Purpose: Somatostatin receptor (SSTR) expression has been reported in estrogen receptor-positive (ER +) metastatic breast cancer (mBC) by pathology and immunohistochemistry studies. We aimed to investigate whether SSTR could be a viable target for PET imaging and potential theranostics in ER + mBC.
Methods: Thirty prospectively recruited patients with ER + mBC underwent PET/CT imaging with [F]FDG and [Ga]Ga-DOTATATE (within three weeks). Detection rates (per-patient, per-region), number of lesions detected, SUVmax values, Krenning scores, SSTR-FDG visual scores, and PET-based staging with both radiotracers were compared.
Results: [F]FDG and [Ga]Ga-DOTATATE PET/CT had similar per-patient detection rates (100% vs 96.7%, P = 1.0). Per-region and per-lesion analyses revealed comparable detection of local/breast lesions, nodal, and skeletal metastases. However, [F]FDG outperformed [Ga]Ga-DOTATATE in detecting visceral/other metastases (235 vs 128 lesions, P = 0.003). [Ga]Ga-DOTATATE resulted in a lower PET-based M-stage compared to [F]FDG in 10% of patients, although T-/N-stages were concordant in all patients. HER2- patients showed a trend of higher [Ga]Ga-DOTATATE lesional SUVmax values compared to the HER2 + sub-group (median 9.0 vs 3.8, P = 0.078). 3/30 (10%) participants had a patient-level Krenning score ≥ 3 ([Ga]Ga-DOTATATE uptake higher than liver background in majority of the lesions), potentially making them suitable for SSTR-targeted radionuclide therapy.
Conclusions: SSTR-targeted theranostics may represent a novel potential alternative in a subset of patients with ER + mBC. Its generalized applicability is limited by poor sensitivity for visceral metastases and significant inter-lesion heterogeneity. Future studies must identify how tumor subtype, proliferation, and prior systemic therapies impact SSTR expression levels in these patients to ensure meaningful clinical translation.
Clinical Trial Registration: Clinical Trials Registry-India: CTRI/2023/03/051025 (prospectively registered on 23.03.2023).
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http://dx.doi.org/10.1007/s10549-025-07651-4 | DOI Listing |
Front Toxicol
February 2025
Istituto Zooprofilattico Sperimentale del Lazio e della Toscana "M. Aleandri", Rome, Italy.
Introduction: The estrogenic and anti-estrogenic effects of endocrine disruptors were examined using two-dimensional 2D and three-dimensional 3D estrogen receptor-positive T47D and MCF7 human breast cancer cells.
Methods: The model system was used to test the plasticizer Bisphenol A (BPA), a known endocrine disruptor (EDs) with estrogen-like action, aga inst 17β-Estradiol (E2), the endogenous nuclear estrogen receptor (nERs) ligand, and the anti-estrogenic drug Fulvestrant (FUL). Spheroid formation and gene expression of estrogen-regulated markers (pS2 and TGFβ3) both in 2D and 3D cultures were used to establish the dose-dependent cellular effects of these substances, evaluated cell viability either by separately treating with the individual substances or in co-treatment.
J Steroid Biochem Mol Biol
March 2025
Department of Biotechnology, SRM University, Delhi-NCR, Sonepat, Haryana 131029, India; Department of Biomedical Engineering, SRM University, Sonepat, Haryana 131029, India. Electronic address:
Estrogen receptor-positive (ER+) breast carcinoma represents a significant portion of breast cancer cases and is characterized by the presence of estrogen receptors that promote tumor growth upon estrogen binding. ER + breast cancer progression involves hormonal influences, interactions within the tumor microenvironment, and genetic mutations that may lead to treatment resistance. Successful therapeutic options include hormonal therapies, particularly aromatase inhibitors (AIs), which aim to block the effects of estrogen or reduce its synthesis.
View Article and Find Full Text PDFBreast Cancer Res
March 2025
Department of Pathology, University of Colorado, Anschutz Medical Campus, Aurora, CO, USA.
Background: Lipid metabolic reprogramming is increasingly recognized as a hallmark of endocrine resistance in estrogen receptor-positive (ER+) breast cancer. In this study, we investigated alterations in lipid metabolism in ER + breast cancer cell lines with acquired resistance to common endocrine therapies and evaluated the efficacy of a clinically relevant fatty acid synthase (FASN) inhibitor.
Methods: ER + breast cancer cell lines resistant to Tamoxifen (TamR), Fulvestrant (FulvR), and long-term estrogen withdrawal (EWD) were derived.
NPJ Precis Oncol
March 2025
Pathology Department, Corewell Health Farmington Hills Hospital, Farmington Hills, MI, USA.
We present a unique case of locally advanced, inflammatory hormone receptor (HR) positive, human epidermal growth factor receptor 2 (HER2)-negative breast cancer in a young woman. A MammaPrint gene signature performed on the core biopsy indicated a very high risk of recurrence (MammaPrint high risk 2, MPH2). BluePrint 80-gene signature was used for the molecular subtyping and identified the tumor as a basal subtype, resembling triple-negative breast cancer (TNBC) despite the strong estrogen receptor (ER) expression on immunohistochemical (IHC) staining.
View Article and Find Full Text PDFSci Rep
March 2025
GROW - Research Institute for Oncology and Reproduction, Maastricht University Medical Center+, Maastricht, The Netherlands.
Tamoxifen is essential in treating estrogen receptor-positive (ER+) breast cancer, primarily through its active metabolite, endoxifen. Emerging research suggests potential interactions between tamoxifen and gut microbiota. This study investigates the effects of tamoxifen on gut microbiota composition in postmenopausal ER+ and human epidermal growth factor receptor 2 negative (HER2-) breast cancer patients and explores correlations between gut microbiota and endoxifen plasma levels.
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