View in EDS PDF Full Text

Mutational Analysis Reveals the Origin and Therapy-Driven Evolution of Recurrent Glioma.

Saved in:
Bibliographic Details
Title: Mutational Analysis Reveals the Origin and Therapy-Driven Evolution of Recurrent Glioma.
Authors: Johnson, Brett E., Mazor, Tali, Chibo Hong, Barnes, Michael, Koki Aihara, McLean, Cory Y., Fouse, Shaun D., Shogo Yamamoto, Hiroki Ueda, Kenji Tatsuno, Asthana, Saurabh, Jalbert, Llewellyn E., Nelson, Sarah J., Bollen, Andrew W., Gustafson, W. Clay, Charron, Elise, Weiss, William A., Smirnov, Ivan V., Song, Jun S., Olshen, Adam B.
Source: Science (pre-March 2025). 1/10/2014, Vol. 343 Issue 6167, p189-193. 5p.
Subjects: Gliomas, Tumors, Genetic mutation, Cancer relapse, Temozolomide, Retinoblastoma gene, Rapamycin, Mutagenesis
Abstract: Tumor recurrence is a leading cause of cancer mortality. Therapies for recurrent disease may fail, at least in part, because the genomic alterations driving the growth of recurrences are distinct from those in the initial tumor. To explore this hypothesis, we sequenced the exornes of 23 initial low-grade gliomas and recurrent tumors resected from the same patients. In 43% of cases, at least half of the mutations in the initial tumor were undetected at recurrence, including driver mutations in TP53, ATRX, SMARCA4, and BRAF] this suggests that recurrent tumors are often seeded by cells derived from the initial tumor at a very early stage of their evolution. Notably, tumors from 6 of 10 patients treated with the chemotherapeutic drug temozolomide (TMZ) followed an alternative evolutionary path to high-grade glioma. At recurrence, these tumors were hypermutated and harbored driver mutations in the RB (retinoblastoma) and Akt-mTOR (mammalian target of rapamycin) pathways that bore the signature of TMZ-induced mutagenesis. [ABSTRACT FROM AUTHOR]
Copyright of Science (pre-March 2025) is the property of American Association for the Advancement of Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
FullText Links:
  – Type: pdflink
Text:
  Availability: 0
Header DbId: pbh
DbLabel: Psychology and Behavioral Sciences Collection
An: 93709284
AccessLevel: 6
PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 0
IllustrationInfo
Items – Name: Title
  Label: Title
  Group: Ti
  Data: Mutational Analysis Reveals the Origin and Therapy-Driven Evolution of Recurrent Glioma.
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AR" term="%22Johnson%2C+Brett+E%2E%22">Johnson, Brett E.</searchLink><br /><searchLink fieldCode="AR" term="%22Mazor%2C+Tali%22">Mazor, Tali</searchLink><br /><searchLink fieldCode="AR" term="%22Chibo+Hong%22">Chibo Hong</searchLink><br /><searchLink fieldCode="AR" term="%22Barnes%2C+Michael%22">Barnes, Michael</searchLink><br /><searchLink fieldCode="AR" term="%22Koki+Aihara%22">Koki Aihara</searchLink><br /><searchLink fieldCode="AR" term="%22McLean%2C+Cory+Y%2E%22">McLean, Cory Y.</searchLink><br /><searchLink fieldCode="AR" term="%22Fouse%2C+Shaun+D%2E%22">Fouse, Shaun D.</searchLink><br /><searchLink fieldCode="AR" term="%22Shogo+Yamamoto%22">Shogo Yamamoto</searchLink><br /><searchLink fieldCode="AR" term="%22Hiroki+Ueda%22">Hiroki Ueda</searchLink><br /><searchLink fieldCode="AR" term="%22Kenji+Tatsuno%22">Kenji Tatsuno</searchLink><br /><searchLink fieldCode="AR" term="%22Asthana%2C+Saurabh%22">Asthana, Saurabh</searchLink><br /><searchLink fieldCode="AR" term="%22Jalbert%2C+Llewellyn+E%2E%22">Jalbert, Llewellyn E.</searchLink><br /><searchLink fieldCode="AR" term="%22Nelson%2C+Sarah+J%2E%22">Nelson, Sarah J.</searchLink><br /><searchLink fieldCode="AR" term="%22Bollen%2C+Andrew+W%2E%22">Bollen, Andrew W.</searchLink><br /><searchLink fieldCode="AR" term="%22Gustafson%2C+W%2E+Clay%22">Gustafson, W. Clay</searchLink><br /><searchLink fieldCode="AR" term="%22Charron%2C+Elise%22">Charron, Elise</searchLink><br /><searchLink fieldCode="AR" term="%22Weiss%2C+William+A%2E%22">Weiss, William A.</searchLink><br /><searchLink fieldCode="AR" term="%22Smirnov%2C+Ivan+V%2E%22">Smirnov, Ivan V.</searchLink><br /><searchLink fieldCode="AR" term="%22Song%2C+Jun+S%2E%22">Song, Jun S.</searchLink><br /><searchLink fieldCode="AR" term="%22Olshen%2C+Adam+B%2E%22">Olshen, Adam B.</searchLink>
– Name: TitleSource
  Label: Source
  Group: Src
  Data: <searchLink fieldCode="JN" term="%22Science+%28pre-March+2025%29%22">Science (pre-March 2025)</searchLink>. 1/10/2014, Vol. 343 Issue 6167, p189-193. 5p.
