ReviewCell communication and signaling : CCS2021
Drug resistance and Cancer stem cells.
Review in Cell communication and signaling : CCS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 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
208 citing papers in PubMed, 1 synthesis or guideline pooled it, 307 citations in OpenAlex.
- Pooled it
- Therapy resistance-related ncRNAs in cervical cancer: biomarkers and therapeutic targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Ellagic Acid and Metformin: In Vitro Synergy and Enhanced Cisplatin Efficacy In Vivo in Resistant Breast Cancer.Nutrients · 2026Article
- Identification of Novel Transcriptional Alleles in Primary Prostate Cancer Cells and Cancer Stem Cells by Bulk RNA-Seq and Single-Cell RNA-Seq Analyses.Biomolecules · 2026Article
- TargetPrior: a miRNA-signature embedded evolutionary learning framework for prioritizing drug targets in acute myeloid leukemia.Bioinformatics (Oxford, England) · 2026Article
- Translational insights and clinical challenges of targeting cancer stem cells.Signal transduction and targeted therapy · 2026Review
- Three-dimensional spheroid models in breast cancer: tumor microenvironment complexity, cancer stem cell-driven resistance, and translational model integration.Journal of translational medicine · 2026Review
- Cancer stem cells and drug resistance in cancer: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
- Beyond Acute EGFR Blockade: Biological Basis and Clinical Evidence for Long-Term Nimotuzumab Therapy.Biomedicines · 2026Review
- Cancer stem cells and their molecular signaling mechanisms in tongue squamous cell carcinoma (Review).Oncology letters · 2026Review
- Plant extracts and phytochemicals in canine and feline mammary cancer models: current evidence and comparative perspectives.Veterinary research communications · 2026Review
- Innovative strategies to overcome cancer drug resistance: from nanodelivery systems to targeted therapeutics.Discover oncology · 2026Review
- Review
- Ferroptosis vulnerability of enzalutamide resistant prostate cancer conferred by ACSL4 overexpression and GPX4 antagonism.Cell death & disease · 2026Article
- The Niche Awakens: Comprehension of Cancer Stem Cells' Microenvironment to Plan New Therapeutic Strategies.Cells · 2026Review
- Two Worlds, One Battle: How Bacteria and Malignancies Converge on Drug Resistance.International journal of molecular sciences · 2026Review
- Article
- The role of theTranslational cancer research · 2026Article
- CDK4 inhibition by luteolin enhances lenvatinib sensitivity in HCC via Wnt/β-catenin modulation.Cancer cell international · 2026Article
- From Signaling Pathways to Combination Therapy: Bioactive Compounds against Cancer Stem Cells.Stem cell reviews and reports · 2026Review
148 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
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Therapy resistance is a major problem when treating cancer patients as cancer cells develop mechanisms that counteract the effect of therapeutic compounds, leading to fit and more aggressive clones that contribute to poor prognosis. Therapy resistance can be both intrinsic and/or acquired. These are multifactorial events, and some are related to factors including adaptations in cancer stem cells (CSCs), epithelial-mesenchymal transition (EMT), deregulation of key signaling pathways, drug efflux through ABC transporters, acquired mutations, evading apoptosis, and activation of DNA damage response among others. Among these factors, CSCs represent the major source of therapy resistance. CSCs are a subset of tumor cells that are capable of self-renewal and multilineage progenitor expansion that are known to be intrinsically resistant to anticancer treatments. Multiple clones of CSCs pre-exist, and some can adopt and expand easily to changes in the tumor microenvironment (TME) and/or in response to radio- and chemotherapy. A combination of both intrinsic and extrinsic factors contributes to CSC-mediated therapy resistance. In this review, we will focus on CSCs and therapy resistance as well as suggest strategies to eliminate CSCs and, therefore, overcome resistance. Video abstract.
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.