neuroectodermal tumors/argininas

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H3.3 G34R mutations in pediatric primitive neuroectodermal tumors of central nervous system (CNS-PNET) and pediatric glioblastomas: possible diagnostic and therapeutic implications?

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Pediatric glioblastomas recently have been exon sequenced with evidence that approximately 30 % of cases harbour mutations of the histone H3.3 gene. Although studies to determinate their role in risk stratification are on-going, it remains to be determined whether H3.3 mutations could be found in

Primitive neuroectodermal tumors of the cerebral hemispheres in two siblings with TP53 germline mutation.

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AWe report on two siblings (brother and sister) who developed cerebral PNETs at the age of 5 years and 6 months, respectively. Both children were treated by operation followed by polychemotherapy. The brother also received cranio-spinal irradiation. Nevertheless, the children died about 12 months

Chemokine receptor CXCR4 as a therapeutic target for neuroectodermal tumors.

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Chemokines (chemotactic cytokines) are a family of proteins associated with the trafficking and activation of leukocytes and other cell types in immune surveillance and inflammatory response. Besides their roles in the immune system, they play pleiotropic roles in tumor initiation, promotion, and

Transcriptional down-regulation through nuclear exclusion of EWS methylated by PRMT1.

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The EWS gene is known to be chromosomally translocated and fused to various members of the DNA-binding transcription factors in Ewing's sarcoma and primitive neuroectodermal tumor. The product of this gene encodes the N-terminal transcriptional activation domain and the C-terminal RNA-binding domain

Genomic structure of the EWS gene and its relationship to EWSR1, a site of tumor-associated chromosome translocation.

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The EWS gene has been identified based on its location at the chromosome 22 breakpoint of the t(11;22)(q24;q12) translocation that characterizes Ewing sarcoma and related neuroectodermal tumors. The EWS gene spans about 40 kb of DNA and is encoded by 17 exons. The nucleotide sequence of the exons is

PMS2 mutations in childhood cancer.

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Until recently, the PMS2 DNA mismatch repair gene has only rarely been implicated as a cancer susceptibility locus. New studies have shown, however, that earlier analyses of this gene have had technical limitations and also that the genetic behavior of mutant PMS2 alleles is unusual, in that, unlike

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