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Genetic Programs Driving Oncogenic Transformation: Lessons from in Vitro Models.

Eros Di Giorgio1, Harikrishnareddy Paluvai1, Raffaella Picco1

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Summary

This study reveals common signaling pathway dysregulation during cancer development, driven by oncogenes like RAS, MYC, and HDAC4. These pathways help tumors adapt and predict patient outcomes, suggesting new therapeutic targets.

Keywords:
DOCK4G0S2HDAC4MYCRASSRPX interferonTCGAinflammation

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Area of Science:

  • Molecular oncology and cancer biology.
  • Transcriptional regulation and gene expression analysis in cancer.

Background:

  • Cancer complexity arises from oncogene/tumor suppressor pleiotropy and tumor micro/macro-environment interactions.
  • Understanding commonalities in cancer progression despite mutational heterogeneity is crucial.

Purpose of the Study:

  • To analyze transcriptional adaptations induced by three key oncogenes (RAS, MYC, HDAC4) during isogenic transformation.
  • To identify common dysregulated pathways and gene signatures predictive of cancer patient outcomes.

Main Methods:

  • A reductionist approach analyzing transcriptional adaptations.
  • Investigated the impact of RAS, MYC, and HDAC4 oncogenes in an isogenic transformation model.
  • Identified common gene signatures regulated by these oncogenes.

Main Results:

  • Common signaling pathways, rather than specific genes, were dysregulated during oncogene-induced transformation.
  • Tumor cells in vitro prime pathways for adapting to environmental challenges like restricted blood supply and immune infiltration.
  • Two gene signatures regulated by RAS, MYC, and HDAC4 predict patient outcomes across various cancer types.

Conclusions:

  • Despite diverse mutational landscapes, common regulatory hubs exist at the intersection of signaling pathways in cancer.
  • These common hubs offer potential therapeutic targets for a broad range of cancers.
  • Transcriptional adaptations driven by oncogenes are key to tumor cell survival, metastasis, and therapeutic vulnerability.