ArticleOncogene2015
The TrkB+ cancer stem cells contribute to post-chemotherapy recurrence of triple-negative breast cancers in an orthotopic mouse model.
Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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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.
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Who cites it
31 citing papers in PubMed, 54 citations in OpenAlex.
- Brain-derived neurotrophic factor in solid tumor angiogenesis and neurovascular-immune interactions (Review).Oncology letters · 2026Review
- Peripheral nerve remodeling in the tumor microenvironment: neuro-immune crosstalk, molecular mechanisms, and precision therapeutic.Frontiers in immunology · 2026Review
- Cetuximab and Paclitaxel Drug Response in Head and Neck Tumor Stem Cells.Biomolecules · 2025Article
- Novel CAR-T cells targeting TRKB for the treatment of solid cancer.Apoptosis : an international journal on programmed cell death · 2024Article
- TNF receptor 2 knockout mouse had reduced lung cancer growth and schizophrenia-like behavior through a decrease in TrkB-dependent BDNF level.Archives of pharmacal research · 2024Article
- Breast cancer stem cells generate immune-suppressive T regulatory cells by secreting TGFβ to evade immune-elimination.Discover oncology · 2023Article
- miR-603 promotes cell proliferation and differentiation by targeting TrkB in acute promyelocytic leukemia.Annals of hematology · 2023Article
- Melatonin, BAG-1 and cortisol circadian interactions in tumor pathogenesis and patterned immune responses.Exploration of targeted anti-tumor therapy · 2023Review
- Oncogenic role of a developmentally regulatedScience advances · 2022Article
- Interactions Among Brain-Derived Neurotrophic Factor and Neuroimmune Pathways Are Key Components of the Major Psychiatric Disorders.Molecular neurobiology · 2022Review
- Neurotrophic receptor tyrosine kinase family members in secretory and non-secretory breast carcinomas.World journal of clinical oncology · 2022Article
- Tumour Microenvironment: Roles of the Aryl Hydrocarbon Receptor, O-GlcNAcylation, Acetyl-CoA and Melatonergic Pathway in Regulating Dynamic Metabolic Interactions across Cell Types-Tumour Microenvironment and Metabolism.International journal of molecular sciences · 2020Review
- TrkB-Targeted Therapy for Mucoepidermoid Carcinoma.Biomedicines · 2020Article
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- Nerves in the Tumor Microenvironment: Origin and Effects.Frontiers in cell and developmental biology · 2020Review
- Identification of Potential Key Genes for Pathogenesis and Prognosis in Prostate Cancer by Integrated Analysis of Gene Expression Profiles and the Cancer Genome Atlas.Frontiers in oncology · 2020Article
- Cancer stem cells-driven tumor growth and immune escape: the Janus face of neurotrophins.Aging · 2019Article
- Evidence for a non-canonical JAK/STAT signaling pathway in the synthesis of the brain's major ion channels and neurotransmitter receptors.BMC genomics · 2019Article
- Estradiol induces BDNF/TrkB signaling in triple-negative breast cancer to promote brain metastases.Oncogene · 2019Article
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 at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer stem cells (CSCs) are believed to have a crucial role in triple-negative breast cancer (TNBC) recurrence. However, the exact mechanisms that are functionally critical in CSCs-mediated recurrence remain unclear. Here, we showed that CSCs derived from recurrent TNBCs are endowed with increased self-renewal capacity as compared with those from the matched primary lesions. Using patient-derived specimens, we demonstrated the existence of paracrine brain-derived neurotrophic factor (BDNF) signaling between differentiated recurrent TNBC cells and CSCs characterized by the expression of TrkB, the receptor of BDNF. We showed that paclitaxel induced BDNF expression and apoptosis simultaneously in a cell cycle-dependent manner. BDNF promotes the self-renewal potential of the TrkB+CSCs through induction of KLF4. The TrkB+CSCs represent a particular subset indispensable for TNBC relapse. In line with this, TrkB is proved to be a superior predictor for TNBC recurrence. Using a genetically engineered mouse model of TNBC, we observed that ablation of the TrkB+CSCs potentially prevents relapse of malignant tumors. Further preclinical investigation of this promising approach may lead to development of a novel therapeutic strategy to improve the devastating prognosis of TNBC patients.
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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.