ArticleMolecular biology reports2015
Towards a systemic paradigm in carcinogenesis: linking epigenetics and genetics.
Article in Molecular biology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 44 citations in OpenAlex.
- A perspective review on factors that influence mutagenicity in medicinal plants and their health implications.Toxicological sciences : an official journal of the Society of Toxicology · 2025Review
- Biochemistry-Not Oncogenes-May Demystify and Defeat Cancer.Oncology and therapy · 2023Review
- The Concept of Cancer Stem Cells: Elaborating on ALDH1B1 as an Emerging Marker of Cancer Progression.Life (Basel, Switzerland) · 2023Review
- Review
- Mutation or not, what directly establishes a neoplastic state, namely cellular immortality and autonomy, still remains unknown and should be prioritized in our research.Journal of Cancer · 2022Review
- Metabolic therapy and bioenergetic analysis: The missing piece of the puzzle.Molecular metabolism · 2021Review
- Review
- From cancer to rejuvenation: incomplete regeneration as the missing link (part II: rejuvenation circle).Future science OA · 2020Review
- Environmental Carcinogenesis and Transgenerational Transmission of Carcinogenic Risk: From Genetics to Epigenetics.International journal of environmental research and public health · 2018Article
- Hospitalizations in Pediatric and Adult Patients for All Cancer Type in Italy: The EPIKIT Study under the E.U. COHEIRS Project on Environment and Health.International journal of environmental research and public health · 2017Article
- Press-pulse: a novel therapeutic strategy for the metabolic management of cancer.Nutrition & metabolism · 2017Article
- Carcinogenetic mechanisms of endocrine disruptors in female cancers (Review).Oncology reports · 2016Review
- Knockdown of long noncoding RNA H19 sensitizes human glioma cells to temozolomide therapy.OncoTargets and therapy · 2016Article
- Strategies to Prevent "Bad Luck" in Cancer.Journal of the National Cancer Institute · 2015Article
- Silencing of Bmi-1 gene enhances chemotherapy sensitivity in human glioblastoma cells.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Potential of epigenetic therapies in the management of solid tumors.Cancer management and research · 2015Review
- Potential Gene Interactions in the Cell Cycles of Gametes, Zygotes, Embryonic Stem Cells and the Development of Cancer.Frontiers in oncology · 2015Review
- Cancer as a mitochondrial metabolic disease.Frontiers in cell and developmental biology · 2015Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For at least 30 years cancer has been defined as a genetic disease and explained by the so-called somatic mutation theory (SMT), which has dominated the carcinogenesis field. Criticism of the SMT has recently greatly increased, although still not enough to force all SMT supporters to recognize its limits. Various researchers point out that cancer appears to be a complex process concerning a whole tissue; and that genomic mutations, although variably deleterious and unpredictably important in determining the establishment of the neoplastic phenotype, are not the primary origin for a malignant neoplasia. We attempt to describe the inadequacies of the SMT and demonstrate that epigenetics is a more logical cause of carcinogenesis. Many previous models of carcinogenesis fall into two classes: (i) in which some biological changes inside cells alone lead to malignancy; and (ii) requiring changes in stroma/extracellular matrix. We try to make clear that in the (ii) model genomic instability is induced by persistent signals coming from the microenvironment, provoking epigenetic and genetic modifications in tissue stem cells that can lead to cancer. In this perspective, stochastic mutations of DNA are a critical by-product rather then the primary cause of cancer. Indirect support for such model of carcinogenesis comes from the in vitro and vivo experiments showing apparent 'reversion' of cancer phenotypes obtained via physiological factors of cellular differentiation (cytokines and other signaling molecules) or drugs, even if the key mutations are not 'reversed'.
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.