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Correction: Corrigendum: Recurrent hormone-binding domain truncated ESR1 amplifications in primary endometrial cancers suggest their implication in hormone independent growth

The Original Article was published on 10 May 2016

Scientific Reports 6: Article number: 25521; published online: 10 May 2016; updated: 30 June 2017

This Article contains errors in the frequencies of ESR1 amplifications concerning uterine corpus endometrioid carcinoma (UCEC) in TCGA, which were incorrectly given as 88 cases (16.3%) and 36 cases (6.7%) for overall and focal amplifications respectively. These numbers represent the regarding amplification frequencies of partial ESR1 sequences that manifest the GISTIC peak.

The correct frequencies of ESR1 amplification in UCEC of TCGA are 90 cases (16.7%) and 39 cases (7.2%) for overall and focal amplification respectively. Accordingly, the seven cases with ESR1 amplifications that appear to truncate the hormone-binding domain encoding region manifest 17.9% instead of 19.4% of cases with focal amplification.

In addition, the GISTIC q-value for ESR1 amplification is incorrectly given as “q = 5.75 × 10−4”. The correct term and number for this value is “residual q = 2.29 × 10−4 after ‘GISTIC peel-off’”.

As a result, in the Results section under subheading ‘Hormone-binding domain truncated ESR1 amplifications in primary endometrial cancers’.

“In the TCGA data subset of 539 endometrial carcinomas analyzed, we identified 88 (16.3%) cases with amplifications encompassing or overlapping ESR1. 46.6% of these were histologically defined serous and 75.0% of the tumors with ESR1 amplification were clustered within the serous like copy-number high molecular subtype according to TCGA. The ESR1 amplifications were focal (less than half a chromosome arm in length) in 36 cases (6.7%) of tumors, and had a significantly higher rate of amplification than the genome-wide average (q = 5.75 × 10−4). Mapping of the overlap between amplifications across tumors identified ESR1 only as the most likely gene target (see methods).

These amplifications appeared to truncate the hormone-binding domain encoding region in seven cases (1.3% of the entire dataset; and 19.4% of cases with focal ESR1 amplification) and to retain exons 1–4 or 1–3, encoding the n-terminal ESR1 transactivation domain (AF1) and DNA-binding domains. Another case without ESR1 amplification exhibited a heterozygous deletion of exons encoding the hormone-binding domain (Fig. 2), for a total apparent ESR1 truncation rate of 1.5% over all tumors. In one additional TCGA case, we detected a hormone-binding domain (exons 4–8) truncating ESR1-SYNE1 mRNA fusion (Appendix B). Eight of these nine tumors were molecularly classified as being in the serous like copy-number high subgroup (4.3% of this subgroup)”.

should read:

“In the TCGA data subset of 539 endometrial carcinomas analyzed, we identified 90 (16.7%) cases with amplifications encompassing or overlapping ESR1. 45.6% of these were histologically defined serous and 75.0% of the tumors with ESR1 amplification were clustered within the serous like copy-number high molecular subtype according to TCGA. The ESR1 amplifications were focal (less than half a chromosome arm in length) in 39 cases (7.2%), and had a significantly higher rate of amplification than the genome-wide average (residual q = 2.29 × 10−4 after “GISTIC peel-off”). Mapping of the overlap between amplifications across tumors identified ESR1 only as the most likely gene target (see methods).

These amplifications appeared to truncate the hormone-binding domain encoding region in seven cases (1.3% of the entire dataset; and 17.9% of cases with focal ESR1 amplification) and to retain exons 1–4 or 1–3, encoding the n-terminal ESR1 transactivation domain (AF1) and DNA-binding domains. Another case without ESR1 amplification exhibited a heterozygous deletion of exons encoding the hormone-binding domain (Fig. 2), for a total apparent ESR1 truncation rate of 1.5% over all tumors. In one additional TCGA case, we detected a hormone-binding domain (exons 4–8) truncating ESR1-SYNE1 mRNA fusion (Appendix B). Eight of these nine tumors were molecularly classified as being in the serous like copy-number high subgroup (4.3% of this subgroup)”.

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The online version of the original article can be found at 10.1038/srep25521

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Holst, F., Hoivik, E., Gibson, W. et al. Correction: Corrigendum: Recurrent hormone-binding domain truncated ESR1 amplifications in primary endometrial cancers suggest their implication in hormone independent growth. Sci Rep 7, 46873 (2017). https://doi.org/10.1038/srep46873

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