PreprintArticleVersion 1Preserved in Portico This version is not peer-reviewed
Secondary Analysis of Human Bulk RNA-seq Dataset Suggest Potential Mechanisms and Transcriptional Biomarkers for Letrozole Resistance in Estrogen Positive (ER+) Breast Cancer
Version 1
: Received: 11 May 2024 / Approved: 13 May 2024 / Online: 14 May 2024 (11:33:07 CEST)
How to cite:
Sutherland, L.; Lang, J.; Gonzalez-Juarbe, N.; Pickett, B. E. Secondary Analysis of Human Bulk RNA-seq Dataset Suggest Potential Mechanisms and Transcriptional Biomarkers for Letrozole Resistance in Estrogen Positive (ER+) Breast Cancer. Preprints2024, 2024050904. https://doi.org/10.20944/preprints202405.0904.v1
Sutherland, L.; Lang, J.; Gonzalez-Juarbe, N.; Pickett, B. E. Secondary Analysis of Human Bulk RNA-seq Dataset Suggest Potential Mechanisms and Transcriptional Biomarkers for Letrozole Resistance in Estrogen Positive (ER+) Breast Cancer. Preprints 2024, 2024050904. https://doi.org/10.20944/preprints202405.0904.v1
Sutherland, L.; Lang, J.; Gonzalez-Juarbe, N.; Pickett, B. E. Secondary Analysis of Human Bulk RNA-seq Dataset Suggest Potential Mechanisms and Transcriptional Biomarkers for Letrozole Resistance in Estrogen Positive (ER+) Breast Cancer. Preprints2024, 2024050904. https://doi.org/10.20944/preprints202405.0904.v1
APA Style
Sutherland, L., Lang, J., Gonzalez-Juarbe, N., & Pickett, B. E. (2024). Secondary Analysis of Human Bulk RNA-seq Dataset Suggest Potential Mechanisms and Transcriptional Biomarkers for Letrozole Resistance in Estrogen Positive (ER+) Breast Cancer. Preprints. https://doi.org/10.20944/preprints202405.0904.v1
Chicago/Turabian Style
Sutherland, L., Norberto Gonzalez-Juarbe and Brett E. Pickett. 2024 "Secondary Analysis of Human Bulk RNA-seq Dataset Suggest Potential Mechanisms and Transcriptional Biomarkers for Letrozole Resistance in Estrogen Positive (ER+) Breast Cancer" Preprints. https://doi.org/10.20944/preprints202405.0904.v1
Abstract
Estrogen receptor-positive (ER+) breast cancer is common among postmenopausal women and is frequently treated with Letrozole. Letrozole inhibits aromatase from synthesizing estrogen from androgens. Decreased estrogen slows the growth of tumors and can be an effective treatment. Letrozole resistance is increasingly being observed, which poses a unique problem for patients. We reanalyzed transcriptomic data comparing individuals who responded to Letrozole therapy (responders) to those who were resistant to treatment (non-responders). We identified SOX11 and S100A9 as two genes that significantly differed between these patients; with “PLK1 signaling events” being the most significant signaling pathway. We also identified PRDX4 and E2F8 as the top transcriptional biomarkers for ER+ treatment resistance. Many of the other significant gene products play a known role in ER+ breast cancer or other types of cancer, which partially validate our results. Several of the gene products we identified do not have a characterized role in ER+ breast cancer. Our analysis identified a set of genes that warrant further research to elucidate the molecular mechanism of Letrozole resistance in this patient population, as well as novel high-performing biomarkers. We anticipate that these findings could contribute to improved therapeutic outcomes in human patients.
Keywords
estrogen receptor; breast cancer; treatment resistance; Letrozole; biomarker
Subject
Biology and Life Sciences, Aging
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
