gms | German Medical Science

73. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Griechischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

29.05. - 01.06.2022, Köln

ENO1 is upregulated in relapsed low-grade glioma

ENO1 ist hochreguliert in rezidivierten LGG

Meeting Abstract

Suche in Medline nach

  • Thuy Diem Dinh - Universitätsklinikum Köln, Klinik für Neurochirurgie, Köln, Deutschland
  • Roland Goldbrunner - Universitätsklinikum Köln, Klinik für Neurochirurgie, Köln, Deutschland
  • presenting/speaker Marco Timmer - Universitätsklinikum Köln, Klinik für Neurochirurgie, Köln, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 73. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Griechischen Gesellschaft für Neurochirurgie. Köln, 29.05.-01.06.2022. Düsseldorf: German Medical Science GMS Publishing House; 2022. DocP054

doi: 10.3205/22dgnc366, urn:nbn:de:0183-22dgnc3668

Veröffentlicht: 25. Mai 2022

© 2022 Dinh et al.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe http://creativecommons.org/licenses/by/4.0/.


Gliederung

Text

Objective: The Warburg effect describes the ability of cancer cells to reorganize their metabolic pathway, so that the glycolysis can take place in normoxic and hypoxic condition. Thus, the increased energy demand of cancer cells can be covered. ENO1 (α-Enolase), a glycolytic enzyme, contributes to the Warburg effect. Upregulation of ENO1 have been detected in several tumors as endometrial carcinoma, melanoma and pancreatic cancer. Our aim was to evaluate whether ENO1 might function as a prognostic marker for low-grade glioma.

Methods: The glioma samples used were extracted via surgery. The samples were divided according to the WHO classification 2007. ENO1 expression was measured through qPCR and SDHA served as housekeeping gene. IDH1-mutations in glioma samples were detected by sequencing amplified cDNA. For the survival analysis we divided the samples into two groups dependent on ENO1 expression (>median and <median) and analyzed the data by using a Log-rank test and visualized it by generating Kaplan-Meier-curves.

Results: Relapsed GII glioma have upregulated ENO1 expression compared to primary GII glioma (p=0.0023). Comparing the relapsed GII with the previously occurred one the ENO1 expression increased (p=0.0472). The progression free survival (PFS) of primary and relapsed GII glioma did not differ significantly dependent ENO1 expression (33.00 months vs. 38.00 months; p=0.9045). However, in primary GII glioma with high ENO1 expression the PFS is significantly elongated in contrast to low ENO1 expression glioma (54.02 months vs. 28.93 months; p=0.0052).

Conclusion: ENO1 might be an interesting marker for glioma especially for relapsed GII glioma and for patient’s PFS.