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Genomic-transcriptomic evolution in lung cancer and metastasis.

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Intratumour heterogeneity drives lung cancer evolution and treatment resistance. This study reveals the transcriptome

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Area of Science:

  • Oncology
  • Genomics
  • Transcriptomics

Background:

  • Intratumour heterogeneity (ITH) is a key driver of lung cancer progression, immune evasion, and therapeutic resistance.
  • Understanding the molecular basis of ITH is crucial for developing effective lung cancer treatments.

Purpose of the Study:

  • To investigate intratumour transcriptomic diversity in non-small cell lung cancer (NSCLC).
  • To explore the relationship between gene expression, ITH, and tumour evolution.
  • To identify RNA-based mechanisms contributing to cancer progression and metastasis.

Main Methods:

  • Paired whole-exome and RNA sequencing of 354 NSCLC tumors and 96 adjacent normal tissues from the TRACERx study.
  • Analysis of 947 tumor regions (primary and metastatic) to assess transcriptomic variation.
  • Application of machine learning to link genomic and transcriptomic data with metastasis potential.

Main Results:

  • The transcriptome significantly contributes to phenotypic variation and ITH in NSCLC.
  • Allele-specific expression, often independent of copy number changes, is linked to epigenomic dysfunction and genomic-transcriptomic parallel evolution.
  • RNA single-base substitution signatures implicate ADAR and APOBEC3A activity, revealing ongoing APOBEC activity.
  • Metastasis-seeding potential is associated with the evolutionary context of mutations and increased proliferation in primary tumors.

Conclusions:

  • The interplay between the genome and transcriptome is critical in shaping ITH and driving lung cancer evolution.
  • Transcriptomic diversity and RNA editing play significant roles in lung cancer progression and therapeutic resistance.
  • Genomic and transcriptomic analyses provide insights into metastasis mechanisms and potential therapeutic targets.