ReviewJournal of biomedical research2016
The more the messier: centrosome amplification as a novel biomarker for personalized treatment of colorectal cancers.
Review in Journal of biomedical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 9 citations in OpenAlex.
- A GPER-PKA-Centrin axis regulates centrosome numbers and centriole integrity in colon cancer cells.Communications biology · 2025Article
- GPER1 links estrogens to centrosome amplification and chromosomal instability in human colon cells.Life science alliance · 2023Article
- Review
- Keep Calm and Carry on with Extra Centrosomes.Cancers · 2022Review
- Overcome cancer drug resistance by targeting epigenetic modifications of centrosome.Cancer drug resistance (Alhambra, Calif.) · 2019Review
- A look into centrosome abnormalities in colon cancer cells, how they arise and how they might be targeted therapeutically.Biochemical pharmacology · 2018Review
- Cyclin A2 regulates symmetrical mitotic spindle formation and centrosome amplification in human colon cancer cells.American journal of translational research · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colon cancer is currently the third most common cancer and second most fatal cancer in the United States, resulting in approximately 600,000 deaths annually. Though colorectal cancer death rates are decreasing by about 3% every year, disease outcomes could be substantially improved with more research into the drivers of colon carcinogenesis, the determinants of aggressiveness in colorectal cancer and the identification of biomarkers that could enable choice of more optimal treatments. Colon carcinogenesis is notably a slow process that can take decades. Known factors that contribute to the development of colon cancer are mutational, epigenetic and environmental, and risk factors include age, history of polyps and family history of colon cancer. Colorectal cancers exhibit heterogeneity in their features and are often characterized by the presence of chromosomal instability, microscopic satellite instability, or CpG island methylator phenotype. In this review, we propose that centrosome amplification may be a widespread occurrence in colorectal cancers and could potently influence tumor biology. Moreover, the quantitation of this cancer-specific anomaly could offer valuable prognostic information and pave the way for further customization of treatment based on the organellar profile of patients. Patient stratification models that take into account centrosomal status could thus potentially reduce adverse side effects and result in improved outcomes for colorectal cancer patients.
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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.