ReviewWorld journal of clinical oncology2025
Cell reprogramming in cancer: Interplay of genetic, epigenetic mechanisms, and the tumor microenvironment in carcinogenesis and metastasis.
Review in World journal of clinical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Genomic innovations in cancer prevention, diagnosis, prognosis and precision therapeutics.Frontiers in genetics · 2026Review
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
No grant is acknowledged in the PubMed record.
Abstract
Cell plasticity, also known as lineage plasticity, refers to the ability of a cell to reprogram and change its phenotypic identity in response to various cues. This phenomenon is context-dependent, playing a crucial role in embryonic development, tissue regeneration, and wound healing. However, when dysregulated, cell plasticity contributes to cancer initiation, progression, metastasis, and therapeutic resistance. Throughout different stages of tumor development, cancer cells exploit various forms of plasticity to evade normal regulatory mechanisms that govern cell division and homeostasis. Recent evidence highlights the complex interplay between genetic and epigenetic factors, the tumor microenvironment, and epithelial-to-mesenchymal transition in driving cancer cell plasticity. This dynamic reprogramming suggests that "deregulated cell plasticity" could be considered an additional hallmark of cancer. Advancements in next-generation sequencing and single-cell RNA analysis, combined with artificial intelligence technologies such as deep learning, along with Google's AlphaFold may help predict the trajectories of cancer cells. By predicting protein three-dimensional structures and identifying both active and potential allosteric binding sites, AlphaFold 2 can accelerate the development of new cancer drugs and therapies. For example, allosteric drugs, bind to the allosteric rather than the active sites, can induce conformational changes in proteins, affecting their activities. This can then alter the conformation of an active site that a drug-resistant mutation has created, permitting a blocked orthosteric drug to bind and this enables the design of more effective drugs that can synergize with traditional orthosteric drugs to bind and regain its efficacy. These innovations could provide deeper insights into the intricate mechanisms of cancer progression and resistance, ultimately paving the way for more precise, durable, and personalized oncologic treatments.
Indexed as
Identifiers
What Socratic 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 Socratic graph.