In 90% to 95% of ES and PNET tumors, the presence of a specific translocation t(11;22) (q24;q11) as a primary event has been well documented [23][24][25] and the t(11;22) is being used successfully in the differential diagnosis of malignant tumors. In our study, two cases of ES were cytogenetically characterized; one of these tumors (case 7) revealed the t(11;22), thus establishing the diagnosis.…”

Section: Ewing Sarcomamentioning

confidence: 99%

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Cytogenetic Characterization of Sarcomas of Bone and Soft Tissues

Akhtar

1995

Annals of Saudi Medicine

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Section: Ewing Sarcomasupporting

confidence: 80%

Section: Ewing Sarcomamentioning

confidence: 99%

Cytogenetic Characterization of Sarcomas of Bone and Soft Tissues

Akhtar

1995

Annals of Saudi Medicine

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“…Inclusion of ENB within the Ewing's sarcoma family of tumours 35 or the primitive neuroectodermal tumours (PNET) 34 has been proposed, 30 because of the identification in some cases of translocation t (11:22), which is regarded as specific for Ewing's sarcoma. 89 Studies with fluorescence in situ hybridisation 39,40 and RT-PCR 31,40 have not confirmed this translocation in ENB.…”

Section: Originmentioning

confidence: 99%

“…These were supplemented by another 19 relevant publications found in references cited. 4,[9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26] The studies were divided into three types, according to their principal objectives: origin and aetiology of ENB, 9,11,15,[17][18][19]21,24,[27][28][29][30][31][32][33][34][35][36][37][38][39][40] histopathological diagnosis; 10,[12][13][14]23,37,[41][42][43][44]…”

Section: Search Strategy and Selection Criteriamentioning

confidence: 99%

Esthesioneuroblastoma: a meta-analysis and review

Dulguerov

Allal

Calcaterra

2001

The Lancet Oncology

541

698

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Our objective was to review recent developments in diagnosis, staging, and treatment of esthesioneuroblastoma (ENB). A meta-analysis of publications between 1990 and 2000 was carried out, and studies were classified according to their main subject: origin/aetiology of ENB, histopathological diagnosis, and treatment. Data so far point to the basal progenitor cells of the olfactory epithelium as the origin of ENB. Histopathological diagnosis remains difficult and is based on results of antigen expression detected through a panel of antibodies by immunohistochemistry. RT-PCR of HASH expression could be a specific marker of ENB. Overall and disease-free survival at 5 years averaged 45% (SD 22) and 41% (SD 21) in the studies included in the meta-analysis. Survival in Hyams' grades I-II was 56% (SD 20) compared with 25% (SD 20) in grades III-IV (odds ratio 6.2). In patients with metastases in cervical lymph nodes (on average 5% of the total) survival was 29%, compared with 64% for patients with N0 disease (odds ratio 5.1). Survival according to treatment modalities was 65% for surgery plus radiotherapy, 51% for radiotherapy and chemotherapy, 48% for surgery, 47% for surgery plus radiotherapy and chemotherapy, and 37% for radiotherapy alone. The histopathological grading according to Hyams and the presence of cervical lymph-node metastases emerged as prognostic factors. A combination of surgery and radiotherapy seems to be the optimum approach to treatment. The exact role of chemotherapy in treatment protocols is still unclear. The role of elective neck dissection is unclear

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“…Although there have been debates on their histogenesis, PNET and ES are currently regarded as tumors of the same spectrum, which share a common chromosomal translocation, t(11;22)(q24;q12), and the elevated expression of CD99 (Bhagirath et al, 1995;McKeon et al, 1988;Scotlandi et al, 1996;Stephenson et al, 1992). PNET/ES cells are believed to originate from the neural crest and share histogenetic similarities with neuroblastoma, another major solid tumor in childhood (Ladanyi et al, 1990;Lipinski et al, 1987).…”

mentioning

confidence: 99%

Activation of trkA Induces Differentiation and Inhibits the Growth of JK-GMS Askin Tumor Cells

Kim

Cho

et al. 2002

Laboratory Investigation

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SUMMARY:Peripheral primitive neuroectodermal tumor (PNET) and Ewing's sarcoma (ES) constitute a unique group of small round cell tumors in childhood and young adults that are characterized by the same chromosomal translocation t(11;22)(q24;q12). Recently, the expression of neurotrophin receptors has been found in various human tumors including PNET/ES, but the functional significance of these receptor expressions has not been documented in PNET/ES. In the present study, we investigated the biologic effects of trkA neurotrophin receptor activation by nerve growth factor (NGF) in a newly established Askin tumor cell line, JK-GMS, which constitutively expresses a high level of trkA. The activation of trkA induced differentiation and inhibited the growth of JK-GMS cells, which was characteristically associated with down-regulation of c-myc and N-myc mRNA expression. NGF did not exert significant changes in two different PNET/ES cell lines, CADO-ES1 and RD-ES, which did not express detectable levels of trkA. The biologic effects mediated by NGF were abrogated by treatment of the cells with K-252a, and the treatment with brain-derived neurotrophic factor did not affect the biologic behavior of JK-GMS cells, indicating that the effects are trkA specific. The results observed were quite similar to those of neuroblastoma cells, another childhood tumor of neural crest origin. Overall findings strongly suggest that the trkA-mediated signaling pathway plays a crucial role in controlling the basic biologic properties of JK-GMS cells. (Lab Invest 2002, 82:221-229).

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Cytogenetic and pathologic aspects of Ewing's sarcoma and neuroectodermal tumors

Cited by 77 publications

References 67 publications

Cytogenetic Characterization of Sarcomas of Bone and Soft Tissues

Cytogenetic Characterization of Sarcomas of Bone and Soft Tissues

Esthesioneuroblastoma: a meta-analysis and review

Activation of trkA Induces Differentiation and Inhibits the Growth of JK-GMS Askin Tumor Cells

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