Primary Intracerebral Angiomatoid Fibrous Histiocytoma

Dunham, Christopher; Hussong, Jerry W.; Seiff, Michael E.; Pfeifer, John D.; Perry, Arie

doi:10.1097/pas.0b013e3181453451

Cited by 89 publications

(21 citation statements)

References 19 publications

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“…Currently, seven members have been identified in the ATF family: ATF1, ATF2, ATF3, ATF4, ATF5, ATF6 and ATF7 [ 24 ]. ATF1 has been linked to multiple cancers, such as clear cell sarcoma [ 25 ], melanoma [ 26 ] and angiomatoid fibrous histiocytoma [ 27 ]. ATF2 has been found to play a dual role in tumorigenesis [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-488 inhibits tongue squamous carcinoma cell invasion and EMT by directly targeting ATF3

et al. 2018

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BackgroundIt has been reported that the expression of activating transcription factor 3 (ATF3) is closely associated with both microRNA (miRNA) processing and the progress of many cancers. Our study aimed to explore the interaction between ATF3 and miR-488 in tongue squamous cell carcinoma (TSCC).MethodsQuantitative real-time PCR was performed to detect the levels of ATF3 and miR-488 in TSCC tissues and cell lines. Cell invasion and epithelial–mesenchymal transition (EMT) were assessed to determine the biological functions of miR-488 and ATF3 in TSCC cells. The mRNA and protein levels of ATF3 were measured using quantitative RT-PCR and western blotting. Luciferase assays were performed to validate ATF3 as an miR-488 target in TSCC cells.ResultsWe found that the level of miR-488 significantly decreased and the expression of ATF3 significantly increased in TSCC tissues and cell lines. A low level of miR-488 was closely associated with increased expression of ATF3 in TSCC tissues. Introducing miR-488 significantly inhibited the invasion and EMT of TSCC cells, and knockdown of miR-488 promoted both processes. The bioinformatics analysis predicted that ATF3 is a potential target gene of miR-488. The luciferase reporter assay showed that miR-488 could directly target ATF3. ATF3 silencing had similar effects to miR-488 overexpression on TSCC cells. Overexpression of ATF3 in TSCC cells partially reversed the inhibitory effects of the miR-488 mimic.ConclusionmiR-488 inhibited cell invasion and EMT of TSCC cells by directly downregulating ATF3 expression.

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Section: Discussionmentioning

confidence: 99%

RETRACTED ARTICLE: MicroRNA-488 inhibits tongue squamous carcinoma cell invasion and EMT by directly targeting ATF3

et al. 2018

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“…Our findings do not refute the existence of intracranial AFH, as two well-documented examples have been reported in the literature showing EWSR1-ATF1 fusion in the occipital lobe of a 25 year-old man and an EWSR1 rearrangement in the temporal lobe of a 35 year-old man. 25,26 We have also identified an additional brain AFH from our files, with classic morphologic features and EWSR1-ATF1 fusion occurring in the temporal lobe of a 59 year-old man.…”

Section: Discussionmentioning

confidence: 92%

EWSR1 Fusions With CREB Family Transcription Factors Define a Novel Myxoid Mesenchymal Tumor With Predilection for Intracranial Location

Kao

Sung

Zhang

et al. 2017

American Journal of Surgical Pathology

116

132

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Recurrent gene fusions involving EWSR1 with members of the cAMP response element binding protein (CREB) family (ATF1 and CREB1) have been reported in a diverse group of tumors including angiomatoid fibrous histiocytoma (AFH), soft tissue and gastrointestinal clear cell sarcoma (CCS), primary pulmonary myxoid sarcoma (PPMS) and hyalinizing clear cell carcinoma of salivary gland. We have recently encountered a group of 5 myxoid mesenchymal tumors positive for EWSR1 fusions with one of the CREB family member (ATF1, CREB1 and CREM), with histologic features distinct from any of the previously described pathologic entities. Tumors occurred in children or young adults (12–23 years; mean 18), with equal gender distribution. All except one were intracranial (intra-axial, 2; meningeal, 2) while one was perirectal. Histologically, the tumors were well-circumscribed, often lobulated, composed of uniform ovoid to round cells, and arranged in cord-like or reticular structures in a myxoid background. All except one displayed unique sunburst amianthoid fibers. Immunohistochemically, tumors were positive for EMA (5/5; 4 focal, 1 diffuse) and desmin (3/5). A novel EWSR1-CREM fusion was identified by RNA sequencing in the peri-rectal tumor, which was further confirmed by FISH and RT-PCR. A 2nd case with similar EWSR1-CREM fusion was identified by RT-PCR and FISH in a meningeal tumor. The remaining cases studied by FISH showed the presence of EWSR1-CREB1 fusion in 2 cases and EWSR1-ATF1 in one. In conclusion, we report a distinct group of myxoid mesenchymal neoplasms occurring in children or young adults with a predilection for intracranial locations. Although the immunoprofile (EMA, desmin) and the fusion type raise the possibility of a myxoid AFH, none of the typical histologic findings of AFH were present, suggesting a novel entity.

