Transcriptome and genome evolution during HER2-amplified breast neoplasia.

Background: The acquisition of oncogenic drivers is a critical feature of cancer progression. For some carcinomas, it is clear that certain genetic drivers occur early in neoplasia and others late. Why these drivers are selected and how these changes alter the neoplasia's fitness is less understood....

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Publicado en:Breast Cancer Research Vol. 23; no. 1; pp. 1 - 16
Autores principales: Lu, Peipei, Foley, Joseph, Zhu, Chunfang, McNamara, Katherine, Sirinukunwattana, Korsuk, Vennam, Sujay, Varma, Sushama, Fehri, Hamid, Srivastava, Arunima, Zhu, Shirley, Rittscher, Jens, Mallick, Parag, Curtis, Christina, West, Robert
Formato: research Journal Article
Publicado: BioMed Central 7/15/2021
Acceso en línea:Ver este registro en EBSCOhost
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        14655411
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      jtl: Breast Cancer Research
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      dt: 7/15/2021
      vid: 23
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      pub: BioMed Central
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        NLM34266469
        151438324
        10.1186/s13058-021-01451-6
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        151438324
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        atl: Transcriptome and genome evolution during HER2-amplified breast neoplasia.
      aug:
        au:
          Lu, Peipei
          Foley, Joseph
          Zhu, Chunfang
          McNamara, Katherine
          Sirinukunwattana, Korsuk
          Vennam, Sujay
          Varma, Sushama
          Fehri, Hamid
          Srivastava, Arunima
          Zhu, Shirley
          Rittscher, Jens
          Mallick, Parag
          Curtis, Christina
          West, Robert
        affil: Department of Pathology, Stanford University, Stanford, CA, USA
      sug:
        subj:
          Breast Neoplasms
          Adenocarcinoma
          Gene Expression Profiling
          Genome, Human
          Receptors, Cell Surface
          Evolution
          Oncogenes
          Gene Amplification
          In Situ Hybridization, Fluorescence
          Genetics
          Signal Transduction
          Breast Neoplasms Pathology
          Adenocarcinoma Pathology
          Extracellular Space
          Interferons Metabolism
          Female
          Human
          Comparative Studies
          Multicenter Studies
          Evaluation Research
          Validation Studies
          Clinical Assessment Tools
          Female
      ab: Background: The acquisition of oncogenic drivers is a critical feature of cancer progression. For some carcinomas, it is clear that certain genetic drivers occur early in neoplasia and others late. Why these drivers are selected and how these changes alter the neoplasia's fitness is less understood.Methods: Here we use spatially oriented genomic approaches to identify transcriptomic and genetic changes at the single-duct level within precursor neoplasia associated with invasive breast cancer. We study HER2 amplification in ductal carcinoma in situ (DCIS) as an event that can be both quantified and spatially located via fluorescence in situ hybridization (FISH) and immunohistochemistry on fixed paraffin-embedded tissue.Results: By combining the HER2-FISH with the laser capture microdissection (LCM) Smart-3SEQ method, we found that HER2 amplification in DCIS alters the transcriptomic profiles and increases diversity of copy number variations (CNVs). Particularly, interferon signaling pathway is activated by HER2 amplification in DCIS, which may provide a prolonged interferon signaling activation in HER2-positive breast cancer. Multiple subclones of HER2-amplified DCIS with distinct CNV profiles are observed, suggesting that multiple events occurred for the acquisition of HER2 amplification. Notably, DCIS acquires key transcriptomic changes and CNV events prior to HER2 amplification, suggesting that pre-amplified DCIS may create a cellular state primed to gain HER2 amplification for growth advantage.Conclusion: By using genomic methods that are spatially oriented, this study identifies several features that appear to generate insights into neoplastic progression in precancer lesions at a single-duct level.
      pubtype: Academic Journal
      doctype:
        research
        Journal Article
      ougenre: Article
    language: English
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