2013
DOI: 10.1158/0008-5472.sabcs13-s3-05
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Abstract S3-05: Patient-derived xenograft study reveals endocrine therapy resistance of ER+ breast cancer caused by distinct ESR1 gene aberrations

Abstract: Endocrine therapy resistance occurs in 50% of estrogen receptor positive (ER+) luminal breast cancers but the underlying mechanisms are poorly understood. To gain insight, we have taken advantage of whole-genome and RNA sequencing data of five late-stage hormone-resistant luminal breast tumors all of which have been successfully established as patient-derived mouse xenograft (PDX) models. Here we describe genetic alterations in ESR1-the gene coding for ERa-in three of these five tumors. They include an ESR1 po… Show more

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Cited by 3 publications
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“…These variations were associated with constitutive ER activation and the ability to grow in an estradiol-independent manner [107]. Similarly, genetic alterations in ESR1 from 3 of 5 late-stage, hormone-resistant luminal breast cancers, based on the establishment of PDX models, revealed three mechanisms that could drive endocrine resistance [108]. These included an ESR1 point mutation (Y537S), a translocation leading to a fusion protein of ESR1/YAP1, and an ESR1 gene amplification.…”
Section: Activation Of Cdk4/6 In Luminal B Breast Cancermentioning
confidence: 99%
“…These variations were associated with constitutive ER activation and the ability to grow in an estradiol-independent manner [107]. Similarly, genetic alterations in ESR1 from 3 of 5 late-stage, hormone-resistant luminal breast cancers, based on the establishment of PDX models, revealed three mechanisms that could drive endocrine resistance [108]. These included an ESR1 point mutation (Y537S), a translocation leading to a fusion protein of ESR1/YAP1, and an ESR1 gene amplification.…”
Section: Activation Of Cdk4/6 In Luminal B Breast Cancermentioning
confidence: 99%