ReviewMolecular carcinogenesis2006
Molecular and cellular targets.
Review in Molecular carcinogenesis, 2006. 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, 44 citations in OpenAlex.
- Molecular and modular intricacies of precision oncology.Frontiers in immunology · 2024Review
- Salivary esterases dramatically reduce biostability of dentin collagen treated with galloylated polyphenols.Dental materials : official publication of the Academy of Dental Materials · 2022Article
- Strategies to better treat glioblastoma: antiangiogenic agents and endothelial cell targeting agents.Future medicinal chemistry · 2021Review
- Article
- A new method to prepare and redefine black tea thearubigins.Journal of chromatography. A · 2018Article
- Synergistic anticancer activity of biologicals from green and black tea on DU 145 human prostate cancer cells.Central-European journal of immunology · 2015Article
- A chrysin derivative suppresses skin cancer growth by inhibiting cyclin-dependent kinases.The Journal of biological chemistry · 2013Article
- Signal transduction and molecular targets of selected flavonoids.Antioxidants & redox signaling · 2013Review
- Functional protein pathway activation mapping of the progression of normal skin to squamous cell carcinoma.Cancer prevention research (Philadelphia, Pa.) · 2012Article
- Effects of the black tea polyphenol theaflavin-2 on apoptotic and inflammatory pathways in vitro and in vivo.Molecular nutrition & food research · 2011Article
- Activity and interactions of antibiotic and phytochemical combinations against Pseudomonas aeruginosa in vitro.International journal of biological sciences · 2010Article
- 7,3',4'-Trihydroxyisoflavone inhibits epidermal growth factor-induced proliferation and transformation of JB6 P+ mouse epidermal cells by suppressing cyclin-dependent kinases and phosphatidylinositol 3-kinase.The Journal of biological chemistry · 2010Article
- Epigallocatechin 3-gallate and green tea catechins: United they work, divided they fail.Cancer prevention research (Philadelphia, Pa.) · 2009Review
- Inhibitory effects of caffeine analogues on neoplastic transformation: structure-activity relationship.Carcinogenesis · 2008Article
- Modulatory effects of polyphenols on apoptosis induction: relevance for cancer prevention.International journal of molecular sciences · 2008Article
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
Abstract
Carcinogenesis is a multistage process consisting of initiation, promotion, and progression stages and each stage may be a possible target for chemopreventive agents. A significant outcome of these investigations on the elucidation of molecular and cellular mechanisms is the explication of signal transduction pathways induced by tumor promoters in cancer development. The current belief today is that cancer may be prevented or treated by targeting specific cancer genes, signaling proteins, and transcription factors. The molecular mechanisms explaining how normal cells undergo neoplastic transformation induced by tumor promoters are rapidly being clarified. Accumulating research evidence suggests that many of dietary factors, including tea compounds, may be used alone or in combination with traditional chemotherapeutic agents to prevent or treat cancer. The potential advantage of many natural or dietary compounds seems to focus on their potent anticancer activity combined with low toxicity and very few adverse side effects. This review summarizes some of our recent work regarding the effects of the various tea components on signal transduction pathways involved in neoplastic cell transformation and carcinogenesis.
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.