ReviewCancers2025
The PI3K/Akt/mTOR Signaling Pathway in Triple-Negative Breast Cancer: A Resistance Pathway and a Prime Target for Targeted Therapies.
Review in Cancers, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed.
- Article
- Cytotoxic, Drug-Interaction, and Apoptosis-Associated Effects of β-Boswellic Acid and Doxorubicin in Murine 4T1 TNBC-like Cells.Biomedicines · 2026Article
- MicroRNAs in Breast Cancer: Biological Functions and Technologies for Experimental and Therapeutic Applications.Cancers · 2026Review
- CK2 in triple-negative breast cancer: oncogenic signaling networks and emerging CK2 inhibitor-based combination therapies.Clinical and experimental medicine · 2026Review
- Unlocking the ferroptotic window: Lipidomic rewiring and metabolic addiction in EMT-driven breast cancer resistance.Cell death discovery · 2026Review
- Molecular Profiling and Selective Pro-Apoptotic Activity of a Pruning-DerivedInternational journal of molecular sciences · 2026Article
- Article
- Beyond Molecular Classification in Metastatic Triple-Negative Breast Cancer: Toward Subtype-Guided Precision Oncology.International journal of molecular sciences · 2026Review
- Dehydrocorydaline Exerts Anti-Pancreatic Cancer Effects Through the PI3K/Akt/mTOR Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Two Worlds, One Battle: How Bacteria and Malignancies Converge on Drug Resistance.International journal of molecular sciences · 2026Review
- Exosomal MicroRNAs as Drivers of Desmoplasia and Treatment Resistance in Breast Cancer: Mechanisms, Biomarker Potential, and Therapeutic Opportunities.Biomolecules · 2026Review
- Article
- Targeting cancer signaling pathways and their therapeutic strategies.Discover oncology · 2026Review
- Ultrasound-Assisted Synthesis and Biological Profiling of 1,3,5-Triazine Derivatives with Antiproliferative Activity in Triple-Negative Breast Cancer.Current issues in molecular biology · 2026Article
- Short and Long Non-Coding RNAs in Renal Cell Carcinoma.Non-coding RNA · 2026Review
- Patient Journey for Triple-Negative Breast Cancer: Optimal Care Pathways vs. Reality of Care in Italian Breast Units.Current oncology (Toronto, Ont.) · 2026Article
- Review
- A comparative analysis of mutational profiles between triple-negative breast cancer and non-triple-negative breast cancer.Discover oncology · 2026Article
- Article
- Extracellular Signal-Regulated Kinase and Reactive Oxygen Species Regulate PD-L1 to Promote Migration and Proliferation of Triple-Negative Breast Cancer MDA-MB-231 Cells.Oncology research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Triple-negative breast cancer is the most aggressive subtype of breast cancer and is associated with the worst prognosis. Conventional chemotherapy remains the gold standard treatment for this disease but is associated with a high relapse rate, highlighting the urgent need for effective targeted therapies. The PI3K/Akt/mTOR pathway, dysregulated in nearly 60% of these cancers, appears to be a prime target. It involves a signaling cascade beginning with PI3K activation followed by activating phosphorylation of Akt and then mTOR complex, which activates oncogenic processes by enhancing protein synthesis, inhibiting apoptosis, dysregulating autophagy and promoting DNA repair that supports tumor cell survival. Moreover, the PI3K/Akt/mTOR pathway plays a central role in the development of chemoresistance. Numerous alterations (activating the mutation of PIK3CA or the loss of tumor suppressor PTEN) may lead to its overactivation. Targeted inhibitors of PI3K, Akt and mTOR have been developed to counteract this dysregulation. However, numerous cancer resistance mechanisms have emerged, reducing their efficacy, for example, reactivation of Akt following mTOR blockade, reactivation of the pathway by insulin signaling or activation of compensatory pathways such as the MAPK pathway, thus limiting their integration into routine practice. To counteract these resistances, combination therapies currently being investigated in clinical trials aim to improve clinical outcomes of PI3K/Akt/mTOR pathway inhibition. The aim of this review was to summarize current therapies developed to target this pathway in TNBC, with a focus on the resistance mechanisms that limit their effectiveness.
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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.