Monitoring treatment efficacy and resistance in breast cancer patients via circulating tumor DNA genomic profiling

Mol Genet Genomic Med. 2020 Feb;8(2):e1079. doi: 10.1002/mgg3.1079. Epub 2019 Dec 23.

Abstract

Background: One of the major challenges in managing invasive breast cancer (BC) is the lack of reliable biomarkers to track response. Circulating tumor DNA (ctDNA) from liquid biopsy, as a candidate biomarker, provides a valuable assessment of BC patients. In this retrospective study, we evaluated the utility of ctDNA to reflect the efficacy of treatment and to monitor resistance mechanisms.

Methods: Targeted next-generation sequencing (NGS) of 416 cancer-relevant genes was performed on 41 plasma biopsy samples of 19 HER2+ and 12 HER2- BC patients. Longitudinal ctDNA samples were analyzed in three BC patients over the treatment course for detecting acquired mutations.

Results: In HER2+ BC patients, ERBB2 somatic copy numbers in ctDNA samples were significantly higher in patients progressed on HER2-targeted therapy than those who were still responding to the treatment. Recurrent acquired mutations were detected in genes including ERBB2, TP53, EGFR, NF1, and SETD2, which may contribute to trastuzumab resistance. In longitudinal analyses, the observed mutation allele frequencies were tracked closely in concordance with treatment responses. A novel ERBB2 p.(Leu869Arg) mutation was acquired in one patient upon resistant to trastuzumab therapy, which was further validated as an oncogenic mutation in vitro and contributed to resistance. In HER2- BC patients with chemotherapy resistance, genetic alterations on TP53, PIK3CA, and DNA damage repair genes were frequently observed.

Conclusions: In summary, ctDNA monitoring, particularly longitudinal analyses, provides valuable insights into the assessment of targeted therapy efficacy and gene alterations underlying trastuzumab resistance and chemotherapy resistance in HER2+ and HER2- BC patients, respectively.

Keywords: ERBB2; breast cancer; chemotherapy; ctDNA; drug resistance; trastuzumab.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antineoplastic Agents, Immunological / therapeutic use
  • Biomarkers, Tumor / blood
  • Biomarkers, Tumor / genetics*
  • Breast Neoplasms / blood
  • Breast Neoplasms / drug therapy
  • Breast Neoplasms / genetics*
  • Circulating Tumor DNA / genetics*
  • Class I Phosphatidylinositol 3-Kinases / genetics
  • Drug Resistance, Neoplasm*
  • ErbB Receptors / genetics
  • Female
  • Histone-Lysine N-Methyltransferase / genetics
  • Humans
  • Mutation
  • Neurofibromin 1 / genetics
  • Receptor, ErbB-2 / genetics
  • Trastuzumab / therapeutic use
  • Tumor Suppressor Protein p53 / genetics

Substances

  • Antineoplastic Agents, Immunological
  • Biomarkers, Tumor
  • Circulating Tumor DNA
  • NF1 protein, human
  • Neurofibromin 1
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • Histone-Lysine N-Methyltransferase
  • SETD2 protein, human
  • Class I Phosphatidylinositol 3-Kinases
  • PIK3CA protein, human
  • EGFR protein, human
  • ERBB2 protein, human
  • ErbB Receptors
  • Receptor, ErbB-2
  • Trastuzumab