The role of progesterone receptor (PR) status on the association between obesity and prognosis of estrogen receptor positive (ER+) breast cancer (BC) remains poorly understood.
We investigated the prognostic impact of a deletion spanning the entire UGT2B17 gene (UGT2B17*2) and genetic variants of the aromatase CYP19A1 and estrogen receptor α (ESR1) in 125 postmenopausal women with ER-positive breast cancer enrolled in a randomized pre-surgical trial.
An eight-lncRNA signature was established to predict the survival of patients with estrogen receptor (ER)-positive breast cancer receiving endocrine therapy.
Endocrine therapy is important for management of patients with estrogen receptor (ER) positive breast cancer, however positive ER staining does not reliably predict therapy response.
Late recurrence accounts for nearly half of the recurrences in estrogen receptor (ER)-positive breast cancer and decreases post-recurrence survival in patients with ER-negative breast cancer.
Endocrine therapy represents a mainstay adjuvant treatment of estrogen receptor-positive (ER+) breast cancer in clinical practice with an overall survival (OS) benefit.
Finally, we observed that PIK3CA mutations co-occurred with mutations in the estrogen receptor (ESR1) in metastatic tumors from ER+ breast cancer patients.
We hypothesize that more vitamin D exposure (through diet, supplements, and sunlight) and higher intake of calcium are associated with decreased risk of estrogen receptor (ER)+ and ER- breast cancer, and of triple-negative breast cancer (TNBC) among black women.
Estrogen receptor 1 and progesterone receptor are distinct biomarkers and prognostic factors in estrogen receptor-positive breast cancer: Evidence from a bioinformatic analysis.
A CYP2D6 gene polymorphism is related to the effect of tamoxifen treatment in patient with estrogen-receptor positive (ER) positive breast cancer and CYP2D6*10 T/T can lead to a poor prognosis in Asian patients.
However, after adjustment for total WGR and WGW intake, women in the highest quartile of relative WGR intake, reflected by the alkylresorcinol C17:0/C21:0 ratio, had a higher risk of overall breast cancer and estrogen-receptor-positive (ER+) breast cancer than women in the lowest quartile of relative WGR intake, while the risk of estrogen-receptor-negative (ER-) breast cancer incidence was unaffected.
Estrogen receptor α (ER) is the target of endocrine therapies in ER-positive breast cancer (BC), but their therapeutic effectiveness diminishes with disease progression.
Survival analyses indicated that a positive to negative conversion of ER was an independent poor prognostic factor in patients with primary ER-positive breast cancer.
The aim of the current study was to identify molecular characteristics of young patients with estrogen receptor (ER)-positive breast cancer by analyzing mutations and copy number variants (CNV), and by applying expression profiling.
The glucocorticoid receptor (NR3C1, GR) is frequently downregulated in breast tumors, and evidence suggests it acts as a tumor suppressor in estrogen receptor-positive (ER+) breast cancer.
The Rearranged during Transfection (RET) protein is overexpressed in a subset of Estrogen Receptor (ER) positive breast cancer, with both signalling pathways functionally interacting.
A potential strategy for patients with estrogen receptor (ER)-positive breast cancer is necessary to replace neoadjuvant chemotherapy which has limited benefit.
These questions have provoked new mechanistic hypotheses that link resistance to endocrine agents to: (1) Specific defects in single strand break repair are associated with increased mortality from ER+ breast cancer [1,2]; (2) Loss/mutations of certain single strand break repair proteins that disrupt estrogen-regulated cell cycle control through the ATM, CHK2, CDK4 axis [1,2] thereby directly coupling endocrine therapy resistance to specific DNA repair defects; (3) Acquired mutations that drive metastasis include the generation of in-frame ESR1 gene fusions that activate epithelial-to-mesenchymal transition (EMT) driven metastasis as well as endocrine drug-resistant proliferation [3].