ArticleScientific reports2025
Characterizing SSTR2 expression and modulation for targeted imaging and therapy in preclinical models of triple-negative breast cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The trial behind it
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Who cites it
7 citing papers in PubMed.
- Epigenetic Dysregulation of Somatostatin Receptors (SSTR) 1-5 and Therapeutic Implications in Neuroendocrine and Non-Neuroendocrine Malignancies.International journal of cancer · 2026Review
- Humanized antibody-drug conjugates for Somatostatin receptor 2 (SSTR2)-positive tumor treatment.Molecular cancer therapeutics · 2026Article
- A photocleavable peptidic Ru(ii) mass-tag enabling targeted DESI and MALDI mass spectrometry imaging in cancer tissues.Chemical science · 2026Article
- SAHA Alters Macrophages in the Tumor-Immune Landscape in Preclinical Models of Triple-Negative Breast Cancer.Pharmaceutics · 2026Article
- Neuroendocrine Neoplasms of the Gastrointestinal Tract: Morphology, WHO 2022 Grading, and Prognostic Perspectives.Cureus · 2026Review
- SSTR2-targeting therapy in EBV-positive and EBV-negative metastatic nasopharyngeal carcinoma.American journal of cancer research · 2026Article
- A Systematic Review of Advances in Plant-Based Phospholipid Liposomes in Breast Cancer Therapy: Characterization, Innovations, Clinical Applications, and Future Directions.Pharmaceuticals (Basel, Switzerland) · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Patients with breast cancer which lack molecular targets, such as human epidermal growth factor receptor 2 (HER2) or hormone receptors, have limited access to targeted therapies. Somatostatin receptor 2 (SSTR2) is overexpressed in some cancers, and SSTR2-targeted radiopharmaceuticals are FDA-approved for theranostic targeted imaging and therapy in neuroendocrine tumors (NETs). Importantly, histone deacetylase (HDAC) inhibitors can epigenetically modulate SSTR2 expression in NETs with low or variable basal expression. The goal of this study is to characterize SSTR2 basal expression and induction via HDAC inhibition as a potential target for imaging and therapy in preclinical models of triple-negative breast cancer (TNBC). SSTR2 expression in mouse samples was assessed via Western blot and immunohistochemistry. Real-time quantitative PCR (qRT-PCR), flow cytometry, and cell binding assays were utilized to determine if HDAC inhibition can upregulate SSTR2 expression. [
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.