ReviewCancer metastasis reviews2012
A new hypothesis for the cancer mechanism.
Review in Cancer metastasis reviews, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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
20 citing papers in PubMed, 59 citations in OpenAlex.
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- An insight into the anticancer potentials of lignan arctiin: A comprehensive review of molecular mechanisms.Heliyon · 2024Review
- Comparison of anti-cancer effects of platinum ribavirin and ribavirin via telomerase and Bcl-2 gene expression.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Potential Carcinogens in Makeup Cosmetics.International journal of environmental research and public health · 2023Article
- Breast cancer: molecular mechanisms of underlying resistance and therapeutic approaches.American journal of cancer research · 2022Review
- Increased co-expression of PSMA2 and GLP-1 receptor in cervical cancer models in type 2 diabetes attenuated by Exendin-4: A translational case-control study.EBioMedicine · 2021Article
- RAGE and Its Ligands: Molecular Interplay Between Glycation, Inflammation, and Hallmarks of Cancer-a Review.Hormones & cancer · 2018Review
- Bioinformatics and functional analyses of key genes and pathways in human clear cell renal cell carcinoma.Oncology letters · 2018Article
- Differential distribution of immune cells in breast invasive carcinoma vs. breast carcinomaInternational journal of clinical and experimental pathology · 2017Article
- Breast cancer epidemic in the early twenty-first century: evaluation of risk factors, cumulative questionnaires and recommendations for preventive measures.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Cancer Biopsy in Ancient Persian Medicine: Do or Not to Do!Iranian journal of public health · 2015Article
- Intracranial Undifferentiated Sarcoma Arising from a Low-Grade Glioma: A Case Report and Literature Review.Journal of Korean Neurosurgical Society · 2015Article
- MTA1--a stress response protein: a master regulator of gene expression and cancer cell behavior.Cancer metastasis reviews · 2014Review
- Hyaluronan and RHAMM in wound repair and the "cancerization" of stromal tissues.BioMed research international · 2014Review
- Trimeric Tn antigen on syndecan 1 produced by ppGalNAc-T13 enhances cancer metastasis via a complex formation with integrin α5β1 and matrix metalloproteinase 9.The Journal of biological chemistry · 2013Article
- If it is not healing, do worry about it!BMJ case reports · 2013Article
- Pathways to breast cancer recurrence.ISRN oncology · 2013Article
- Multiscale models of breast cancer progression.Annals of biomedical engineering · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Several observations have led us to a new hypothesis for cancer mechanism. First, that cancer appears only on those multicellular organisms with complicated wound-healing capacities. Second, that wounds considered as risk factors can be identified in all cancers in clinics. And finally, that oncogene activation appears not only in cancer, but also in normal physiology and noncancer pathology processes. Our proposed hypothesis is that cancer is a natural wound healing-related process, which includes oncogene activations, cytokine secretions, stem cell recruitment differentiation, and tissue remodeling. Wounds activate oncogenes of some cells and the latter secrete cytokines to recruit stem cells to heal the wounds. However, if the cause of the wound or if the wound persists, such as under the persistent UV and carcinogen exposures, the continuous wound healing process will lead to a clinical cancer mass. There is no system in nature to stop or reverse the wound healing process in the middle stage when the wound exists. The outcome of the cancer mechanism is either healing the wound or exhausting the whole system (death). The logic of this cancer mechanism is consistent with the rationales of the other physiological metabolisms in the body-for survival. This hypothesis helps to understand many cancer mysteries derived from the mutation theory, such as why cancer only exists in a small proportion of multicellular organisms, although they are all under potential mutation risks during DNA replications. The hypothesis can be used to interpret and guide cancer prevention, recurrence, metastasis, in vitro and in vivo studies, and personalized treatments.
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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.