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“…Rearrangement of EWSR1 is found in intracranial Ewing sarcomas that involve the inner table of the skull and extraosseous meningeal ‘peripheral’ primitive neuroectodermal tumors [35,52]. Additionally, exceptional examples of other intracranial neoplasms with an EWSR1 rearrangement and variable malignancy have been reported [13,18]. However, this is the first report of such a fusion gene in a primary neuroepithelial tumor.…”

Section: Discussionmentioning

confidence: 99%

Genetic alterations in uncommon low-grade neuroepithelial tumors: BRAF, FGFR1, and MYB mutations occur at high frequency and align with morphology

et al. 2016

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Low-grade neuroepithelial tumors (LGNTs) are diverse CNS tumors presenting in children and young adults, often with a history of epilepsy. While the genetic profiles of common LGNTs, such as the pilocytic astrocytoma and ‘adult-type’ diffuse gliomas, are largely established, those of uncommon LGNTs remain to be defined. In this study, we have used massively parallel sequencing and various targeted molecular genetic approaches to study alterations in 91 LGNTs, mostly from children but including young adult patients. These tumors comprise dysembryoplastic neuroepithelial tumors (DNETs; n=22), diffuse oligodendroglial tumors (d-OTs; n=20), diffuse astrocytomas (DAs; n=17), angiocentric gliomas (n=15), and gangliogliomas (n=17). Most LGNTs (84%) analyzed by whole-genome sequencing (WGS) were characterized by a single driver genetic alteration. Alterations of FGFR1 occurred frequently in LGNTs composed of oligodendrocyte-like cells, being present in 82% of DNETs and 40% of d-OTs. In contrast, a MYB-QKI fusion characterized almost all angiocentric gliomas (87%), and MYB fusion genes were the most common genetic alteration in DAs (41%). A BRAF:p.V600E mutation was present in 35% of gangliogliomas and 18% of DAs. Pathogenic alterations in FGFR1/2/3, BRAF, or MYB/MYBL1 occurred in 78% of the series. Adult-type d-OTs with an IDH1/2 mutation occurred in four adolescents, the youngest aged 15 years at biopsy. Despite a detailed analysis, novel genetic alterations were limited to two fusion genes, EWSR1-PATZ1 and SLMAP-NTRK2, both in gangliogliomas. Alterations in BRAF, FGFR1, or MYB account for most pathogenic alterations in LGNTs, including pilocytic astrocytomas, and alignment of these genetic alterations and cytologic features across LGNTs has diagnostic implications. Additionally, therapeutic options based upon targeting the effects of these alterations are already in clinical trials.

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Primary Intracerebral Angiomatoid Fibrous Histiocytoma

Cited by 89 publications

References 19 publications

RETRACTED ARTICLE: MicroRNA-488 inhibits tongue squamous carcinoma cell invasion and EMT by directly targeting ATF3

RETRACTED ARTICLE: MicroRNA-488 inhibits tongue squamous carcinoma cell invasion and EMT by directly targeting ATF3

EWSR1 Fusions With CREB Family Transcription Factors Define a Novel Myxoid Mesenchymal Tumor With Predilection for Intracranial Location

Genetic alterations in uncommon low-grade neuroepithelial tumors: BRAF, FGFR1, and MYB mutations occur at high frequency and align with morphology

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