ReviewBritish journal of clinical pharmacology2016
The therapeutic potential of mTOR inhibitors in breast cancer.
Review in British journal of clinical pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed.
- Pharmacokinetic Optimization of Everolimus Dosing in Oncology: A Randomized Crossover Trial.Clinical pharmacokinetics · 2018Trial
- Intracellular GRP78-Directed Delivery of Rapamycin by Biomolecular Condensates of Hydra-Elastin-like Polypeptides.Biomacromolecules · 2026Article
- Polymeric rapamycin nanoparticles encapsulating ponatinib cause regression of venous malformations in mice.Science translational medicine · 2026Article
- Integrating RNA-seq and scRNA-seq to explore the prognostic features and immune landscape of exosome-related genes in breast cancer metastasis.Annals of medicine · 2025Article
- mTOR Levels and Metastasis in Luminal Breast Cancer: Implications for Prognosis and Treatment.Asian Pacific journal of cancer prevention : APJCP · 2025Article
- Real-world evidence couples genomic biomarkers with therapeutic outcomes for canine hemangiosarcoma.Scientific reports · 2025Article
- Article
- Decoding estrogen receptor and GPER biology: structural insights and therapeutic advances in ERα-positive breast cancer.Frontiers in oncology · 2025Review
- AEGAN-Pathifier: a data augmentation method to improve cancer classification for imbalanced gene expression data.BMC bioinformatics · 2024Article
- SnoRNA U50A mediates everolimus resistance in breast cancer through mTOR downregulation.Translational oncology · 2024Article
- Predictive, preventive, and personalized medicine in breast cancer: targeting the PI3K pathway.Journal of translational medicine · 2024Review
- A modular microfluidic platform to study how fluid shear stress alters estrogen receptor phenotype in ERMicrosystems & nanoengineering · 2024Article
- Exemestane-Everolimus-Induced Angioedema in a Woman With Metastatic Breast Cancer: A Case Report and Review.Cureus · 2023Article
- A modular microfluidic platform to study how fluid shear stress alters estrogen receptor phenotype in ERResearch square · 2023Article
- Role of the Dietary Phytochemical Curcumin in Targeting Cancer Cell Signalling Pathways.Plants (Basel, Switzerland) · 2023Review
- Aquaporins in Tumor.Advances in experimental medicine and biology · 2023Article
- A prognostic model related to necrotizing apoptosis of breast cancer based on biorthogonal constrained depth semi-supervised nonnegative matrix decomposition and single-cell sequencing analysis.American journal of cancer research · 2023Article
- Multiplexed and reproducible high content screening of live and fixed cells using Dye Drop.Nature communications · 2022Article
- Focal Adhesion Kinase Provides a Collateral Vulnerability That Can Be Leveraged to Improve mTORC1 Inhibitor Efficacy.Cancers · 2022Article
- Identifying drivers of breast cancer metastasis in progressively invasive subpopulations of zebrafish-xenografted MDA-MB-231.Molecular biomedicine · 2022Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rapamycin and modified rapamycins (rapalogs) have been used to prevent allograft rejection after organ transplant for over 15 years. The mechanistic target of rapamycin (mTOR) has been determined to be a key component of the mTORC1 complex which consists of the serine/threonine kinase TOR and at least five other proteins which are involved in regulating its activity. Some of the best characterized substrates of mTORC1 are proteins which are key kinases involved in the regulation of cell growth (e.g., p70S6K) and protein translation (e.g., 4E-BP1). These proteins may in some cases serve as indicators to sensitivity to rapamycin-related therapies. Dysregulation of mTORC1 activity frequently occurs due to mutations at, or amplifications of, upstream growth factor receptors (e.g., human epidermal growth factor receptor-2, HER2) as well as kinases (e.g., PI3K) and phosphatases (e.g., PTEN) critical in the regulation of cell growth. More recently, it has been shown that certain rapalogs may enhance the effectiveness of hormonal-based therapies for breast cancer patients who have become resistant to endocrine therapy. The combined treatment of certain rapalogs (e.g., everolimus) and aromatase inhibitors (e.g., exemestane) has been approved by the United States Food and Drug Administration (US FDA) and other drug regulatory agencies to treat estrogen receptor positive (ER+) breast cancer patients who have become resistant to hormonal-based therapies and have progressed. This review will summarize recent basic and clinical research in the area and evaluate potential novel therapeutic approaches.
Indexed as
Identifiers
What OpenQuestion holds
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.