ReviewOncotarget2015
EMT, CTCs and CSCs in tumor relapse and drug-resistance.
Review in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 300 papers, 1 of them a synthesis that pooled it.
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
300 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Human papillomavirus, vaginal microbiota and metagenomics: the interplay between development and progression of cervical cancer.Frontiers in microbiology · 2024Pooled it
- Advanced Image Generation for Cancer and Stem Cell Biology Using Diffusion Models.Methods in molecular biology (Clifton, N.J.) · 2027Article
- Epithelial-Mesenchymal Plasticity in Cancer: Transcriptional Regulation, Biomarker Challenges, and Emerging Therapeutic Opportunities.Cell biochemistry and function · 2026Review
- Hyperglycaemia-Induced Metabolic Stress Promotes EMT-Driven Therapeutic Resistance in Cancer: Evidence of a Deleterious Feed-Forward Cycle.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Epithelial-mesenchymal transition and its role in drug resistance of cervical cancer.Molecular biology reports · 2026Review
- Breast cancer stem cells and circulating tumor cells: Dual drivers of progression and relapse.World journal of stem cells · 2025Review
- Design, synthesis and molecular modeling of new coumarin-thiazole derivatives as dual EGFR/HDAC1 inhibitors:RSC advances · 2025Article
- Polydatin: A natural compound with multifaceted anticancer properties.Journal of traditional and complementary medicine · 2025Review
- Tfcp2l1 as a central integrator of hypoxia, dedifferentiation, and tumor progression.Journal of experimental & clinical cancer research : CR · 2025Review
- Yin Yang 1 (YY1) as a Central Node in Drug Resistance Pathways: Potential for Combination Strategies in Cancer Therapy.Biomolecules · 2025Review
- hsa-miR-5688 inhibits FOXC1-OCT4/SOX2 feedforward loop that drives chemoresistance in breast cancer stem cells.Molecular therapy. Oncology · 2025Article
- Intercellular contractile force attenuates chemosensitivity through Notch-MVP-mediated nuclear drug export.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Enhanced potency of immune checkpoint inhibitors against poorly immunological solid tumors by immune stimulatory oncolytic adenoviruses-mediated remodeling of the tumor microenvironment.Molecular medicine (Cambridge, Mass.) · 2025Article
- Exploring the role of EMT in ovarian cancer progression using a multiscale mathematical model.NPJ systems biology and applications · 2025Article
- Neuropilin-1: A Multifaceted Target for Cancer Therapy.Current oncology (Toronto, Ont.) · 2025Review
- Integrated molecular and microenvironmental drivers of drug resistance in gastrointestinal cancers: mechanisms, immunotherapy challenges, and precision strategies.Frontiers in oncology · 2025Review
- Nano-biomaterials in cancer therapy: Advances in targeting and overcoming cancer stem cell resistance.ADMET & DMPK · 2025Review
- Circulating tumor cell markers for early detection and drug resistance assessment through liquid biopsy.Frontiers in oncology · 2025Review
- Exploring COX-Independent Pathways: A Novel Approach for Meloxicam and Other NSAIDs in Cancer and Cardiovascular Disease Treatment.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Review
240 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
3 authors.
Funding
Abstract
Tumor relapse and metastasis are the primary causes of poor survival rates in patients with advanced cancer despite successful resection or chemotherapeutic treatment. A primary cause of relapse and metastasis is the persistence of cancer stem cells (CSCs), which are highly resistant to chemotherapy. Although highly efficacious drugs suppressing several subpopulations of CSCs in various tissue-specific cancers are available, recurrence is still common in patients. To find more suitable therapy for relapse, the mechanisms underlying metastasis and drug-resistance associated with relapse-initiating CSCs need to be identified. Recent studies in circulating tumor cells (CTCs) of some cancer patients manifest phenotypes of both CSCs and epithelial-mesenchymal transition (EMT). These patients are unresponsive to standard chemotherapies and have low progression free survival, suggesting that EMT-positive CTCs are related to co-occur with or transform into relapse-initiating CSCs. Furthermore, EMT programming in cancer cells enables in the remodeling of extracellular matrix to break the dormancy of relapse-initiating CSCs. In this review, we extensively discuss the association of the EMT program with CTCs and CSCs to characterize a subpopulation of patients prone to relapses. Identifying the mechanisms by which EMT-transformed CTCs and CSCs initiate relapse could facilitate the development of new or enhanced personalized therapeutic regimens.
Indexed as
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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.