Primary Ewing's Sarcoma/Primitive Neuroectodermal Tumor of Kidney with Caval Involvement in a Pregnant Woman

2016 ◽  
Vol 97 (3) ◽  
pp. 365-368 ◽  
Author(s):  
Yinghui Ding ◽  
Zhenlin Huang ◽  
Yafei Ding ◽  
Zhankui Jia ◽  
Chaohui Gu ◽  
...  
Keyword(s):  
Pregnant Woman ◽  
Primitive Neuroectodermal Tumor ◽  
Ewing’S Sarcoma ◽  
Ewing's Sarcoma ◽  
Neuroectodermal Tumor

Primitive neuroectodermal tumor/Ewing's sarcoma: a case report and literature review

2017 ◽  
Vol 176 (10) ◽  
Author(s):  
Izabela S. Alves ◽  
Luiz G. Berriel ◽  
Rafael T. Alves ◽  
Mateus O. Potratz ◽  
Marcele B. Pinto ◽  
...  
Keyword(s):  
Case Report ◽  
Literature Review ◽  
Primitive Neuroectodermal Tumor ◽  
Ewing’S Sarcoma ◽  
Ewing's Sarcoma ◽  
Neuroectodermal Tumor

scholarly journals Primary Pulmonary Ewing's Sarcoma/Primitive Neuroectodermal Tumor in a 67-year-old Man

2007 ◽  
Vol 22 (Suppl) ◽  
pp. S159 ◽  
Author(s):  
Yoon Young Lee ◽  
Do Hoon Kim ◽  
Ji Hye Lee ◽  
Jong Sang Choi ◽  
Kwang Ho In ◽  
...  
Keyword(s):  
Primitive Neuroectodermal Tumor ◽  
Ewing’S Sarcoma ◽  
Ewing's Sarcoma ◽  
Neuroectodermal Tumor

Detection of circulating tumor cells in patients with Ewing's sarcoma and peripheral primitive neuroectodermal tumor.

1997 ◽  
Vol 15 (2) ◽  
pp. 583-588 ◽  
Author(s):  
D C West ◽  
H E Grier ◽  
M M Swallow ◽  
G D Demetri ◽  
L Granowetter ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Tumor Cells ◽  
Primitive Neuroectodermal Tumor ◽  
Ewing’S Sarcoma ◽  
Ewing's Sarcoma ◽  
Residual Disease ◽  
Neuroectodermal Tumor ◽  
Peripheral Primitive Neuroectodermal Tumor ◽  
Rt Pcr ◽  
Relapsed Disease

PURPOSE To determine the feasibility of detecting Ewing's sarcoma (ES) or peripheral primitive neuroectodermal tumor (PNET) through a reverse-transcriptase polymerase chain reaction (RT-PCR) of the t(11;22)(q24;q12) fusion transcript in blood and bone marrow samples from patients with these neoplasms. PATIENTS AND METHODS Peripheral-blood (PB) and/or bone marrow aspirate (BM) samples were obtained from 28 patients with ES or PNET at initial presentation or at relapse. Patients were divided into two groups: newly diagnosed patients with nonmetastatic disease and those with metastatic/relapsed disease. RNA was extracted from fractionated BM and PB samples, and RT-PCR was performed for the EWS/HumFLI1 fusion mRNA was transcribed across the t(11;22) breakpoint. RESULTS Among the 16 patients with nonmetastatic disease, three of 16 were RT-PCR positive for EWS/HumFLI1 RNA in BM and three of 10 were positive in PB. The total number of nonmetastatic patients who were positive in either PB or BM was four of 16 (25%). Among patients with metastatic/relapsed disease, two of six were positive in BM and five of 10 were positive in PB. The total fraction of patients with metastatic/relapsed disease that was positive in either BM or PB was six of 12 (50%). CONCLUSION In this study, we show that it is possible to amplify the EWS/HumFLI1 RNA by RT-PCR from the BM and PB of a subset of patients with both nonmetastatic and metastatic ES or PNET, which implies that occult tumor cells are present at these sites. The true biologic and clinical meaning of this information is unknown. However, it does suggest a possible application of RT-PCR for the monitoring of residual disease in patients who are undergoing therapy for ES or PNET. This approach may permit early identification of patients who may benefit from alternative therapy or who may be spared possible overtreatment.

scholarly journals The Ewing's sarcoma EWS/FLI-1 fusion gene encodes a more potent transcriptional activator and is a more powerful transforming gene than FLI-1.

1993 ◽  
Vol 13 (12) ◽  
pp. 7393-7398 ◽  
Author(s):  
W A May ◽  
S L Lessnick ◽  
B S Braun ◽  
M Klemsz ◽  
B C Lewis ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Primitive Neuroectodermal Tumor ◽  
Ewing’S Sarcoma ◽  
Ewing's Sarcoma ◽  
Fusion Gene ◽  
Consensus Sequence ◽  
Transcriptional Activator ◽  
Neuroectodermal Tumor ◽  
Amino Terminal ◽  
Transforming Gene

EWS/FLI-1 is a chimeric protein formed by a tumor-specific 11;22 translocation found in both Ewing's sarcoma and primitive neuroectodermal tumor of childhood. EWS/FLI-1 has been shown to be a potent transforming gene, suggesting that it plays an important role in the genesis of these human tumors. We now demonstrate that EWS/FLI-1 has the characteristics of an aberrant transcription factor. Subcellular fractionation experiments localized the EWS/FLI-1 protein to the nucleus of primitive neuroectodermal tumor cells. EWS/FLI-1 specifically bound in vitro an ets-2 consensus sequence similarly to normal FLI-1. When coupled to a GAL4 DNA-binding domain, the amino-terminal EWS/FLI-1 region was a much more potent transcriptional activator than the corresponding amino-terminal domain of FLI-1. Finally, EWS/FLI-1 efficiently transformed NIH 3T3 cells, but FLI-1 did not. These data suggest that EWS/FLI-1, functioning as a transcription factor, leads to a phenotype dramatically different from that of cells expressing FLI-1. EWS/FLI-1 could disrupt normal growth and differentiation either by more efficiently activating FLI-1 target genes or by inappropriately modulating genes normally not responsive to FLI-1.

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