ArticleBMC cancer2015
Acquired genetic alterations in tumor cells dictate the development of high-risk neuroblastoma and clinical outcomes.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 78 citations in OpenAlex.
- Peroxisome Carrier SLC25A17: Potential Biomarker for Peroxisome Dysfunction and Human Disease.International journal of molecular sciences · 2026Review
- Cellular Identity Crisis: RD3 Loss Fuels Plasticity and Immune Silence in Progressive Neuroblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- MAL2 and rab17 selectively redistribute invadopodia proteins to laterally-induced protrusions in hepatocellular carcinoma cells.Molecular biology of the cell · 2025Article
- SLC25A17 inhibits autophagy to promote triple-negative breast cancer tumorigenesis by ROS-mediated JAK2/STAT3 signaling pathway.Cancer cell international · 2024Article
- Multiomics data analyses to identify SLC25A17 as a novel biomarker to predict the prognosis and immune microenvironment in head and neck squamous cell carcinoma.BMC bioinformatics · 2023Article
- The MAL Family of Proteins: Normal Function, Expression in Cancer, and Potential Use as Cancer Biomarkers.Cancers · 2023Review
- FOXP2 regulates thyroid cancer cell proliferation and apoptosis via transcriptional activation of RPS6KA6.Experimental and therapeutic medicine · 2022Article
- L3MBTL2-mediated CGA transcriptional suppression promotes pancreatic cancer progression through modulating autophagy.iScience · 2022Article
- A novel hypoxia-driven gene signature that can predict the prognosis of hepatocellular carcinoma.Bioengineered · 2022Article
- The transcribed ultraconserved region uc.160+ enhances processing and A-to-I editing of the miR-376 cluster: hypermethylation improves glioma prognosis.Molecular oncology · 2022Article
- The polymerase δ-interacting protein family and their emerging roles in diseases.Frontiers in medicine · 2022Review
- Significance of hematopoietic surface antigen CD34 in neuroblastoma prognosis and the genetic landscape of CD34-expressing neuroblastoma CSCs.Cell biology and toxicology · 2021Article
- DNA methylation in cord blood in association with prenatal depressive symptoms.Clinical epigenetics · 2021Article
- Aberrant splicing in neuroblastoma generates RNA-fusion transcripts and provides vulnerability to spliceosome inhibitors.Nucleic acids research · 2021Article
- FOXA2-Interacting FOXP2 Prevents Epithelial-Mesenchymal Transition of Breast Cancer Cells by Stimulating E-Cadherin and PHF2 Transcription.Frontiers in oncology · 2021Article
- Transcriptome analysis identifies putative multi-gene signature distinguishing benign and malignant pancreatic head mass.Journal of translational medicine · 2020Article
- Impact of extracellular matrix stiffness on genomic heterogeneity in MYCN-amplified neuroblastoma cell line.Journal of experimental & clinical cancer research : CR · 2020Article
- A fast score test for generalized mixture models.Biometrics · 2020Article
- MAL2-Induced Actin-Based Protrusion Formation is Anti-Oncogenic in Hepatocellular Carcinoma.Cancers · 2020Article
- TTLL12 expression in ovarian cancer correlates with a poor outcome.International journal of clinical and experimental pathology · 2020Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundDetermining the driving factors and molecular flow-through that define the switch from favorable to aggressive high-risk disease is critical to the betterment of neuroblastoma cure.
methodsIn this study, we examined the cytogenetic and tumorigenic physiognomies of distinct population of metastatic site- derived aggressive cells (MSDACs) from high-risk tumors, and showed the influence of acquired genetic rearrangements on poor patient outcomes.
resultsKaryotyping in SH-SY5Y and MSDACs revealed trisomy of 1q, with additional non-random chromosomal rearrangements on 1q32, 8p23, 9q34, 15q24, 22q13 (additions), and 7q32 (deletion). Array CGH analysis of individual clones of MSDACs revealed genetic alterations in chromosomes 1, 7, 8, and 22, corresponding to a gain in the copy numbers of LOC100288142, CD1C, CFHR3, FOXP2, MDFIC, RALYL, CSMD3, SAMD12-AS1, and MAL2, and a loss in ADAM5, LOC400927, APOBEC3B, RPL3, MGAT3, SLC25A17, EP300, L3MBTL2, SERHL, POLDIP3, A4GALT, and TTLL1. QPCR analysis and immunoblotting showed a definite association between DNA-copy number changes and matching transcriptional/translational expression in clones of MSDACs. Further, MSDACs exert a stem-like phenotype. Under serum-free conditions, MSDACs demonstrated profound tumorosphere formation ex vivo. Moreover, MSDACs exhibited high tumorigenic capacity in vivo and prompted aggressive metastatic disease. Tissue microarray analysis coupled with automated IHC revealed significant association of RALYL to the tumor grade in a cohort of 25 neuroblastoma patients. Clinical outcome association analysis showed a strong correlation between the expression of CFHR3, CSMD3, MDFIC, FOXP2, RALYL, POLDIP3, SLC25A17, SERHL, MGAT3, TTLL1, or LOC400927 and overall and relapse-free survival in patients with neuroblastoma.
conclusionTogether, these data highlight the ongoing acquired genetic rearrangements in undifferentiated tumor-forming neural crest cells, and suggest that these alterations could switch favorable neuroblastoma to high-risk aggressive disease, promoting poor clinical outcomes.
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