CoChat
Sign Up
Cited by 69

The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.

Genetic Architectures and Cell-of-Origin in Glioblastoma

Kim, Hyun Jung, Park, Jung Won, Lee, Jeong Ho·2021·Frontiers in Oncology
DOI 10.3389/fonc.2020.615400PMC PMC7859479
Open this paper in CoChat — free account

Abstract

An aggressive primary brain cancer, glioblastoma (GBM) is the most common cancer of the central nervous system in adults. However, an inability to identify its cell-of-origin has been a fundamental issue hindering further understanding of the nature and pathogenesis of GBM, as well as the development of novel therapeutic targets. Researchers have hypothesized that GBM arises from an accumulation of somatic mutations in neural stem cells (NSCs) and glial precursor cells that confer selective growth advantages, resulting in uncontrolled proliferation. In this review, we outline genomic perspectives on IDH-wildtype and IDH-mutant GBMs pathogenesis and the cell-of-origin harboring GBM driver mutations proposed by various GBM animal models. Additionally, we discuss the distinct neurodevelopmental programs observed in either IDH-wildtype or IDH-mutant GBMs. Further research into the cellular origin and lineage hierarchy of GBM will help with understanding the evolution of GBMs and with developing effective targets for treating GBM cancer cells.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fonc.2020.615400

Cites

9 of 9 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 Overview of genetic alterations and cell-of-origin in IDH-wildtype and IDH-mutant GBMs. (Upper panel) Frequently occurring driver mutations and CNVs in IDH-wildtype and IDH-mutant high-grade gliomas (WHO grade 3 & 4) were listed as above. The frequencies were obtained from published data using cBioPortal (19, 20). (Lower panel) Multipotent neural stem cells (NSCs) have capability to self-renewal and differentiate into progenitors with restricted potential including glial precursor cells (GPCs), oligodendrocyte precursor cells (OPCs), astrocyte precursor cells (APCs), and neural progenitor cells (NPCs). Using specific genetic alterations and cell-specific promoters, NSCs and progenitor cells can be transformed to generate either IDH-wildtype or IDH-mutant GBMs in GEMMs.
Figure 1 Overview of genetic alterations and cell-of-origin in IDH-wildtype and IDH-mutant GBMs. (Upper panel) Frequently occurring driver mutations and CNVs in IDH-wildtype and IDH-mutant high-grade gliomas (WHO grade 3 & 4) were listed as above. The frequencies were obtained from published data using cBioPortal (19, 20). (Lower panel) Multipotent neural stem cells (NSCs) have capability to self-renewal and differentiate into progenitors with restricted potential including glial precursor cells (GPCs), oligodendrocyte precursor cells (OPCs), astrocyte precursor cells (APCs), and neural progenitor cells (NPCs). Using specific genetic alterations and cell-specific promoters, NSCs and progenitor cells can be transformed to generate either IDH-wildtype or IDH-mutant GBMs in GEMMs.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 57

