ArticleJournal of biosciences2013
The aging of the 2000 and 2011 Hallmarks of Cancer reviews: a critique.
Article in Journal of biosciences, 2013. 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.
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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.
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Who cites it
44 citing papers in PubMed, 120 citations in OpenAlex.
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- Systemic structural analysis of alterations reveals a common structural basis of driver mutations in cancer.NAR cancer · 2023Article
- Metabolic regulation of endothelial senescence.Frontiers in cardiovascular medicine · 2023Review
- Revisiting Epithelial Carcinogenesis.International journal of molecular sciences · 2022Article
- 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
- Matrix Metalloproteinases Shape the Tumor Microenvironment in Cancer Progression.International journal of molecular sciences · 2021Review
- The Most Competent Plant-Derived Natural Products for Targeting Apoptosis in Cancer Therapy.Biomolecules · 2021Review
- Metabolic Reprogramming in Cancer: Role of HPV 16 Variants.Pathogens (Basel, Switzerland) · 2021Review
- Super-enhancer-associated long noncoding RNA AC005592.2 promotes tumor progression by regulating OLFM4 in colorectal cancer.BMC cancer · 2021Article
- Pro-Tumorigenic Macrophage Infiltration in Oral Squamous Cell Carcinoma and Possible Macrophage-Aimed Therapeutic Interventions.Frontiers in oncology · 2021Review
- Obacunone reduces inflammatory signalling and tumour occurrence in mice with chronic inflammation-induced colorectal cancer.Pharmaceutical biology · 2020Article
- Chemopreventive and Anticancer Effects of Thymoquinone: Cellular and Molecular Targets.Journal of cancer prevention · 2020Review
- The evolution of interventional oncology in the 21st century.The British journal of radiology · 2020Review
- Modulating Tumor Cell Functions by Tunable Nanopatterned Ligand Presentation.Nanomaterials (Basel, Switzerland) · 2020Review
- Ophiopogon Saponin C1 Inhibits Lung Tumors by Stabilizing Endothelium Permeability via Inhibition of PKCδ.International journal of biological sciences · 2020Article
- CD206Scientific reports · 2019Article
- Unexpected Discoveries Should Be Reconsidered in Science-A Look to the Past?International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Two review articles published in 2000 and 2011 by Hanahan and Weinberg have dominated the discourse about carcinogenesis among researchers in the recent past. The basic tenets of their arguments favour considering cancer as a cell-based, genetic disease whereby DNA mutations cause uncontrolled cell proliferation. Their explanation of cancer phenotypes is based on the premises adopted by the somatic mutation theory (SMT) and its cell-centered variants. From their perspective, eight broad features have been identified as so-called 'Hallmarks of Cancer'. Here, we criticize the value of these features based on the numerous intrinsic inconsistencies in the data and in the rationale behind SMT. An alternative interpretation of the same data plus data mostly ignored by Hanahan and Weinberg is proposed, based instead on evolutionarily relevant premises. From such a perspective, cancer is viewed as a tissue-based disease. This alternative, called the tissue organization field theory, incorporates the premise that proliferation and motility are the default state of all cells, and that carcinogenesis is due to alterations on the reciprocal interactions among cells and between cells and their extracellular matrix. In this view, cancer is development gone awry.
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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.