Mutational analysis reveals the origin and therapy-driven evolution of recurrent glioma
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Back 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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IDH1 mutations are early events in glial cancer development, raising the possibility that additional oncogenic mutations render GBM tumors less dependent on mutant IDH for proliferation and progression.
“IDH1 mutations are early events in the development of glial cancer (Watanabe et al., 2009), raising the possibility that IDH mutations are important for tumor initiation, but accumulation of additional oncogenic mutations renders GBM tumors less dependent on constitutive expression of mutant IDH for tumor proliferation and progression (Johnson et al., 2014; Wakimoto et al., 2014).”
From Targeting Metabolism for Cancer Therapy (2017) · cites this paper as Johnson et al., 2014
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- Authors
- Johnson, B. E., Mazor, T., Hong, C., Barnes, M., Aihara, K., McLean, C. Y., Fouse, S. D., Yamamoto, S., Ueda, H., Tatsuno, K., Asthana, S., Jalbert, L. E., Nelson, S. J., Bollen, A. W., Gustafson, W. C., Charron, E., Weiss, W. A., Smirnov, I. V., Song, J. S., Olshen, A. B., Cha, S., Zhao, Y., Moore, R. A., Mungall, A. J., Jones, S. J. M., Hirst, M., Marra, M. A., Saito, N., Aburatani, H., Mukasa, A., Berger, M. S., Chang, S. M., Taylor, B. S., & Costello, J. F.
- Affiliations
- University of California, San Francisco (US)
- Research Center for Advanced Science and Technology, The University of Tokyo (JP)
- BC Cancer Agency (CA)
- The University of Tokyo (JP)
- Corresponding author
- Johnson, Brett E.
- Mazor, Tali
- Taylor, Barry S.
- Costello, Joseph F.
- ORCID
- Johnson, Brett E.
- Mazor, Tali
- McLean, Cory Y.
- Yamamoto, Shogo
- Ueda, Hiroki
- Tatsuno, Kenji
- Nelson, Sarah J.
- Bollen, Andrew W.
- Gustafson, W. Clay
- Weiss, William A.
- Song, Jun S.
- Olshen, Adam B.
- Cha, Soonmee
- Zhao, Yongjun
- Moore, Richard A.
- Mungall, Andrew J.
- Jones, Steven J. M.
- Hirst, Martin
- Marra, Marco A.
- Saito, Nobuhito
- Aburatani, Hiroyuki
- Mukasa, Akitake
- Berger, Mitchel S.
- Chang, Susan M.
- Taylor, Barry S.
- Costello, Joseph F.
- Venue
- Science
- Published
- 2014-01-10
- Volume
- 343
- Issue
- 6167
- Pages
- 189-193
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC3998672
- OpenAlex
- W2115276344
- Cited by
- 1,362
- References
- 60
- Citations by year
- 2026: 40 · 2025: 56 · 2024: 82 · 2023: 90 · 2022: 121 · 2021: 144 · 2020: 111 · 2019: 141 · 2018: 125 · 2017: 146 · 2016: 121 · 2015: 110 · 2014: 73 · 2013: 2
- FWCI
- 50.15
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- Japan Society for the Promotion of Science (23390343, 24221011)
- National Cancer Institute (P01CA81403, P01CA081403, P30-CA82103, 1T32CA15102201, R01CA169316, P30CA082103, R01CA163336, T32CA151022, T32CA128583, P50CA097257)
- National Institute of General Medical Sciences (T32GM008568)
- National Institute of Neurological Disorders and Stroke (R25NS070680, K08NS079485)
- Topics
- Health Sciences › Medicine › Genetics › Glioma Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- recurrent glioma, low-grade glioma, tumor recurrence, temozolomide, chemoresistance, TP53, ATRX, SMARCA4, BRAF, Rb pathway, Akt/mTOR signaling, hypermutated tumors, mutagenesis, driver mutations, tumor heterogeneity
- MeSH terms
- X-linked Nuclear Protein, Temozolomide, Brain, Brain Neoplasms, Dacarbazine, DNA Mutational Analysis, DNA Helicases, Glioma, Humans, Neoplasm Recurrence, Local, Nuclear Proteins, Transcription Factors, Tumor Suppressor Protein p53, Mutagenesis, Antineoplastic Agents, Alkylating, Proto-Oncogene Proteins B-raf, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases, Neoplasm Grading
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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