Expression of MYCN in pediatric synovial sarcoma

Somers, Gino R.; Zieleńska, Maria; Alaqel, Shaker; Sherman, Christopher; Chan, Suzanne; Thorner, Paul

doi:10.1038/modpathol.3800792

Cited by 11 publications

(8 citation statements)

References 41 publications

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“…Our results concerning the first evidence of nestin expression in osteosarcomas, some previously reported findings on nestin expression in soft-tissue sarcomas [ 25 , 37 , 38 ], and particularly our detection of CSCs features in osteosarcoma-derived cell lines indicate the importance of such research with regard to the bone and soft-tissue sarcomas. Therefore, the present study is a first step to further detailed investigation of the cells exhibiting CSCs markers in osteosarcoma tumor tissue, especially in view of the clinical course of the disease.…”

Section: Discussionsupporting

confidence: 81%

“…However, there is only a minimum of similar findings in soft tissue sarcomas; the only one evidence of nestin was given in pediatric rhabdomyosarcomas [ 25 ] and angiosarcomas [ 37 ]. In synovial sarcomas, nestin expression was documented in approximately 10% of pediatric synovial sarcomas [ 38 ] but it was not detected in the same tumor type in another study [ 39 ]. Not very surprisingly, nestin expression was also sporadically showed in Ewing sarcomas/PNETs [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

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Nestin expression in osteosarcomas and derivation of nestin/CD133 positive osteosarcoma cell lines

et al. 2008

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Background: Nestin was originally identified as a class VI intermediate filament protein that is expressed in stem cells and progenitor cells in the mammalian CNS during development. This protein is replaced in the adult organism by other intermediate filament proteins; however, nestin may be re-expressed under certain pathological conditions such as ischemia, inflammation, brain injury, and neoplastic transformation. Nestin has been detected in many kinds of tumors, especially in tumors derived from the CNS. Co-expression of nestin and the CD133 surface molecule is considered to be a marker for cancer stem cells in neurogenic tumors. Our work was aimed at a detailed study of nestin expression in osteosarcomas and osteosarcoma-derived cell lines.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Nestin expression in osteosarcomas and derivation of nestin/CD133 positive osteosarcoma cell lines

et al. 2008

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“…With the exception of SH‐SY5Y, the highest MYCN protein concentrations were found in cell lines IMR‐32, SK‐N‐BE, 2 CHP‐126 and CHP‐134, which are all derived from MYCN ‐amplified tumors. The ES cell lines as well as non‐ MYCN amplified SH‐SY5Y and Askin Tumor model SK‐N‐MC show basic expression of MYCN protein, which is in agreement with other reports 26 …”

Section: Resultssupporting

confidence: 92%

Cross contamination meets misclassification: Awakening of CHP‐100 from sleeping beauty sleep—A reviewed model for Ewing's sarcoma

Dirks

Capes‐Davis

Eberth

et al. 2021

Intl Journal of Cancer

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A human cell line of neuroblastic tissue, which was believed to have been lost to science due to its unavailability in public repositories, is revived and reclassified. In the 1970s, a triple set of neuroblastoma (NB) cell lines became available for research as MYCN‐amplified vs nonamplified models (CHP‐126/‐134 and CHP‐100, respectively). Confusingly, CHP‐100 was used in subsequent years as a model for NB and, since the 1990s, as a model for neuroepithelioma and later as a model for Ewing's sarcoma (ES), which inevitably led to non‐reproducible results. A deposit at a bioresource center revealed that globally available stocks of CHP‐100 were identical to the prominent NB cell line IMR‐32 and CHP‐100 was included into the list of misidentified cell lines. Now we report on the rediscovery of an authentic CHP‐100 cell line and provide evidence of incorrect classification during establishment. We show that CHP‐100 cells carry a t(11;22)(q24;q12) type II EWSR1‐FLI1 fusion and identify it as a classic ES. Although the question of whether CHP‐100 was a virtual and never existing cell line from the beginning is now clarified, the results of all relevant publications should be considered questionable. Neither the time of the cross‐contamination event with IMR‐32 is known nor was the final classification as a model for Ewing family of tumors available with an associated short tandem repeat profile. After a long road of errors and confusion, authentic CHP‐100 is now characterized as a type II EWSR1‐FLI1 fusion model 44 years after its establishment.

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“…None were shown to contain translocations associated with ES, ARMS, SS, or infantile sarcoma (see Somers and colleagues [1] for further detail), and all showed nuclear positivity for INI1 [1]. Some of the other sarcomas used in this study have been previously published in unrelated studies, including the RMSs [36], the SSs, and the MPNSTs [39]. The study was performed with the approval of the Hospital for Sick Children's Research Ethics Board.…”

Section: Methodsmentioning

confidence: 99%

Immunohistochemical Expression and Cluster Analysis of Mesenchymal and Neural Stem Cell–Associated Proteins in Pediatric Soft Tissue Sarcomas

Sadiković

Graham

et al. 2011

Pediatr Dev Pathol

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Pediatric undifferentiated soft tissue sarcomas (USTSs) are a group of malignancies composed predominantly of primitive round cell sarcomas, the histogenesis of which is uncertain. Thus, diagnosis and therapy remain a challenge. The aims of the current study were to determine whether differential expression of stem cell-associated proteins could be used to aid in determining the histogenesis of pediatric USTSs and to determine whether pediatric USTSs expressed a unique panel of stem cell-associated proteins to aid diagnosis. Tumors included 28 Ewing sarcoma/primitive neuroectodermal tumors (ESs), 22 embryonal rhabdomyosarcomas (ERMSs), 8 alveolar rhabdomyosarcomas (ARMSs), 5 synovial sarcomas (SSs), 5 malignant peripheral nerve sheath tumors (MPNSTs), and 13 USTSs. Stem cell antibodies included 3 mesenchymal stem cell markers (CD44, CD105, and CD166) and 5 neural stem cell markers (CD15, CD29, CD56, CD133, and nestin). Sections were scored followed by statistical analysis, clustering analysis, and visualizations using Partek Genomic Suite Software. The Euclidean clustering divided the tumors into 2 major groups. ESs and USTSs formed the majority of the 1st group, whereas ERMSs, ARMSs, MPNSTs, and SSs formed the 2nd group. Reduced expression of CD56 was strongly associated with the ES/USTS cluster (P < 0.0001). ESs and USTSs were further separated by CD166 staining, wherein increased expression was associated with ES (P < 0.0001). The 2nd group included the majority of other sarcomas, with no consistent separation between subtypes. The current study demonstrates the usefulness of applying stem cell markers to pediatric sarcomas and indicates that USTSs and ESs are closely related and may share a common histogenesis.

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Expression of MYCN in pediatric synovial sarcoma

Cited by 11 publications

References 41 publications

Nestin expression in osteosarcomas and derivation of nestin/CD133 positive osteosarcoma cell lines

Nestin expression in osteosarcomas and derivation of nestin/CD133 positive osteosarcoma cell lines

Cross contamination meets misclassification: Awakening of CHP‐100 from sleeping beauty sleep—A reviewed model for Ewing's sarcoma

Immunohistochemical Expression and Cluster Analysis of Mesenchymal and Neural Stem Cell–Associated Proteins in Pediatric Soft Tissue Sarcomas

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