– Name: Subject
  Label: Subjects
  Group: Su
  Data: <searchLink fieldCode="DE" term="%22Gliomas%22">Gliomas</searchLink><br /><searchLink fieldCode="DE" term="%22Tumors%22">Tumors</searchLink><br /><searchLink fieldCode="DE" term="%22Genetic+mutation%22">Genetic mutation</searchLink><br /><searchLink fieldCode="DE" term="%22Cancer+relapse%22">Cancer relapse</searchLink><br /><searchLink fieldCode="DE" term="%22Temozolomide%22">Temozolomide</searchLink><br /><searchLink fieldCode="DE" term="%22Retinoblastoma+gene%22">Retinoblastoma gene</searchLink><br /><searchLink fieldCode="DE" term="%22Rapamycin%22">Rapamycin</searchLink><br /><searchLink fieldCode="DE" term="%22Mutagenesis%22">Mutagenesis</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Tumor recurrence is a leading cause of cancer mortality. Therapies for recurrent disease may fail, at least in part, because the genomic alterations driving the growth of recurrences are distinct from those in the initial tumor. To explore this hypothesis, we sequenced the exornes of 23 initial low-grade gliomas and recurrent tumors resected from the same patients. In 43% of cases, at least half of the mutations in the initial tumor were undetected at recurrence, including driver mutations in TP53, ATRX, SMARCA4, and BRAF] this suggests that recurrent tumors are often seeded by cells derived from the initial tumor at a very early stage of their evolution. Notably, tumors from 6 of 10 patients treated with the chemotherapeutic drug temozolomide (TMZ) followed an alternative evolutionary path to high-grade glioma. At recurrence, these tumors were hypermutated and harbored driver mutations in the RB (retinoblastoma) and Akt-mTOR (mammalian target of rapamycin) pathways that bore the signature of TMZ-induced mutagenesis. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Science (pre-March 2025) is the property of American Association for the Advancement of Science and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
PLink https://search.ebscohost.com/login.aspx?direct=true&site=eds-live&db=pbh&AN=93709284
RecordInfo BibRecord:
  BibEntity:
    Identifiers:
      – Type: doi
        Value: 10.1126/science.1239947
    Languages:
      – Code: eng
        Text: English
    PhysicalDescription:
      Pagination:
        PageCount: 5
        StartPage: 189
    Subjects:
      – SubjectFull: Gliomas
        Type: general
      – SubjectFull: Tumors
        Type: general
      – SubjectFull: Genetic mutation
        Type: general
      – SubjectFull: Cancer relapse
        Type: general
      – SubjectFull: Temozolomide
        Type: general
      – SubjectFull: Retinoblastoma gene
        Type: general
      – SubjectFull: Rapamycin
        Type: general
      – SubjectFull: Mutagenesis
        Type: general
    Titles:
      – TitleFull: Mutational Analysis Reveals the Origin and Therapy-Driven Evolution of Recurrent Glioma.
        Type: main
  BibRelationships:
    HasContributorRelationships:
      – PersonEntity:
          Name:
            NameFull: Johnson, Brett E.
      – PersonEntity:
          Name:
            NameFull: Mazor, Tali
      – PersonEntity:
          Name:
            NameFull: Chibo Hong
      – PersonEntity:
          Name:
            NameFull: Barnes, Michael
      – PersonEntity:
          Name:
            NameFull: Koki Aihara
      – PersonEntity:
          Name:
            NameFull: McLean, Cory Y.
      – PersonEntity:
          Name:
            NameFull: Fouse, Shaun D.
      – PersonEntity:
          Name:
            NameFull: Shogo Yamamoto
      – PersonEntity:
          Name:
            NameFull: Hiroki Ueda
      – PersonEntity:
          Name:
            NameFull: Kenji Tatsuno
      – PersonEntity:
          Name:
            NameFull: Asthana, Saurabh
      – PersonEntity:
          Name:
            NameFull: Jalbert, Llewellyn E.
      – PersonEntity:
          Name:
            NameFull: Nelson, Sarah J.
      – PersonEntity:
          Name:
            NameFull: Bollen, Andrew W.
      – PersonEntity:
          Name:
            NameFull: Gustafson, W. Clay
      – PersonEntity:
          Name:
            NameFull: Charron, Elise
      – PersonEntity:
          Name:
            NameFull: Weiss, William A.
      – PersonEntity:
          Name:
            NameFull: Smirnov, Ivan V.
      – PersonEntity:
          Name:
            NameFull: Song, Jun S.
      – PersonEntity:
          Name:
            NameFull: Olshen, Adam B.
    IsPartOfRelationships:
      – BibEntity:
          Dates:
            – D: 10
              M: 01
              Text: 1/10/2014
              Type: published
              Y: 2014
          Identifiers:
            – Type: issn-print
              Value: 00368075
          Numbering:
            – Type: volume
              Value: 343
            – Type: issue
              Value: 6167
          Titles:
            – TitleFull: Science (pre-March 2025)
              Type: main
ResultId 1