AI Article Synopsis

  • The study focused on diffuse midline gliomas (DMG) with H3K27M mutations, which have unique genetic traits and a poor prognosis, aiming to understand their clinical characteristics and survival outcomes.
  • Researchers analyzed data from 43 patients (aged 3 to 75) treated in China from 2017 to 2019, assessing various clinical and molecular factors related to their condition.
  • Key findings revealed that a low preoperative Karnofsky Performance Score (KPS), lack of radiotherapy, and P53 overexpression were linked to a significantly shorter overall survival of about 12.83 months in these patients.

Article Abstract

Purpose: Diffuse midline gliomas (DMG) with H3K27M mutations have been identified as a rare distinctive entity with unique genetic features, varied molecular alterations, and poor prognosis. The current study aimed to evaluate the clinical characteristics and profile of molecular markers on patients with a DMG harboring H3K27M mutations, and explore the impact of this genetic makeup on overall survival.

Methods: We retrospectively analyzed 43 consecutive patients diagnosed with a DMG harboring H3K27M mutations (age range 3 to 75 years) and treated in a tertiary institution within China between January 2017 to December 2019. Various clinical and molecular factors were evaluated to assess their prognostic value in this unique patient cohort.

Results: The median overall survival (OS) was 12.83 months. Preoperative Karnofsky Performance Score (KPS) and adjuvant radiotherapy were found to be independent clinical parameters influencing the OS by multivariate analysis ( = 0.027 and < 0.001 respectively). Whereas extent of tumor resection failed to demonstrate statistical significance. For molecular markers, P53 overexpression was identified as a negative prognostic factor for overall survival by multivariate analysis ( = 0.030).

Conclusion: Low preoperative KPS, absence of radiotherapy and P53 overexpression were identified as predictors of a dismal overall survival in patients with DMG and H3K27M mutations.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7917281PMC
http://dx.doi.org/10.3389/fonc.2020.602553DOI Listing

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