Scientific article

Natural HLA class I ligands from glioblastoma: extending the options for immunotherapy

Published inJournal of neuro-oncology, vol. 111, no. 3, p. 285-294
Publication date2013

Glioblastoma multiforme is the most frequent and most malignant primary brain tumor with poor prognosis despite surgical removal and radio-chemotherapy. In this setting, immunotherapeutical strategies have great potential, but the reported repertoire of tumor associated antigens is only for HLA-A 02 positive tumors. We describe the first analysis of HLA-peptide presentation patterns in HLA-A 02 negative glioma tissue combined with gene expression profiling of the tumor samples by oligonucleotide microarrays. We identified numerous candidate peptides for immunotherapy. These are peptides derived from proteins with a well-described role in glioma tumor biology and suitable gene expression profiles such as PTPRZ1, EGFR, SEC61G and TNC. Information obtained from complementary analyses of HLA-A 02 negative tumors not only contributes to the discovery of novel shared glioma antigens, but most importantly provides the opportunity to tailor a patient-individual cocktail of tumor-associated peptides for a personalized, targeted immunotherapeutic approach in HLA-A 02 negative patients.

  • Brain Neoplasms/classification/metabolism/pathology
  • Gene Expression Regulation, Neoplastic/physiology
  • Glial Fibrillary Acidic Protein/metabolism
  • Glioblastoma/classification/metabolism/pathology
  • HLA Antigens/metabolism
  • Humans
  • Ligands
  • Membrane Proteins/metabolism
  • Peptides/metabolism
  • Receptor, Epidermal Growth Factor/metabolism
  • Receptor-Like Protein Tyrosine Phosphatases, Class 5/metabolism
  • Tandem Mass Spectrometry
Citation (ISO format)
NEIDERT, Marian Christoph et al. Natural HLA class I ligands from glioblastoma: extending the options for immunotherapy. In: Journal of neuro-oncology, 2013, vol. 111, n° 3, p. 285–294. doi: 10.1007/s11060-012-1028-8
Main files (1)
Article (Published version)
ISSN of the journal0167-594X

Technical informations

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