ArticleEpigenetics2014
Reprogramming cancer cells to pluripotency: an experimental tool for exploring cancer epigenetics.
Article in Epigenetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 17 citations in OpenAlex.
- Merits and challenges of iPSC-derived organoids for clinical applications.Frontiers in cell and developmental biology · 2023Review
- "Reprogram Enablement" as an Assay for Identifying Early Oncogenic Pathways by Their Ability to Allow Neoplastic Cells to Reacquire an Epiblast State.Stem cell reports · 2020Article
- Cancer cell reprogramming: a promising therapy converting malignancy to benignity.Cancer communications (London, England) · 2019Review
- Review
- Immortalized murine fibroblast cell lines are refractory to reprogramming to pluripotent state.Oncotarget · 2018Article
- Oncofetal Epigenetic Bivalency in Breast Cancer Cells: H3K4 and H3K27 Tri-Methylation as a Biomarker for Phenotypic Plasticity.Journal of cellular physiology · 2016Article
- In vitro models of cancer stem cells and clinical applications.BMC cancer · 2016Review
- Reprogramming strategies for the establishment of novel human cancer models.Cell cycle (Georgetown, Tex.) · 2016Review
- Addressing the elephant in the room, therapeutic resistance in non-small cell lung cancer, with epigenetic therapies.Oncotarget · 2016Review
- Using induced pluripotent stem cells as a tool for modelling carcinogenesis.World journal of stem cells · 2015Review
- Application of induced pluripotency in cancer studies.Reports of practical oncology and radiotherapy : journal of Greatpoland Cancer Center in Poznan and Polish Society of Radiation OncologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The epigenetic marks displayed by a cancer cell originate from two separate processes: The most prominent epigenetic signatures are associated with the cell of origin, i.e., the lineage and cell type identity imposed during development. The second set comprises those aberrant cancer-specific epigenetic marks that appear during tumor initiation or subsequent malignant progression. These are generally thought to associate with tumor-promoting pathways. As biochemical pathways regulating epigenetic mechanisms are potentially "druggable" and reversible, there is considerable interest in defining their roles in tumor genesis and growth, as they may represent therapeutic targets for treatment of human neoplasias. (1) However, despite the potential importance of epigenetic modifications in human cancer, it has been difficult to determine when, where and how epigenetic disruptions occur, and if they have important functional roles in sustaining the malignant state.
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.