ArticleBMC cancer2010
Clinical significance of phosphatidyl inositol synthase overexpression in oral cancer.
Article in BMC cancer, 2010. 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
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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
7 citing papers in PubMed, 19 citations in OpenAlex.
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- Gene dosage changes in KCTD13 result in penile and testicular anomalies via diminished androgen receptor function.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Role of Metabolic Reprogramming in Epithelial⁻Mesenchymal Transition (EMT).International journal of molecular sciences · 2019Review
- Discovery of potential biomarkers in human melanoma cells with different metastatic potential by metabolic and lipidomic profiling.Scientific reports · 2017Article
- Present and Future of EGFR Inhibitors for Head and Neck Squamous Cell Cancer.Journal of oncology · 2012Article
- Guggulsterone targets smokeless tobacco induced PI3K/Akt pathway in head and neck cancer cells.PloS one · 2011Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWe reported increased levels of phosphatidyl inositol synthase (PI synthase), (enzyme that catalyses phosphatidyl inositol (PI) synthesis-implicated in intracellular signaling and regulation of cell growth) in smokeless tobacco (ST) exposed oral cell cultures by differential display. This study determined the clinical significance of PI synthase overexpression in oral squamous cell carcinoma (OSCC) and premalignant lesions (leukoplakia), and identified the downstream signaling proteins in PI synthase pathway that are perturbed by smokeless tobacco (ST) exposure.
methodsTissue microarray (TMA) Immunohistochemistry, Western blotting, Confocal laser scan microscopy, RT-PCR were performed to define the expression of PI synthase in clinical samples and in oral cell culture systems.
resultsSignificant increase in PI synthase immunoreactivity was observed in premalignant lesions and OSCCs as compared to oral normal tissues (p = 0.000). Further, PI synthase expression was significantly associated with de-differentiation of OSCCs, (p = 0.005) and tobacco consumption (p = 0.03, OR = 9.0). Exposure of oral cell systems to smokeless tobacco (ST) in vitro confirmed increase in PI synthase, Phosphatidylinositol 3-kinase (PI3K) and cyclin D1 levels.
conclusionCollectively, increased PI synthase expression was found to be an early event in oral cancer and a target for smokeless tobacco.
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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.