Mutational Analysis Reveals the Origin and Therapy-Driven Evolution of Recurrent Glioma
2013; American Association for the Advancement of Science; Volume: 343; Issue: 6167 Linguagem: Inglês
10.1126/science.1239947
ISSN1095-9203
AutoresBrett Johnson, Tali Mazor, Chibo Hong, Michael J. Barnes, Koki Aihara, Cory Y. McLean, Shaun D. Fouse, Shogo Yamamoto, Hiroki Ueda, Kenji Tatsuno, Saurabh Asthana, Llewellyn E. Jalbert, Sarah J. Nelson, Andrew W. Bollen, W. Clay Gustafson, Elise Charron, William A. Weiss, Ivan Smirnov, Jun S. Song, Adam B. Olshen, Soonmee Cha, Yongjun Zhao, Richard A. Moore, Andrew J. Mungall, Steven J.M. Jones, Martin Hirst, Marco A. Marra, Nobuhito Saito, Hiroyuki Aburatani, Akitake Mukasa, Mitchel S. Berger, Susan M. Chang, Barry S. Taylor, J Costello,
Tópico(s)Epigenetics and DNA Methylation
ResumoBack with a Vengeance After surgery, gliomas (a type of brain tumor) recur in nearly all patients and often in a more aggressive form. Johnson et al. (p. 189 , published online 12 December 2013) used exome sequencing to explore whether recurrent tumors harbor different mutations than the primary tumors and whether the mutational profile in the recurrences is influenced by postsurgical treatment of patients with temozolomide (TMZ), a chemotherapeutic drug known to damage DNA. In more than 40% of cases, at least half of the mutations in the initial glioma were undetected at recurrence. The recurrent tumors in many of the TMZ-treated patients bore the signature of TMZ-induced mutagenesis and appeared to follow an evolutionary path to high-grade glioma distinct from that in untreated patients.
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