ReviewJournal of Nippon Medical School = Nippon Ika Daigaku zasshi2011
Development and maintenance of cancer stem cells under chronic inflammation.
Review in Journal of Nippon Medical School = Nippon Ika Daigaku zasshi, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Targeting pattern recognition receptors for cancer therapy: Mechanisms and strategies.Acta pharmaceutica Sinica. B · 2025Review
- PPIC-labeled CAFs: Key players in neoadjuvant chemotherapy resistance for gastric cancer.Translational oncology · 2024Article
- Blocking the Hormone Receptors Modulates NLRP3 in LPS-Primed Breast Cancer Cells.International journal of molecular sciences · 2023Article
- Small cell lung cancer stem cells display mesenchymal properties and exploit immune checkpoint pathways in activated cytotoxic T lymphocytes.Cancer immunology, immunotherapy : CII · 2022Article
- Ruxolitinib Reduces Oxidative Stress in Patients With Primary Myelofibrosis: A Multicenter Study.Cureus · 2022Article
- Differences and similarities between cancer and somatic stem cells: therapeutic implications.Stem cell research & therapy · 2020Review
- Heme oxygenase promotes B-Raf-dependent melanosphere formation.Pigment cell & melanoma research · 2020Article
- Synergic Crosstalk between Inflammation, Oxidative Stress, and Genomic Alterations in BCR-ABL-Negative Myeloproliferative Neoplasm.Antioxidants (Basel, Switzerland) · 2020Review
- Senescence-Associated Pro-inflammatory Cytokines and Tumor Cell Plasticity.Frontiers in molecular biosciences · 2020Review
- Role of the NLRP3 Inflammasome: Insights Into Cancer Hallmarks.Frontiers in immunology · 2020Review
- Comprehensive characterization of cancer-testis genes in testicular germ cell tumor.Cancer medicine · 2019Article
- NF-κB, inflammation, immunity and cancer: coming of age.Nature reviews. Immunology · 2018Review
- NLRP3 inflammasome activation promotes inflammation-induced carcinogenesis in head and neck squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2017Article
- Cytokine-producing function of human blood cells in chronic atrophic gastritis and gastric adenomas and adenocarcinomas.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2016Article
- Inflammation Promotes Expression of Stemness-Related Properties in HBV-Related Hepatocellular Carcinoma.PloS one · 2016Article
- Prostaglandin E2 Promotes Colorectal Cancer Stem Cell Expansion and Metastasis in Mice.Gastroenterology · 2015Article
- Laparoscopic surgery for colorectal cancer is not associated with an increase in the circulating levels of several inflammation-related factors.Cancer biology & therapy · 2015Article
- Transient TNF regulates the self-renewing capacity of stem-like label-retaining cells in sphere and skin equivalent models of melanoma.Cell communication and signaling : CCS · 2014Article
- Chronic disease burden among cancer survivors in the California Behavioral Risk Factor Surveillance System, 2009-2010.Journal of cancer survivorship : research and practice · 2014Article
- Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
In many human cancers, tumorigenic potential is not equally shared by all cells but is restricted to phenotypically distinct subpopulations termed cancer stem cells. Cancer stem cells are also capable of both self-renewal and differentiation, and these functional properties have been suggested to play major roles in tumor initiation and progression. The factors responsible for the development of cancer stem cells and their subsequent regulation are unclear, but several chronic inflammatory states have been associated with an increased risk of malignancy. Therefore, it is possible that specific processes associated with chronic inflammation, as well as the adaptation to cellular stress, regulate cancer stem cells. Several factors associated with chronic inflammation, including cytokines, oxidative stress, and hypoxia, induce the activation of specific cellular response programs that can affect the survival, proliferation, metabolism, and differentiation of cancer cells, as well as the self-renewal and quiescence of normal stem cells. In this review, we discuss how these adaptive processes potentially become subverted to enhance the development and function of cancer stem cells.
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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.