Recurrent breakpoints at 9q31 and 22q12.2 in extraskeletal myxoid chondrosarcoma☆
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Cited by (93)
Ewing sarcoma genomics and recent therapeutic advancements
2023, Pediatric Hematology Oncology JournalA literature Review: The genomic landscape of spinal chondrosarcoma and potential diagnostic, prognostic & therapeutic implications
2022, Interdisciplinary Neurosurgery: Advanced Techniques and Case ManagementCitation Excerpt :The overall prevalence of gene fusion in EMC is reported in the literature to be as high as 75 % [42]. Of note, EMC has been shown to have a distinctive t(9;22) chromosomal translocation associated with it [43–47]. More specifically, there is a balanced translocation involving the NR4A3 (TEC) gene on chromosome 9 that in 75 % of cases results in a t (9;22) (q22;q12) [48].
Mesenchymal Tumors with EWSR1 Gene Rearrangements
2019, Surgical Pathology ClinicsCitation Excerpt :EMC shows variable, focal, often weak S100 protein expression, and some cases are variably immunoreactive for neuroendocrine markers (synaptophysin and sometimes chromogranin). EMC most frequently harbor the t(9;22)(q22;q12) in which EWSR1 fuses with NR4A3 (formerly CHN).53,140 Rarer translocations are t(9;17)(q22;q11), t(3;9)(q12;q22), and t(9;15)(q22;q21) in which NR4A3 fuses with TAF15 (associated with some EMC with neuroendocrine differentiation),141 TFG and TCF12, as well as a variant FUS-NR4A3 t(9;16)(q22;p11.2).142
Cytogenetic and Molecular Pathology of Pediatric Cancer
2009, Oncology of Infancy and Childhood: Expert Consult - Online and PrintTurning cell cycle controller genes into cancer drugs: A role for an antiproliferative cytokine (βGBP)
2003, Biochemical PharmacologyCitation Excerpt :Significantly, selective elimination of cancer cells in the organism must be based on naturally occurring molecules with ability to exploit the differential dependence of normal and cancer cells on mechanisms which control mitogen activation and programmed cell death. One molecule which has been shown to have these properties is β galactoside binding protein (βGBP) a 15 kDa protein [21,22] whose gene maps in the SIS/PDGF homology region on murine chromosome 15E/human chromosome 22q12–q13 [23,24], a syntenic group found to undergo deletions and translocations in a number of human tumours [25–28]. Secreted by CD4+ and CD8+ activated T cells [29], but also by somatic cells [21], βGBP binds with high affinity (Kd 10−10 M) to ∼5×104 receptor sites per cell to negatively control the cell cycle by downregulating tyrosine kinase receptor-activated signalling and affecting cell cycle controller genes to induce a cell cycle pause before cell commitment to mitosis [21,30].
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Supported in part by Grants CA-14555 and CA-41183 from the National Cancer Institute.
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Dr. Turc-Carel is a Fellow of the Association pour la Recherche sur le Cancer.
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C. T-C., P. D. C., and A. A. S. are presently at The Cancer Center, Southwest Biomedical Research Institute, Scottsdale, AZ.