AI Article Synopsis

  • TGFbeta is a promising target for treating glioblastomas, as its overproduction has been linked to these aggressive tumors, but comprehensive studies on TGFbeta signaling in large patient cohorts are lacking.
  • Researchers compiled a gene set related to TGFbeta activation and analyzed its impact in high-grade gliomas, revealing varying levels of activation in glioblastoma samples.
  • The study identified two distinct subgroups of glioblastomas based on their TGFbeta activation patterns, indicating potential differences in how these groups might respond to anti-TGFbeta treatments.

Article Abstract

Background: TGFbeta has emerged as an attractive target for the therapeutic intervention of glioblastomas. Aberrant TGFbeta overproduction in glioblastoma and other high-grade gliomas has been reported, however, to date, none of these reports has systematically examined the components of TGFbeta signaling to gain a comprehensive view of TGFbeta activation in large cohorts of human glioma patients.

Methods: TGFbeta activation in mammalian cells leads to a transcriptional program that typically affects 5-10% of the genes in the genome. To systematically examine the status of TGFbeta activation in high-grade glial tumors, we compiled a gene set of transcriptional response to TGFbeta stimulation from tissue culture and in vivo animal studies. These genes were used to examine the status of TGFbeta activation in high-grade gliomas including a large cohort of glioblastomas. Unsupervised and supervised classification analysis was performed in two independent, publicly available glioma microarray datasets.

Results: Unsupervised and supervised classification using the TGFbeta-responsive gene list in two independent glial tumor gene expression data sets revealed various levels of TGFbeta activation in these tumors. Among glioblastomas, one of the most devastating human cancers, two subgroups were identified that showed distinct TGFbeta activation patterns as measured from transcriptional responses. Approximately 62% of glioblastoma samples analyzed showed strong TGFbeta activation, while the rest showed a weak TGFbeta transcriptional response.

Conclusion: Our findings suggest heterogeneous TGFbeta activation in glioblastomas, which may cause potential differences in responses to anti-TGFbeta therapies in these two distinct subgroups of glioblastomas patients.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2655274PMC
http://dx.doi.org/10.1186/1479-5876-7-12DOI Listing

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