ReviewJournal of molecular medicine (Berlin, Germany)2009
Cancer stem cells-clinical relevance.
Review in Journal of molecular medicine (Berlin, Germany), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Role of microRNA-regulated cancer stem cells in recurrent hepatocellular carcinoma.World journal of hepatology · 2022Review
- Inhibition of sonic hedgehog and PI3K/Akt/mTOR pathways cooperate in suppressing survival, self-renewal and tumorigenic potential of glioblastoma-initiating cells.Molecular and cellular biochemistry · 2019Article
- Induction of multiple myeloma cancer stem cell apoptosis using conjugated anti-ABCG2 antibody with epirubicin-loaded microbubbles.Stem cell research & therapy · 2018Article
- Inhibition of sonic hedgehog pathway and pluripotency maintaining factors regulate human pancreatic cancer stem cell characteristics.International journal of cancer · 2012Article
- Sulforaphane synergizes with quercetin to inhibit self-renewal capacity of pancreatic cancer stem cells.Frontiers in bioscience (Elite edition) · 2011Article
- Controversies in cancer stem cells.Journal of molecular medicine (Berlin, Germany) · 2009Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
Therapeutic advances over the past three decades now allow most cancer patients to achieve major clinical responses. Although clinical responses can clearly decrease side effects and improve quality of life, most cancer patients still eventually relapse and die of their disease. Many cancers have now been shown to harbor cells that are phenotypically and biologically similar to normal cells with self-renewal capacity; these so-called cancer stem cells (CSC) typically constitute only a small fraction of the total tumor burden, but theoretically harbor all the self-renewal capacity. Moreover, the CSC appears to be relatively resistant to standard anticancer therapies by co-opting normal stem cells' intrinsic defense mechanisms, such as quiescence, efflux pumps, and detoxifying enzymes. However, the clinical importance of CSC, if any, remains unproven. Nevertheless, emerging evidence suggests that initial responses in cancer represent therapeutic effectiveness against the bulk cancer cells, while the rare CSC is responsible for relapse. Better understanding of the biology of CSC, as well as reexamining both our preclinical and clinical drug development paradigms to include the CSC concept, has the potential to revolutionize the treatment of many cancers.
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.