ReviewCarcinogenesis2015
The potential for chemical mixtures from the environment to enable the cancer hallmark of sustained proliferative signalling.
Review in Carcinogenesis, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 39 citations in OpenAlex.
- The Influence of Environmental Exposure to Xenoestrogens on the Risk of Cancer Development.International journal of molecular sciences · 2024Review
- Total Effective Xenoestrogen Burden in Serum Samples and Risk of Endometrial Cancer in the Spanish Screenwide Case-Control Study.Environmental health perspectives · 2024Article
- Environmental and Occupational Triggers of Dry Eye Symptoms in the Ahsa Region of Saudi Arabia: A Cross-Sectional Study.Clinical ophthalmology (Auckland, N.Z.) · 2024Article
- Single-Cell Proliferation Microfluidic Device for High Throughput Investigation of Replicative Potential and Drug Resistance of Cancer Cells.Cellular and molecular bioengineering · 2023Article
- Small Molecules Targeting Programmed Cell Death in Breast Cancer Cells.International journal of molecular sciences · 2021Review
- Effect of High-Dose Topical Minoxidil on Erythrocyte Quality in SKH1 Hairless Mice.Animals : an open access journal from MDPI · 2020Article
- Curation of cancer hallmark-based genes and pathways for in silico characterization of chemical carcinogenesis.Database : the journal of biological databases and curation · 2020Article
- Blockade of α7 nicotinic acetylcholine receptors inhibit nicotine-induced tumor growth and vimentin expression in non-small cell lung cancer through MEK/ERK signaling way.Oncology reports · 2017Article
- The various aspects of genetic and epigenetic toxicology: testing methods and clinical applications.Journal of translational medicine · 2017Review
- Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells.Current genomics · 2017Article
- Low-Dose Mixture Hypothesis of Carcinogenesis Workshop: Scientific Underpinnings and Research Recommendations.Environmental health perspectives · 2017Article
- A Perspective Discussion on Rising Pesticide Levels and Colon Cancer Burden in Brazil.Frontiers in public health · 2017Article
- Evaluating the mechanistic evidence and key data gaps in assessing the potential carcinogenicity of carbon nanotubes and nanofibers in humans.Critical reviews in toxicology · 2017Review
- Four microRNAs Signature for Survival Prognosis in Colon Cancer using TCGA Data.Scientific reports · 2016Article
- Total Effective Xenoestrogen Burden in Serum Samples and Risk for Breast Cancer in a Population-Based Multicase-Control Study in Spain.Environmental health perspectives · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
32 authors at 20 institutions in 13 countries.
Funding
Abstract
The aim of this work is to review current knowledge relating the established cancer hallmark, sustained cell proliferation to the existence of chemicals present as low dose mixtures in the environment. Normal cell proliferation is under tight control, i.e. cells respond to a signal to proliferate, and although most cells continue to proliferate into adult life, the multiplication ceases once the stimulatory signal disappears or if the cells are exposed to growth inhibitory signals. Under such circumstances, normal cells remain quiescent until they are stimulated to resume further proliferation. In contrast, tumour cells are unable to halt proliferation, either when subjected to growth inhibitory signals or in the absence of growth stimulatory signals. Environmental chemicals with carcinogenic potential may cause sustained cell proliferation by interfering with some cell proliferation control mechanisms committing cells to an indefinite proliferative span.
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.