Advertisement

Journal of Neuro-Oncology

, Volume 138, Issue 3, pp 659–666 | Cite as

Molecular profiles for insular low-grade gliomas with putamen involvement

  • Chunyao Zhou
  • Yongheng Wang
  • Xing Liu
  • Yuchao Liang
  • Ziwen Fan
  • Tao Jiang
  • Yinyan Wang
  • Lei Wang
Clinical Study

Abstract

Background

The newly proposed putamen classification system shows good prognostic value in patients with insular LGGs, yet no study towards the molecular profiles of putamen involved LGGs has been proposed.

Methods

Clinical information and imaging data of patients diagnosed with insular low-grade gliomas were collected retrospectively. Genetic information of the 34 tumors was assessed using RNA-sequencing. Gene set enrichment analysis was further performed to identify the genes showing differential expression between putamen-involved tumors and putamen non-involved tumors. The level of Ki-67 expression was also evaluated.

Results

There were 843 genes identified to be differentially expressed between putamen-involved and non-involved gliomas. Specifically, Gene set enrichment analysis discovered 13 Kyoto Encyclopedia of Genes and Genomes pathways and 37 Gene Ontology Biological Process term were upregulated in putamen-involved low-grade glioma cells. The enriched GO sets with the highest gene counts included cell cycle (42 genes), mitotic cell cycle (24 genes), and cell division (19 genes). Furthermore, high expression of Ki-67 was associated with putamen involvement in insular gliomas.

Conclusions

There is clear genetic variation between putamen-involved and non-involved insular low-grade gliomas. The differential expression of genes related to the processes of cell proliferation, cell migration, or DNA repair may lead to putamen involvement. The findings suggest that among the two subtypes, putamen-involved insular low-grade gliomas have higher malignancy, and the clinical treatment towards the putamen-involved insular low-grade gliomas should be more active.

Keywords

Insular glioma Molecular profile Genomic feature Putamen Prognosis 

Notes

Funding

This work was supported by National Basic Research Program of China (No. 2015CB755500), National Natural Science Foundation of China (No. 81601452), Beijing Natural Science Foundation (No. 7174295) and Key science and technology research project of the Hebei provincial health and Family Planning Commission (No. 20171258).

Compliance with ethical standards

Conflict of interest

We report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Ethical approval

This retrospective study was approved by the institutional review board of Beijing Tiantan hospital, written consent was obtained from all of our enrolled patients.

Supplementary material

11060_2018_2837_MOESM1_ESM.xlsx (12 kb)
Supplementary material 1 (XLSX 11 KB)
11060_2018_2837_MOESM2_ESM.xlsx (10 kb)
Supplementary material 2 (XLSX 10 KB)
11060_2018_2837_MOESM3_ESM.xlsx (25 kb)
Supplementary material 3 (XLSX 25 KB)

