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Poster session 02

223P - Gene expression profiles in endocrine-resistant breast cancer

Date

10 Sep 2022

Session

Poster session 02

Topics

Translational Research;  Endocrine Therapy;  Cancer Diagnostics

Tumour Site

Breast Cancer

Presenters

Caroline Schagerholm

Citation

Annals of Oncology (2022) 33 (suppl_7): S88-S121. 10.1016/annonc/annonc1040

Authors

C. Schagerholm1, S. Robertson1, E.G. Sifakis1, L. Hases2, C. Williams3, J. Hartman4

Author affiliations

  • 1 Oncology-pathology, Karolinska Institutet, SE-17177 - Stockholm/SE
  • 2 Gene Expression Laboratory, The Salk Institute for Biological Studies, 92037 - La Jolla/US
  • 3 Biosciences And Nutrition, Science for Life Laboratory (SciLifeLab), 171 65 - Solna/SE
  • 4 Oncology-pathology, Karolinska Institutet, 171 77 - Stockholm/SE

Resources

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Abstract 223P

Background

Around 75% of breast cancer (BC) patients' tumors express the treatment-predictive biomarker estrogen receptor alpha (ER/ESR1) and are accordingly offered endocrine therapy. One-third of patients develop endocrine resistance, a majority with tumors that retain ER expression. For most patients, the resistance mechanism is still unknown but factors such as alterations in ER downstream signaling have been investigated. This study aims to examine the gene expression programs of endocrine-resistant tumors.

Methods

A cohort of verified endocrine-resistant BC patients diagnosed in 2005-2006 and 2008-2012 was retrospectively collected at the Karolinska University Hospital in Stockholm, Sweden. Cases (N=56) were defined as patients with an ER+ and human epidermal growth factor receptor 2 (HER2)-negative primary tumor who developed an ER+/HER2- relapse during endocrine therapy. Patients with an ER+/HER2- tumor without progression or relapse at 10 years of follow-up were defined as controls (N=56). RNA was extracted from formalin-fixed paraffin-embedded tissue and analyzed using Affymetrix Clariom D microarrays. Transcriptome Analysis Console (TAC) Software, Gene Set Enrichment (GSEA) application, and R were used for gene expression data analysis.

Results

The initial analysis generated differentially expressed genes, where in general more genes were upregulated in primary tumors of cases who eventually relapse versus controls and downregulated in relapse versus primary tumors of cases. Subsequent investigation of gene sets showed upregulations in epithelial-mesenchymal transition, androgen response, MYC targets, and reactive oxygen species in primary tumors of cases versus controls. We found upregulation in metabolism-associated gene sets and downregulation of estrogen response, epithelial-mesenchymal transition, androgen response, and ESR1 regulation in relapses of cases compared to their primary tumors.

Conclusions

This study of a unique cohort of endocrine-resistant tumors suggests that specific signaling pathways are associated with the development of endocrine resistance in BC. These gene expression signatures may guide further studies on the resistance mechanisms and develop future diagnostic tools for therapy response prediction.

Clinical trial identification

Editorial acknowledgement

Legal entity responsible for the study

Karolinska Institutet.

Funding

Has not received any funding.

Disclosure

S. Robertson: Financial Interests, Full or part-time Employment: Stratipath AB. J. Hartman: Other, Personal, Advisory Board: Roche; Financial Interests, Institutional, Funding: Cepheid, Novartis, Roche; Financial Interests, Personal, Ownership Interest: Stratipath AB; Other, Personal, Speaker’s Bureau, Speakers honoraria: Roche, Novartis, Pfizer, Eli Lilly, MSD, Veracyte, ExactSciences. All other authors have declared no conflicts of interest.

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