  1. Louis, 2016, The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary, Acta Neuropathol, 131, 10.1007/s00401-016-1545-1 · DOI
  2. Stupp, 2005, Radiotherapy plus concomitant and adjuvant temozolomide for glioblastoma, N Engl J Med, 352, 10.1056/NEJMoa043330 · DOI · Paper page
  3. Cancer Genome Atlas Research, 2008, Comprehensive genomic characterization defines human glioblastoma genes and core pathways, Nature, 455, 10.1038/nature07385 · DOI · Paper page
  4. Nathanson, 2014, Targeted therapy resistance mediated by dynamic regulation of extrachromosomal mutant EGFR DNA, Science, 343, 10.1126/science.1241328 · DOI
  5. Visvader, 2011, Cells of origin in cancer, Nature, 469, 10.1038/nature09781 · DOI
  6. Batista, 2014, Adult neurogenesis and glial oncogenesis: when the process fails, BioMed Res Int, 2014, 10.1155/2014/438639 · DOI
  7. Bradshaw, 2016, Cancer Stem Cell Hierarchy in Glioblastoma Multiforme, Front Surg, 3, 10.3389/fsurg.2016.00021 · DOI
  8. Gimple, 2019, Glioblastoma stem cells: lessons from the tumor hierarchy in a lethal cancer, Genes Dev, 33, 591, 10.1101/gad.324301.119 · DOI · Paper page
  9. Parsons, 2008, An integrated genomic analysis of human glioblastoma multiforme, Science, 321, 10.1126/science.1164382 · DOI · Paper page
  10. Ceccarelli, 2016, Molecular Profiling Reveals Biologically Discrete Subsets and Pathways of Progression in Diffuse Glioma, Cell, 164, 10.1016/j.cell.2015.12.028 · DOI
  11. Korber, 2019, Evolutionary Trajectories of IDH(WT) Glioblastomas Reveal a Common Path of Early Tumorigenesis Instigated Years ahead of Initial Diagnosis, Cancer Cell, 35, 692, 10.1016/j.ccell.2019.02.007 · DOI
  12. Wang, 2016, Clonal evolution of glioblastoma under therapy, Nat Genet, 48, 10.1038/ng.3590 · DOI · Paper page
  13. Miller, 2019, Tracking tumour evolution in glioma through liquid biopsies of cerebrospinal fluid, Nature, 565, 10.1038/s41586-019-0882-3 · DOI
  14. Jonsson, 2019, Genomic Correlates of Disease Progression and Treatment Response in Prospectively Characterized Gliomas, Clin Cancer Res, 25, 10.1158/1078-0432.CCR-19-0032 · DOI
  15. Cerami, 2012, The cBio cancer genomics portal: an open platform for exploring multidimensional cancer genomics data, Cancer Discovery, 2, 10.1158/2159-8290.CD-12-0095 · DOI · Paper page
  16. Gao, 2013, Integrative analysis of complex cancer genomics and clinical profiles using the cBioPortal, Sci Signal, 6, pl1, 10.1126/scisignal.2004088 · DOI · Paper page
  17. Killela, 2013, TERT promoter mutations occur frequently in gliomas and a subset of tumors derived from cells with low rates of self-renewal, Proc Natl Acad Sci USA, 110, 10.1073/pnas.1303607110 · DOI · Paper page
  18. Lee, 2018, Human glioblastoma arises from subventricular zone cells with low-level driver mutations, Nature, 560, 10.1038/s41586-018-0389-3 · DOI · Paper page
  19. Barthel, 2018, Reconstructing the molecular life history of gliomas, Acta Neuropathol, 135, 10.1007/s00401-018-1842-y · DOI
  20. Nobusawa, 2009, IDH1 mutations as molecular signature and predictive factor of secondary glioblastomas, Clin Cancer Res, 15, 10.1158/1078-0432.CCR-09-0715 · DOI
  21. Ichimura, 2009, IDH1 mutations are present in the majority of common adult gliomas but rare in primary glioblastomas, Neuro Oncol, 11, 10.1215/15228517-2009-025 · DOI
  22. Yan, 2009, IDH1 and IDH2 mutations in gliomas, N Engl J Med, 360, 10.1056/NEJMoa0808710 · DOI · Paper page
  23. Barthel, 2019, Longitudinal molecular trajectories of diffuse glioma in adults, Nature, 576, 10.1038/s41586-019-1775-1 · DOI
  24. Liu, 2012, Frequent ATRX mutations and loss of expression in adult diffuse astrocytic tumors carrying IDH1/IDH2 and TP53 mutations, Acta Neuropathol, 124, 10.1007/s00401-012-1031-3 · DOI
  25. Jiao, 2012, CIC, FUBP1 and IDH1 mutations refine the classification of malignant gliomas, Oncotarget, 3, 10.18632/oncotarget.588 · DOI
  26. Verhaak, 2010, Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1, Cancer Cell, 17, 98, 10.1016/j.ccr.2009.12.020 · DOI · Paper page
  27. Wang, 2017, Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment, Cancer Cell, 32, 42, 10.1016/j.ccell.2017.06.003 · DOI
  28. Lei, 2011, Glioblastoma models reveal the connection between adult glial progenitors and the proneural phenotype, PLoS One, 6, e20041, 10.1371/journal.pone.0020041 · DOI
  29. Sanai, 2004, Unique astrocyte ribbon in adult human brain contains neural stem cells but lacks chain migration, Nature, 427, 10.1038/nature02301 · DOI
  30. Tomasetti, 2017, Stem cell divisions, somatic mutations, cancer etiology, and cancer prevention, Science, 355, 10.1126/science.aaf9011 · DOI
  31. Chen, 2012, Malignant glioma: lessons from genomics, mouse models, and stem cells, Cell, 149, 36, 10.1016/j.cell.2012.03.009 · DOI
