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Rapid and convergent evolution in the glioblastoma multiforme genome. | LitMetric

Rapid and convergent evolution in the glioblastoma multiforme genome.

Genomics

NeuroTexas Institute, St. David's Healthcare, Austin, TX 78705, United States; Center for Systems and Synthetic Biology, University of Texas at Austin, Austin, TX 78712, United States; Texas Advanced Computing Center, University of Texas at Austin, Austin, TX 78758, United States.

Published: March 2015

AI Article Synopsis

  • The study investigates which gene mutations are responsible for the progression of Glioblastoma multiforme (GBM), a type of brain cancer, by analyzing genetic changes and their impact on tumor development.
  • It was found that most mutated genes in GBM show high selection values (ω), but these are largely due to weaker purifying selection rather than strong positive selection, with only a few genes significantly favored.
  • The researchers also identified recurring mutations linked to patient survival, indicating that these mutations could be useful for diagnosing and monitoring the progression of GBM.

Article Abstract

Determining which mutations drive tumor progression is a defining question in cancer genomics. We analyzed sequence evolution in Glioblastoma multiforme (GBM) by computing the number of parallel mutations and by estimating ω=dN/dS, a measure of the strength and direction of selection. The ω values of almost all 7617 mutated genes in GBM are much higher than in germline genes. We identified only 21 genes under significant positive selection in GBM, as well as 29 genes under significant purifying selection, including several zinc finger proteins. Therefore, most of the high ω values in the GBM genome are due to weaker purifying selection rather than positive selection. We also found multiple recurrent mutations in GBM, several of which are associated with patient survival time. Our results suggest that convergence and neutral evolution play a significant role in GBM, and that sites with recurrent mutations can serve as molecular diagnostics of the clinical course of GBM tumors.

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Source
http://dx.doi.org/10.1016/j.ygeno.2014.12.010DOI Listing

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