Abstract: The present invention relates to gene promoters whose methylation status correlates with the clinical survival outcome of glioblastoma patients treated according to the Stupp protocol. More specifically, the invention provides methods and kits for the prognosis of survival outcome and/or treatment response in glioblastoma patients.

Abstract: The present invention relates to the identification and use of biomarkers with clinical relevance to high grade gliomas (HGGs). In particular, the invention provides the identity of four genes, CHAF1B, PDLIM4, EDNRB and HJURP, whose expression, at the transcriptome and proteome levels, is correlated with HGG grading and clinical survival outcome. Methods and kits are provided for using these biomarkers in the prognostication of HGGs, and in the selection and/or monitoring of treatment regimens.

Abstract: The present invention relates to adrenoleukodystrophy proteins and uses thereof. More particularly, the invention relates to human adrenoleukodystrophy proteins. Mutations of the adrenoleukodystrophy protein cause adrenoleukodystrophy or adrenomyelopathy.

Abstract: A method for the treatment of adrenoleukodystrophy or adrenomyeloneuropathy, in which there is administered to a human patient in need of the same an effective amount of hematopoietic cells modified ex vivo by infection with a retroviral vector containing a nucleic acid fragment comprising a sequence as represented on FIG. 2 (SEQ. ID No: 1) or FIG. 6 (SEQ. ID. No: 4-17) or FIG. 7 (SEQ. ID No: 18-23). Also, human hematopoietic cells can be treated ex vivo to correct the content of very long chain fatty acids in them, by providing human hematopoietic cells of a patient affected by adrenoleukodystrophy or adrenomyeloneuropathy, and infecting them ex vivo with a retroviral vector containing, operably linked to a promoter, a nucleic acid fragment as above. The expression of the nucleic acid in the hematopoietic cells corrects the content of very long chain fatty acids in the hematopoietic cells.

Abstract: The cDNA and genomic DNA sequences encoding the human adrenoleukodystrophy protein are provided. Mutations of the adrenoleukodystrophy protein cause adrenoleukodystrophy or adrenomyelopathy.