This article is a correction to:
ESR1 fusions and therapeutic resistance in metastatic breast cancer
Zsuzsanna Nagy1,2,3*
Rinath Jeselsohn1,2,3,4*- 1Center for Functional Cancer Epigenetics, Dana Farber Cancer Institute, Harvard Medical School, Boston, MA, United States
- 2Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA, United States
- 3Department of Medicine, Harvard Medical School, Boston, MA, United States
- 4Susan F. Smith Center for Women’s Cancers, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, United States
A Corrigendum on
ESR1 fusions and therapeutic resistance in metastatic breast cancer
by Nagy Z and Jeselsohn R (2023) 12:1037531. doi: 10.3389/fonc.2022.1037531
In the published article, there was an error. In the main text, some ESR1-e6>fusions that Gou and colleagues characterized were incorrectly referred to as transcriptionally inactive.
A correction has been made to “Structure and function of ESR1- e6>fusion proteins in MBC” section, Paragraph 2. This sentence previously stated:
“ESR1-e6>YAP1, ESR1-e6>SOX9, ESR1- e6>ARNT2, ESR1-e6>LPP, and ESR1-e6>NCOA1 produce active fusion proteins that are positive regulators of transcription (80, 81). In contrast to transcriptionally active ESR1-e6>fusions, multiple ESR1-e6>fusions (ESR1-e6>TCF12, ESR1-e6>ARID1B, ESR1- e6>PCDH11X, ESR1-e6>NOP2, ESR1-e6>DAB2, ESR1- e6>CLINT1, ESR1-e6>GRIP1 and ESR1-e6>TNRC6B) were identified as transcriptionally inactive despite producing stable fusion protein, adding to the complex landscape of ESR1- e6>fusion proteins.”
The corrected sentence appears below:
“The number of studies investigating the activity of ESR1-e6>fusions is limited, the function of some fusions are still unknown. Further studies are required to investigate and fully validate the stability and activity of ESR1-e6>fusions. Some ESR1-e6>fusions such as ESR1-e6>YAP1, ESR1-e6>SOX9, ESR1- e6>ARNT2, ESR1-e6>LPP, ESR1-e6>NCOA1, ESR1-e6->PCDH11X, ESR1-e6>CLINT1, ESR1-e6>GRIP1 and ESR1-e6>TNRC6B produce stable and active fusion proteins that are positive regulators of transcription (80, 81). ESR1-e6->DAB2 has cell type specific transcriptional activity- active in MCF7 but not T47D cells. In contrast to transcriptionally active ESR1-e6>fusions, multiple ESR1-e6>fusions (e.g. ESR1-e6>TCF12, ESR1-e6>ARID1B, ESR1-e6>NOP2) were identified as transcriptionally inactive despite producing stable fusion protein, adding to the complex landscape of ESR1- e6>fusion proteins.”
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
Publisher’s note
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Keywords: breast cancer, estrogen receptor, ESR1 fusion, endocrine therapy resistance, SERD
Citation: Nagy Z and Jeselsohn R (2023) Corrigendum: ESR1 fusions and therapeutic resistance in metastatic breast cancer. Front. Oncol. 13:1155540. doi: 10.3389/fonc.2023.1155540
Received: 31 January 2023; Accepted: 01 February 2023;
Published: 06 March 2023.
Edited and approved by:
Ariella Hanker, University of Texas Southwestern Medical Center, United StatesCopyright © 2023 Nagy and Jeselsohn. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Rinath Jeselsohn, Rinath_Jeselsohn@dfci.harvard.edu; Zsuzsanna Nagy, Zsuzsanna_Nagy@dfci.harvard.edu