Literature DB >> 32795465

Chromosome 3p loss of heterozygosity and reduced expression of H3K36me3 correlate with longer relapse-free survival in sacral conventional chordoma.

Guo Gord Zhu1, Daniel Ramirez2, Wen Chen3, Chao Lu4, Lu Wang5, Denise Frosina6, Achim Jungbluth6, Peter Ntiamoah6, Khedoudja Nafa6, Patrick J Boland7, Meera R Hameed8.   

Abstract

Conventional chordoma is a rare slow-growing malignant tumor of notochordal origin primarily arising at the base of the skull and sacrococcygeal bones. Chordoma may arise from its benign counterpart, benign notochordal cell tumors, and can also undergo dedifferentiation progressing into dedifferentiated chordoma. No study has directly compared the genomic alterations among these tumors comprising a morphologic continuum. Our prior study identified frequent chromosome 3p loss of heterozygosity and minimal deleted regions on chromosome 3 encompassing SETD2, encoding a histone methyltransferase involved in histone H3 lysine 36 trimethylation (H3K36me3). In the present study, we expanded our study to include 65 sacral conventional chordoma cases, 3 benign notochordal cell tumor cases, and 2 dedifferentiated chordoma cases using single nucleotide polymorphism (SNP) array, targeted next-generation sequencing analysis, and immunohistochemistry. We performed immunohistochemical analysis of histone, H3K36me3, and investigated whether there is any association between the clinical behavior and recurrent chromosome or aneuploidy or H3K36me3 protein expression. We found that there is increased genomic instability from benign notochordal cell tumor to conventional chordoma to dedifferentiated chordoma. The highly recurrent genomic aberration, chromosome 3p loss of heterozygosity (occurred in 70% of conventional chordomas), is correlated with longer relapse-free survival, but not with overall survival or metastasis-free survival in sacral chordoma. Chordomas demonstrate variable patterns and levels of H3K36me3 expression, and reduced expression of H3K36me3 showed marginally significant correlation with longer relapse-free survival. Copy number alterations in the genes encoding the H3K36me3 methylation transferase complex and demethylase may account for the altered H3K36me3 expression levels.
Copyright © 2020 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Chordoma; Epigenetics; Genetics; H3K36me3; Relapse-free survival

Year:  2020        PMID: 32795465     DOI: 10.1016/j.humpath.2020.07.002

Source DB:  PubMed          Journal:  Hum Pathol        ISSN: 0046-8177            Impact factor:   3.466


  3 in total

1.  Recurrent loss of chromosome 22 and SMARCB1 deletion in extra-axial chordoma: A clinicopathological and molecular analysis.

Authors:  Xiaoyun Wen; Robert Cimera; Ruth Aryeequaye; Mohanty Abhinta; Edward Athanasian; John Healey; Nicola Fabbri; Patrick Boland; Yanming Zhang; Meera Hameed
Journal:  Genes Chromosomes Cancer       Date:  2021-08-26       Impact factor: 5.006

Review 2.  H3K36 trimethylation-mediated biological functions in cancer.

Authors:  Chu Xiao; Tao Fan; He Tian; Yujia Zheng; Zheng Zhou; Shuofeng Li; Chunxiang Li; Jie He
Journal:  Clin Epigenetics       Date:  2021-10-29       Impact factor: 6.551

3.  Prognostic molecular biomarkers in chordomas: A systematic review and identification of clinically usable biomarker panels.

Authors:  Franco Rubino; Christopher Alvarez-Breckenridge; Kadir Akdemir; Anthony P Conley; Andrew J Bishop; Wei-Lien Wang; Alexander J Lazar; Laurence D Rhines; Franco DeMonte; Shaan M Raza
Journal:  Front Oncol       Date:  2022-09-29       Impact factor: 5.738

  3 in total

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