References

  1. 1.
    Yasargil MG (1994) Microneurosurgery, vol 4b. Thieme, StuttgartGoogle Scholar
  2. 2.
    Yasargil MG, von Ammon K, Cavazos E, Doczi T, Reeves JD, Roth P (1992) Tumours of the limbic and paralimbic systems. Acta Neurochir 118(1–2):40–52CrossRefPubMedGoogle Scholar
  3. 3.
    Ozyurt E, Kaya AH, Yanriverdi T et al (2003) New classification for insular tumors and surgical results of 40 patients. Neurosurg Q 13:138–148CrossRefGoogle Scholar
  4. 4.
    Saito R, Kumabe T, Kanamori M, Sonoda Y, Tominaga T (2010) Insulo-opercular gliomas: four different natural progression patterns and implications for surgical indications. Neurol Med Chir 50(4):286–290CrossRefGoogle Scholar
  5. 5.
    Mandonnet E, Capelle L, Duffau H (2006) Extension of paralimbic low grade gliomas: toward an anatomical classification based on white matter invasion patterns. J Neurooncol 78(2):179–185CrossRefPubMedGoogle Scholar
  6. 6.
    Moshel YA, Marcus JD, Parker EC, Kelly PJ (2008) Resection of insular gliomas: the importance of lenticulostriate artery position. J Neurosurg 109(5):825–834CrossRefPubMedGoogle Scholar
  7. 7.
    Ebeling U, Kothbauer K (1995) Circumscribed low grade astrocytomas in the dominant opercular and insular region: a pilot study. Acta Neurochir 132(1–3):66–74CrossRefPubMedGoogle Scholar
  8. 8.
    Sanai N, Polley MY, Berger MS (2010) Insular glioma resection: assessment of patient morbidity, survival, and tumor progression. J Neurosurg 112(1):1–9CrossRefPubMedGoogle Scholar
  9. 9.
    Tang C, Zhang ZY, Chen LC et al (2016) Subgroup characteristics of insular low-grade glioma based on clinical and molecular analysis of 42 cases. J Neurooncol 126(3):499–507CrossRefPubMedGoogle Scholar
  10. 10.
    Wang Y, Wang Y, Fan X et al (2017) Putamen involvement and survival outcomes in patients with insular low-grade gliomas. J Neurosurg 126(6):1788–1794CrossRefPubMedGoogle Scholar
  11. 11.
    Bao ZS, Chen HM, Yang MY et al (2014) RNA-seq of 272 gliomas revealed a novel, recurrent PTPRZ1-MET fusion transcript in secondary glioblastomas. Genome Res 24(11):1765–1773CrossRefPubMedPubMedCentralGoogle Scholar
  12. 12.
    Huang da W, Sherman BT, Lempicki RA (2009) Systematic and integrative analysis of large gene lists using DAVID bioinformatics resources. Nat Protoc 4(1):44–57CrossRefPubMedGoogle Scholar
  13. 13.
    Supek F, Bosnjak M, Skunca N, Smuc T (2011) REVIGO summarizes and visualizes long lists of gene ontology terms. PLoS ONE 6(7):e21800CrossRefPubMedPubMedCentralGoogle Scholar
  14. 14.
    Stillman B (1996) Cell Cycle Control of DNA replication. Science 274:1659–1663CrossRefPubMedGoogle Scholar
  15. 15.
    Lawo S, Bashkurov M, Mullin M et al (2009) HAUS, the 8-subunit human Augmin complex, regulates centrosome and spindle integrity. Curr Biol 19(10):816–826CrossRefPubMedGoogle Scholar
  16. 16.
    DeGregori J (2002) The genetics of the E2F family of transcription factors: shared functions and unique roles. Biochim Biophys Acta 1602:131–150PubMedGoogle Scholar
  17. 17.
    Jorissen R (2003) Epidermal growth factor receptor: mechanisms of activation and signalling. Exp Cell Res 284(1):31–53CrossRefPubMedGoogle Scholar
  18. 18.
    Kourtidis A, Lu R, Pence LJ, Anastasiadis PZ (2017) A central role for cadherin signaling in cancer. Exp Cell Res 358(1):78–85CrossRefPubMedPubMedCentralGoogle Scholar
  19. 19.
    Canel M, Serrels A, Frame MC, Brunton VG (2013) E-cadherin-integrin crosstalk in cancer invasion and metastasis. J Cell Sci 126(Pt 2):393–401CrossRefPubMedGoogle Scholar
  20. 20.
    Craig SE, Brady-Kalnay SM (2011) Cancer cells cut homophilic cell adhesion molecules and run. Cancer Res 71(2):303–309CrossRefPubMedGoogle Scholar
  21. 21.
    Wells A (1999) EGF receptor. Int J Biochem Cell Biol 31:637–643CrossRefPubMedGoogle Scholar
  22. 22.
    Verhaak RG, Hoadley KA, Purdom E et al (2010) Integrated genomic analysis identifies clinically relevant subtypes of glioblastoma characterized by abnormalities in PDGFRA, IDH1, EGFR, and NF1. Cancer Cell 17(1):98–110CrossRefPubMedPubMedCentralGoogle Scholar
  23. 23.
    Murat A, Migliavacca E, Gorlia T et al (2008) Stem cell-related “self-renewal” signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma. J Clin Oncol 26(18):3015–3024CrossRefPubMedGoogle Scholar
  24. 24.
    Zhou BBS, Elledge SJ (2000) The DNA damage response: putting checkpoints in perspective. Nature 408:433CrossRefPubMedGoogle Scholar
  25. 25.
    Goode EL, Ulrich CM, Potter JD (2002) Polymorphisms in DNA repair genes and associations with cancer risk. Cancer Epidemiol Biomarkers Prev 11(12):1513–1530PubMedGoogle Scholar
  26. 26.
    Helleday T, Petermann E, Lundin C, Hodgson B, Sharma RA (2008) DNA repair pathways as targets for cancer therapy. Nat Rev Cancer 8(3):193–204CrossRefPubMedGoogle Scholar
  27. 27.
    Bao S, Wu Q, McLendon RE et al (2006) Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Nature 444(7120):756–760CrossRefPubMedGoogle Scholar
  28. 28.
    Scrima A, Konickova R, Czyzewski BK et al (2008) Structural basis of UV DNA-damage recognition by the DDB1-DDB2 complex. Cell 135(7):1213–1223CrossRefPubMedPubMedCentralGoogle Scholar
  29. 29.
    Krynetskaia NF, Phadke MS, Jadhav SH, Krynetskiy EY (2009) Chromatin-associated proteins HMGB1/2 and PDIA3 trigger cellular response to chemotherapy-induced DNA damage. Mol Cancer Ther 8(4):864–872CrossRefPubMedPubMedCentralGoogle Scholar
  30. 30.
    Sanai N, Berger MS (2008) Glioma extent of resection and its impact on patient outcome. Neurosurgery 62(4):753–764 (discussion 264–756)CrossRefPubMedGoogle Scholar

Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of Neurosurgery, Beijing Tiantan HospitalCapital Medical UniversityBeijingChina
  2. 2.Beijing Neurosurgical InstituteCapital Medical UniversityBeijingChina
  3. 3.Department of NeurosurgeryQinhuangdao First HospitalHebeiChina
  4. 4.Center of Brain TumorBeijing Institute for Brain DisordersBeijingChina

Personalised recommendations