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Integrated multi-omics profiling of nonfunctioning pituitary adenomas.

Zhenqing Wei1,2, Cuiqi Zhou3, Minghui Li4

  • 1Department of Neurosurgery, Peking Union Medical College Hospital, Beijing, China. weizhqdl@126.com.

Pituitary
|November 18, 2020
PubMed
Summary

This study reveals genetic and epigenetic changes in highly proliferative nonfunctioning pituitary adenomas (NFPAs). Integrated multi-omics data identified aberrant copy number variations and DNA methylation impacting gene expression, offering insights into NFPA molecular drivers.

Keywords:
Copy number variationDNA methylationGene expressionMulti-omics profilingNonfunctioning pituitary adenoma

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Area of Science:

  • Endocrinology and Molecular Biology
  • Genetics and Genomics
  • Cancer Research

Background:

  • Pituitary adenomas are common tumors, with nonfunctioning pituitary adenomas (NFPAs) comprising a significant subset.
  • The molecular mechanisms underlying the pathogenesis of proliferative NFPAs remain incompletely understood.
  • Genetic and epigenetic alterations are implicated in tumor development, but their specific roles in NFPAs require further elucidation.

Purpose of the Study:

  • To investigate the integrated multi-omics profiles, including copy number variation (CNV), DNA methylation, and gene expression, in proliferative NFPAs.
  • To identify molecular alterations and aberrant pathways associated with highly proliferative NFPAs (hpNFPAs).
  • To elucidate the molecular basis of hpNFPA development.

Main Methods:

  • Analysis of 8 NFPAs, categorized into highly proliferative (Ki-67 ≥ 3) and lowly proliferative (Ki-67 ≤ 1) groups.
  • Comprehensive assessment of CNV, DNA methylation (using Illumina HumanMethylation450 BeadChip), and gene expression (using Affymetrix GeneChip PrimeView Human Gene Expression Array).
  • Ingenuity Pathway Analysis (IPA) for differentially expressed genes and delineation of protein-protein networks for key genes.

Main Results:

  • Aberrant arm-level CNV and dysregulated DNA methylation impacting gene expression were observed in early-occurring hpNFPAs.
  • Chromosomal losses correlated with reduced DNA methyltransferase expression, influencing global methylation.
  • IPA revealed activated pathways (e.g., PPARα/RXRα, dopamine, cAMP, calcium signaling) and inhibited pathways (e.g., p38 MAPK, ERK5) in hpNFPAs. Key gene networks showed concurrent methylation and expression changes.

Conclusions:

  • This study provides a comprehensive multi-omics view of CNV, DNA methylation, and gene expression in NFPAs.
  • Pathway and network analyses offer critical insights into the molecular underpinnings of highly proliferative NFPAs.
  • The findings contribute to understanding the pathogenesis of pituitary adenomas and may guide future therapeutic strategies.