ReviewAmerican journal of cancer research2016
Breast cancer molecular subtypes: from TNBC to QNBC.
Review in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers.
What it found
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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
113 citing papers in PubMed, 184 citations in OpenAlex.
- Trial
- Genomic Alterations in Quadruple-Negative Breast Cancer Tumors.International journal of molecular sciences · 2026Article
- Deep interpretable radiogenomic workflow deciphers tumor microenvironment from breast MRI and identifies clinician-interpretable biomarkers.NPJ precision oncology · 2026Article
- The role of circular RNAs as miRNA sponges in the mechanisms and therapeutic potential of triple negative breast cancer.Discover oncology · 2026Review
- The emerging role of machine learning-based methods in cancer classification using microRNA.Biochemistry and biophysics reports · 2026Review
- Pivotal Factors in Breast Cancer Molecular Subtypes Apoptosis Induction by ELF-EMF; Ki-67, ROS Level, HER-2, and SODs.The breast journal · 2026Article
- Whole-exome sequencing for identification of specific gene mutations in an Indian cohort of triple-negative breast cancer patients.Discover oncology · 2025Article
- Article
- PFDN1 silencing disrupts critical cancer pathways in triple-negative breast cancer: investigating migration, cell cycle, and apoptosis as a new target therapy.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Small molecule inhibitors for treating breast cancer: drug analysis based on the pathogenesis of breast cancer.Future medicinal chemistry · 2025Review
- Cardio-Oncology Considerations for Breast Cancer: Risk Stratification, Monitoring, and Treatment.Oncology (Williston Park, N.Y.) · 2025Review
- C/EBPβ increases tumor aggressiveness by enhancing KIFC1 expression in androgen receptor negative triple negative breast cancer.Cell communication and signaling : CCS · 2025Article
- ComparingCancers · 2025Article
- Classifications of triple-negative breast cancer: insights and current therapeutic approaches.Cell & bioscience · 2025Review
- Triple-Negative Breast Cancer Progression and Drug Resistance in the Context of Epithelial-Mesenchymal Transition.Cancers · 2025Review
- Cyclometalated iridium(III) complex based on isoquinoline alkaloid synergistically elicits the ICD response and IDO inhibitionActa pharmaceutica Sinica. B · 2025Article
- Multimodal diagnostic models and subtype analysis for neoadjuvant therapy in breast cancer.Frontiers in immunology · 2025Article
- Article
- Review
- Review
53 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
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Treatment protocols for breast cancer depend predominantly on receptor status with respect to estrogen (estrogen receptor alpha), progesterone (progesterone receptor) and human epidermal growth factor [human epidermal growth factor receptor 2 (HER2)]. The presence of one or more of these receptors suggests that a treatment targeting these pathways might be effective, while the absence of, or in the case of HER2, lack of overexpression of, all of these receptors, termed triple negative breast cancer (TNBC), indicates a need for the more toxic chemotherapy. In an effort to develop targeted therapies for TNBC, it will be necessary to differentiate among specific TNBC subtypes. The subset of TNBC that expresses androgen receptor (AR) has been determined to express genes consistent with a luminal subtype and therefore may be amenable to therapies targeting either AR, itself, or other pathways typical of a luminal subtype. Recent investigations of the AR signal pathway within breast cancer lead to AR as a significant target for breast cancer therapy with several clinical trials currently in progress. The subclass of TNBC that lacks AR, which we have termed quadruple negative breast cancer (QNBC) currently lacks a defined targetable pathway. Unlike AR-positive TNBC, QNBC predominantly exhibits a basal-like molecular subtype. Several subtypes and related pathway proteins are preferentially expressed in QNBC that may serve as effective targets for treatment, such as ACSL4, SKP2 and EGFR. ACSL4 expression has been demonstrated to be inversely correlated with expression of hormone/growth factor receptors and may thus serve as a biomarker for QNBC as well as a target for therapy. In the following review we summarize some of the current efforts to develop alternatives to chemotherapy for TNBC and QNBC.
Indexed as
Identifiers
27725895PMC5043099W2530991050What 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.