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E-Poster Display

385P - Molecular profiling and molecular features of progression in Chinese glioma

Date

17 Sep 2020

Session

E-Poster Display

Topics

Tumour Site

Central Nervous System Malignancies

Presenters

Fan Fei

Citation

Annals of Oncology (2020) 31 (suppl_4): S396-S408. 10.1016/annonc/annonc269

Authors

F. Fei1, L. Zhang2, T. He3, T. Han4, X. Li5, Q. Duan6, G. Lu4

Author affiliations

  • 1 Department Of Neurosurgery, Sichuan Academy of Medical Science and Sichuan Provincial People’s Hospital, 610031 - Chengdu/CN
  • 2 Physical Examination Center, Changhai Hospital, the First Affiliated Hospital of Naval Medical University, Shanghai/CN
  • 3 Department Of Breast Surgery, West China Hospital, West China School of Medicine,Sichuan University, Chengdu/CN
  • 4 Department Of Medicine - Genetic Counseling, Jiangsu xiansheng medical diagnosis co. LTD, Nanjing/CN
  • 5 Bioinformatics Department - Tumor Bioinformatics Group, Jiangsu xiansheng medical diagnosis co. LTD, Nanjing/CN
  • 6 Department Of Medicine - Regional Medicine, Jiangsu xiansheng medical diagnosis co. LTD, Nanjing/CN

Resources

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Abstract 385P

Background

Oligodendroglioma (OD), generally harboring both IDH mutations and 1p/19q co-deletion, represents a group of gliomas with a favorable but still variable survival. Although we have a good knowledge of the molecular features of gliomas, the molecular mechanism of OD progression also remains elusive. Molecular profiling comparison between grade II and grade III OD may reveal the effector factors of the progression.

Methods

We performed 131-gene panel targeted sequencing and mass spectrometry (MS)-based assay on tumor samples from 30 OD (with both IDH mutations and 1p/19q co-deletion) and 75 GBM patients in a CAP certified laboratory. Somatic mutations, copy number variations, fusion genes, and tumor susceptibility related germline mutations were detected by following the standard operating procedure (SOP). The methylation ratio was measured by the MS-based assay.

Results

In our cohort, MGMT promoter methylation was significantly higher in OD than in GBMs (p = 0.0018). Although TP53 mutation and 1p19q co-deletion are usually exclusive, we detected 4 out of 9 grade III OD patients with TP53 mutations. Interestingly, mutations were significantly enriched in radiation pathway in OD (p < 0.001) but not in GBM (p = 0.11). No germline mutation was found in OD, but 7 germline mutations were found in GBM, involving TP53, BRCA2, POLE, MUTYH, FANCC, and SLX4 genes, suggesting a potential relationship between hereditary factors and bad prognosis.

Conclusions

Our molecular profiling analysis of Chinese glioma patients revealed features of progression on methylation, gene mutation, and pathway levels, providing hints for further clinical research to better understand the effects of genetic progression on treatment and prognosis.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

The authors.

Funding

Has not received any funding.

Disclosure

All authors have declared no conflicts of interest.

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