ER positive

Immunofluorescence analysis of tumor tissues post-treatment revealed the localized induction of thermal stress and upregulation of Heat Shock Protein 70 (HSP-70), a biomarker linked to enhanced immune cell infiltration and activation within the tumor microenvironment. Overall, this study presents a methodical effort to explore the effectiveness of cobalt-zinc-ferrite nanoprobe for chemo-magnetic hyperthermia effects that can be used for efficient, patient-specific, targeted, controlled anticancer therapy through chemodynamic-magnetic-thermal synergistic therapy.

In this cohort, patients treated at public institutions had lower QOL. Younger age (< 60 years), presence of comorbidities, and ovarian suppression associated with ET were key predictors of poor QOL. These findings provide insights for guiding the development of tailored interventions for the Brazilian population.

The observed effect was ESR1-dependent and effectively blocked by tamoxifen, revealing a ligand-independent activation mechanism...The presence of PSNPs also mitigated AgNPs-induced reduction of BRCA1 expression. This study highlights how nanomaterial-induced ESR1 activation can lead to enhanced epithelial-mesenchymal transition and cell cycle progression, suggesting potential adverse effects of nanomaterials in ER+ cancer proliferation via protein kinase-mediated ESR1 modulation.

&lsqb;18F]FES PET/CT imaging provides prognostic insight beyond static ER testing by identifying functional heterogeneity in mBC. Lesion-level FES heterogeneity based on an SUVmax threshold of 1.8 may help stratify patients unlikely to benefit from ET, guiding more personalized treatment strategies.

Propylparaben may promote the occurrence and progression of estrogen receptor-positive breast cancer by upregulating SLC2A1 and KIF11, activating metabolic and proliferative pathways, and simultaneously suppressing tumor-suppressive signals.

Patients with ER+ HER2- ABC in this study preferred oral to IM ET owing to convenience, and disliked the pain associated with IM ET and travel to receive injections. Compared to IM fulvestrant, oral SERDs may offer an alternative with less burden on the lives of people living with cancer.

Moreover, it suppressed β-catenin expression, unlike NBDHEX; however, it retained GSTP1 inhibitory potency, indicating its add-on therapeutic potential. Therefore, NHSe-2 could be a potential anticancer agent and can be considered for further analysis for its multimodal activity in the realm of cancer research in the future.

Based on preclinical studies showing synergism with simultaneous inhibition of the estrogen receptor (ER), CDK4/6 and PI3K pathways and based on window of opportunity studies showing that metformin suppresses PI3K/mTOR signaling in endometrial cancer (EC), we conduct a non-randomized phase 2 study of letrozole/abemaciclib/metformin in ER positive endometrioid EC (NCT03675893). There are no objective responses among TP53 mutated ECs and among NSMP (no specific molecular profile) tumors with RB1 or CCNE1 alterations; CTNNB1 mutations correlate with clinical benefit. Pharmacokinetic analyses demonstrate that administration of letrozole and abemaciclib with metformin result in a more than 3-fold increase in metformin exposure.

In September 2025, imlunestrant was approved for the treatment of adults with ER+, HER2-, ESR1-mutated advanced or metastatic breast cancer with disease progression following at least one line of endocrine therapy in the USA. This article summarizes the milestones in the development of imlunestrant leading to this first approval for use in patients with ER+, HER2-, ESR1-mutated advanced or metastatic breast cancer.

We previously showed that PR mediates expansion of cancer stem-like cell (CSC) populations and promotes tamoxifen resistance in nuclear ER/PR transcriptional complexes...The UPR activator ErSO, but not UPR inhibitors, blocked expansion of CSCs in WT as well as Y537S ER + models. Together, our findings demonstrate a critical interplay between PR and mutant ER function and provide insight into PR-driven pathways including hyperactivation of the stress-sensing UPR that can be exploited as potential therapeutic avenues in advanced ER+ breast cancer.

We identified unique periods of susceptibility to NO2 and PM2.5 for breast cancer risk by ER status.