scholarly journals Selective cancer-germline gene expression in pediatric brain tumors

2008 ◽  
Vol 88 (3) ◽  
pp. 273-280 ◽  
Author(s):  
Joannes F. M. Jacobs ◽  
Oliver M. Grauer ◽  
Francis Brasseur ◽  
Peter M. Hoogerbrugge ◽  
Pieter Wesseling ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Tumors ◽  
Pediatric Brain Tumors ◽  
Germline Gene ◽  
Pediatric Brain ◽  
Cancer Germline

scholarly journals Changes in the Expression of Pre-Replicative Complex Genes in hTERT and ALT Pediatric Brain Tumors

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1028 ◽  
Author(s):  
Aurora Irene Idilli ◽  
Francesca Pagani ◽  
Emanuela Kerschbamer ◽  
Francesco Berardinelli ◽  
Manuel Bernabé ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Tumors ◽  
Cancer Cells ◽  
Pediatric Brain Tumors ◽  
Telomere Maintenance ◽  
Telomeric Dna ◽  
Maintenance Mechanism ◽  
Alternative Lengthening ◽  
Differential Gene ◽  
Pediatric Brain

Background: The up-regulation of a telomere maintenance mechanism (TMM) is a common feature of cancer cells and a hallmark of cancer. Routine methods for detecting TMMs in tumor samples are still missing, whereas telomerase targeting treatments are becoming available. In paediatric cancers, alternative lengthening of telomeres (ALT) is found in a subset of sarcomas and malignant brain tumors. ALT is a non-canonical mechanism of telomere maintenance developed by cancer cells with no-functional telomerase. Methods: To identify drivers and/or markers of ALT, we performed a differential gene expression analysis between two zebrafish models of juvenile brain tumors, that differ only for the telomere maintenance mechanism adopted by tumor cells: one is ALT while the other is telomerase-dependent. Results: Comparative analysis of gene expression identified five genes of the pre-replicative complex, ORC4, ORC6, MCM2, CDC45 and RPA3 as upregulated in ALT. We searched for a correlation between telomerase levels and expression of the pre-replicative complex genes in a cohort of paediatric brain cancers and identified a counter-correlation between telomerase expression and the genes of the pre-replicative complex. Moreover, the analysis of ALT markers in a group of 20 patients confirmed the association between ALT and increased RPA and decreased H3K9me3 localization at telomeres. Conclusions: Our study suggests that telomere maintenance mechanisms may act as a driver of telomeric DNA replication and chromatin status in brain cancers and identifies markers of ALT that could be exploited for precise prognostic and therapeutic purposes.

scholarly journals Expression of Bmi-1 in Pediatric Brain Tumors as a New Independent Prognostic Marker of Patient Survival

2013 ◽  
Vol 2013 ◽  
pp. 1-5 ◽  
Author(s):  
Shirin Farivar ◽  
Reza Zati Keikha ◽  
Reza Shiari ◽  
Farzaneh Jadali
Keyword(s):  
Gene Expression ◽  
Brain Tumors ◽  
Prognostic Marker ◽  
Patient Survival ◽  
Insertion Site ◽  
Pediatric Brain Tumors ◽  
High Expression ◽  
Low Grade ◽  
Normal Brain ◽  
Pediatric Brain

Objectives. The B-cell-specific moloney leukemia virus insertion site 1 (the Bmi-1) gene is an important member in the family of polycomb group (PcG) genes that plays an oncogenic role in several types of cancer, but it’s expression as a prognostic marker in pediatric brain tumors has not been indicated.Materials and Methods. The Bmi-1 gene expression, clinic pathological and prognostic significance in a series of pediatric brain tumors were examined by real-time PCR method in 56 pediatric brain tumors.Results. The Bmi-1 gene expression in various types of pediatric brain tumors compared to that in normal brain tissue was 4.85-fold. The relative expression varied from 8.64-fold in ependymomas to 2.89-fold in other types. Expression level in high-grade tumors compared to that in low-grade tumors was 2.5 times. In univariate survival analysis of the pediatric brain tumors, a significant association of high expression of the Bmi-1 with patient survival was demonstrated. In multivariate analysis, the Bmi-1 high expression provided significant independent prognostic factors.Conclusion. Increased expression of the Bmi-1 in pediatric brain tumors may be important in the acquisition of an aggressive phenotype. In addition, it can be used as a strong and independent molecular marker of prognosis in pediatric brain tumors.