  32. Zong, 2015, Cell of origin for malignant gliomas and its implication in therapeutic development, Cold Spring Harb Perspect Biol, 7, a020610, 10.1101/cshperspect.a020610 · DOI
  33. Alcantara Llaguno, 2016, Cell of origin of glioma: biological and clinical implications, Br J Cancer, 115, 10.1038/bjc.2016.354 · DOI
  34. Alcantara Llaguno, 2009, Malignant astrocytomas originate from neural stem/progenitor cells in a somatic tumor suppressor mouse model, Cancer Cell, 15, 45, 10.1016/j.ccr.2008.12.006 · DOI · Paper page
  35. Jacques, 2010, Combinations of genetic mutations in the adult neural stem cell compartment determine brain tumour phenotypes, EMBO J, 29, 10.1038/emboj.2009.327 · DOI · Paper page
  36. Zuckermann, 2015, Somatic CRISPR/Cas9-mediated tumour suppressor disruption enables versatile brain tumour modelling, Nat Commun, 6, 7391, 10.1038/ncomms8391 · DOI · Paper page
  37. Alcantara Llaguno, 2015, Adult Lineage-Restricted CNS Progenitors Specify Distinct Glioblastoma Subtypes, Cancer Cell, 28, 10.1016/j.ccell.2015.09.007 · DOI
  38. Galvao, 2014, Transformation of quiescent adult oligodendrocyte precursor cells into malignant glioma through a multistep reactivation process, Proc Natl Acad Sci USA, 111, 10.1073/pnas.1414389111 · DOI
  39. Liu, 2011, Mosaic analysis with double markers reveals tumor cell of origin in glioma, Cell, 146, 10.1016/j.cell.2011.06.014 · DOI
  40. Lu, 2016, Olig2-Dependent Reciprocal Shift in PDGF and EGF Receptor Signaling Regulates Tumor Phenotype and Mitotic Growth in Malignant Glioma, Cancer Cell, 29, 10.1016/j.ccell.2016.03.027 · DOI
  41. Alcantara Llaguno, 2019, Cell-of-origin susceptibility to glioblastoma formation declines with neural lineage restriction, Nat Neurosci, 22, 10.1038/s41593-018-0333-8 · DOI
  42. Chow, 2011, Cooperativity within and among Pten, p53, and Rb pathways induces high-grade astrocytoma in adult brain, Cancer Cell, 19, 10.1016/j.ccr.2011.01.039 · DOI
  43. Friedmann-Morvinski, 2012, Dedifferentiation of neurons and astrocytes by oncogenes can induce gliomas in mice, Science, 338, 10.1126/science.1226929 · DOI
  44. Friedmann-Morvinski, 2014, Dedifferentiation and reprogramming: origins of cancer stem cells, EMBO Rep, 15, 10.1002/embr.201338254 · DOI
  45. Xiong, 2019, Cellular Reprogramming as a Therapeutic Target in Cancer, Trends Cell Biol, 29, 10.1016/j.tcb.2019.05.001 · DOI
  46. Bardella, 2016, Expression of Idh1(R132H) in the Murine Subventricular Zone Stem Cell Niche Recapitulates Features of Early Gliomagenesis, Cancer Cell, 30, 10.1016/j.ccell.2016.08.017 · DOI
  47. Philip, 2018, Mutant IDH1 Promotes Glioma Formation In Vivo, Cell Rep, 23, 10.1016/j.celrep.2018.03.133 · DOI
  48. Nunez, 2019, IDH1-R132H acts as a tumor suppressor in glioma via epigenetic up-regulation of the DNA damage response, Sci Transl Med, 11, eaaq1427, 10.1126/scitranslmed.aaq1427 · DOI
  49. Zhang, 2019, Mutant IDH Sensitizes Gliomas to Endoplasmic Reticulum Stress and Triggers Apoptosis via miR-183-Mediated Inhibition of Semaphorin 3E, Cancer Res, 79, 4994, 10.1158/0008-5472.CAN-19-0054 · DOI
  50. Wang, 2020, Cell Lineage-Based Stratification for Glioblastoma, Cancer Cell, 38, 366, 10.1016/j.ccell.2020.06.003 · DOI
  51. Francis, 2014, EGFR variant heterogeneity in glioblastoma resolved through single-nucleus sequencing, Cancer Discovery, 4, 10.1158/2159-8290.CD-13-0879 · DOI · Paper page
  52. Muller, 2016, Single-cell sequencing maps gene expression to mutational phylogenies in PDGF- and EGF-driven gliomas, Mol Syst Biol, 12, 889, 10.15252/msb.20166969 · DOI
  53. Neftel, 2019, An Integrative Model of Cellular States, Plasticity, and Genetics for Glioblastoma, Cell, 178, 835, 10.1016/j.cell.2019.06.024 · DOI · Paper page
  54. Couturier, 2020, Single-cell RNA-seq reveals that glioblastoma recapitulates a normal neurodevelopmental hierarchy, Nat Commun, 11, 3406, 10.1038/s41467-020-17186-5 · DOI
  55. Tirosh, 2016, Single-cell RNA-seq supports a developmental hierarchy in human oligodendroglioma, Nature, 539, 10.1038/nature20123 · DOI
  56. Venteicher, 2017, Decoupling genetics, lineages, and microenvironment in IDH-mutant gliomas by single-cell RNA-seq, Science, 355, 10.1126/science.aai8478 · DOI
  57. Canoll, 2008, The interface between glial progenitors and gliomas, Acta Neuropathol, 116, 10.1007/s00401-008-0432-9 · DOI

Cited by

Sorted by citations

See all 69

Metadata

Authors
Kim, H. J., Park, J. W., & Lee, J. H.
Venue
Frontiers in Oncology
Publisher
Frontiers Media SA
Published
2021-01-21
Volume
10
ISSN
2234-943X
DOI
10.3389/fonc.2020.615400
PMC
PMC7859479
Cited by
69
References
9
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
National Research Foundation of Korea

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.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review