ReviewCell & bioscience2017
Tumorigenesis as a process of gradual loss of original cell identity and gain of properties of neural precursor/progenitor cells.
Review in Cell & bioscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 82 citations in OpenAlex.
- LINE-1 transposable element is expressed in Kaposi's sarcoma and regulates gene expression in KSHV-infected cells.bioRxiv : the preprint server for biology · 2026Article
- Cancer neuroscience: signaling pathways and new therapeutic strategies for cancer.Signal transduction and targeted therapy · 2026Review
- The influence of neuro-tumor interactions on tumorigenesis and therapeutic response.Experimental hematology & oncology · 2026Review
- Understanding cancer as a systemic disease through comprehension of neural stemness as the core property of cancer cell and the basic rules it dictates.Frontiers in cell and developmental biology · 2026Review
- Using single-cell perturbation screens to decode the regulatory architecture of splicing factor programs.Nucleic acids research · 2025Article
- Chronic stress: a fourth etiology in tumorigenesis?Molecular cancer · 2025Review
- Gene Expression Analysis of (Paired) Primary and Relapsed Wilms Tumor Samples to Unravel the Underlying Factors Driving Tumor Recurrence.Cancer medicine · 2025Article
- A metabolic shift to the serine pathway induced by lipids fosters epigenetic reprogramming in nontransformed breast cells.Science advances · 2025Article
- Identification of the EBF1/ETS2/KLF2-miR-126-Gene Feed-Forward Loop in Breast Carcinogenesis and Stemness.International journal of molecular sciences · 2025Article
- Adverse Outcome Pathways Mechanistically Describing Hepatotoxicity.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Lack of basic rationale in epithelial-mesenchymal transition and its related concepts.Cell & bioscience · 2024Review
- MAPP unravels frequent co-regulation of splicing and polyadenylation by RNA-binding proteins and their dysregulation in cancer.Nature communications · 2024Article
- Allicin and Cancer Hallmarks.Molecules (Basel, Switzerland) · 2024Review
- Loss of Upk1a and Upk1b expression is linked to stage progression in urothelial carcinoma of the bladder.International urology and nephrology · 2024Article
- Review
- Review
- Neural cell state shifts and fate loss in ageing and age-related diseases.Nature reviews. Neurology · 2023Review
- Mechanisms of Action and Limitations of Monoclonal Antibodies and Single Chain Fragment Variable (scFv) in the Treatment of Cancer.Biomedicines · 2023Review
- An Overview of the Role of MicroRNAs on Carcinogenesis: A Focus on Cell Cycle, Angiogenesis and Metastasis.International journal of molecular sciences · 2023Review
- Nucleoli and the nucleoli-centromere association are dynamic during normal development and in cancer.Molecular biology of the cell · 2023Article
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer is a complex disease without a unified explanation for its cause so far. Our recent work demonstrates that cancer cells share similar regulatory networks and characteristics with embryonic neural cells. Based on the study, I will address the relationship between tumor and neural cells in more details. I collected the evidence from various aspects of cancer development in many other studies, and integrated the information from studies on cancer cell properties, cell fate specification during embryonic development and evolution. Synthesis of the information strongly supports that cancer cells share much more similarities with neural progenitor/stem cells than with mesenchymal-type cells and that tumorigenesis represents a process of gradual loss of cell or lineage identity and gain of characteristics of neural cells. I also discuss cancer EMT, a concept having been under intense debate, and possibly the true meaning of EMT in cancer initiation and development. This synthesis provides fresh insights into a unified explanation for and a previously unrecognized nature of tumorigenesis, which might not be revealed by studies on individual molecular events. The review will also present some brief suggestions for cancer research based on the proposed model of tumorigenesis.
Indexed as
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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.