Different pediatric brain tumors are associated with different gene expression profiling

2015 ◽  
Vol 117 (4-5) ◽  
pp. 477-485 ◽  
Author(s):  
Michelino Di Rosa ◽  
Cristina Sanfilippo ◽  
Massimo Libra ◽  
Giuseppe Musumeci ◽  
Lucia Malaguarnera
Keyword(s):  
Gene Expression ◽  
Brain Tumors ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Pediatric Brain Tumors ◽  
Pediatric Brain

scholarly journals A pediatric brain tumor atlas of genes deregulated by somatic genomic rearrangement

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yiqun Zhang ◽  
Fengju Chen ◽  
Lawrence A. Donehower ◽  
Michael E. Scheurer ◽  
Chad J. Creighton
Keyword(s):  
Brain Tumor ◽  
Brain Tumors ◽  
Tyrosine Kinases ◽  
Pediatric Brain Tumor ◽  
Pediatric Brain Tumors ◽  
Altered Expression ◽  
Critical Pathways ◽  
Cis Regulation ◽  
Or Gene ◽  
Pediatric Brain

AbstractThe global impact of somatic structural variants (SSVs) on gene expression in pediatric brain tumors has not been thoroughly characterised. Here, using whole-genome and RNA sequencing from 854 tumors of more than 30 different types from the Children’s Brain Tumor Tissue Consortium, we report the altered expression of hundreds of genes in association with the presence of nearby SSV breakpoints. SSV-mediated expression changes involve gene fusions, altered cis-regulation, or gene disruption. SSVs considerably extend the numbers of patients with tumors somatically altered for critical pathways, including receptor tyrosine kinases (KRAS, MET, EGFR, NF1), Rb pathway (CDK4), TERT, MYC family (MYC, MYCN, MYB), and HIPPO (NF2). Compared to initial tumors, progressive or recurrent tumors involve a distinct set of SSV-gene associations. High overall SSV burden associates with TP53 mutations, histone H3.3 gene H3F3C mutations, and the transcription of DNA damage response genes. Compared to adult cancers, pediatric brain tumors would involve a different set of genes with SSV-altered cis-regulation. Our comprehensive and pan-histology genomic analyses reveal SSVs to play a major role in shaping the transcriptome of pediatric brain tumors.

scholarly journals RONC-19. TWO CASES OF RE-IRRADIATION FOR LATE RECURRENT OR RADIATION-INDUCED TUMOR AFTER RADIATION THERAPY FOR PEDIATRIC BRAIN TUMORS

2020 ◽  
Vol 22 (Supplement_3) ◽  
pp. iii459-iii459
Author(s):  
Takashi Mori ◽  
Shigeru Yamaguchi ◽  
Rikiya Onimaru ◽  
Takayuki Hashimoto ◽  
Hidefumi Aoyama
Keyword(s):  
Radiation Therapy ◽  
Brain Tumors ◽  
Tumor Resection ◽  
Intensity Modulated Radiation Therapy ◽  
Late Recurrence ◽  
Pediatric Brain Tumors ◽  
Suprasellar Region ◽  
Radiation Induced ◽  
Pediatric Brain

Abstract BACKGROUND As the outcome of pediatric brain tumors improves, late recurrence and radiation-induced tumor cases are more likely to occur, and the number of cases requiring re-irradiation is expected to increase. Here we report two cases performed intracranial re-irradiation after radiotherapy for pediatric brain tumors. CASE 1: 21-year-old male. He was diagnosed with craniopharyngioma at eight years old and underwent a tumor resection. At 10 years old, the local recurrence of suprasellar region was treated with 50.4 Gy/28 fr of stereotactic radiotherapy (SRT). After that, other recurrent lesions appeared in the left cerebellopontine angle, and he received surgery three times. The tumor was gross totally resected and re-irradiation with 40 Gy/20 fr of SRT was performed. We have found no recurrence or late effects during the one year follow-up. CASE 2: 15-year-old female. At three years old, she received 18 Gy/10 fr of craniospinal irradiation and 36 Gy/20 fr of boost to the posterior fossa as postoperative irradiation for anaplastic ependymoma and cured. However, a anaplastic meningioma appeared on the left side of the skull base at the age of 15, and 50 Gy/25 fr of postoperative intensity-modulated radiation therapy was performed. Two years later, another meningioma developed in the right cerebellar tent, and 54 Gy/27 fr of SRT was performed. Thirty-three months after re-irradiation, MRI showed a slight increase of the lesion, but no late toxicities are observed. CONCLUSION The follow-up periods are short, however intracranial re-irradiation after radiotherapy for pediatric brain tumors were feasible and effective.

Sign in / Sign up

Export Citation Format

Share Document