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As a result, a number of studies have been carried out showing that the polymorphic structure of the mitochondrial genome has tumorigenesis inducer and promoter effects.
At the same time, we examine the effect of Grail on stress-induced apoptosis and tumorigenesis using fluorescence-activated cell sorting (FACS) analysis and an anchor-independent assay, respectively.
Despite the role of mortalin in tumorigenesis is not fully elucidated, it is thought to exert its tumorigenic effects through various binding partners including p53 (23).
These results suggested that dysregulation of GPNMB expression might be associated with the tumorigenesis of human cervical cancer.
In summary, loss of TIP30 expression might be associated with BUC tumorigenesis and is an independent predictor for OS in patients with BUC.
To examine the function of EI24 on pancreatic cancer tumorigenesis in vivo, we performed tumor formation assays in Balb/c nude mice.
In this review, we discuss the molecular mechanisms by which let-7 microRNAs regulate the colonic tumorigenesis, tumor progression, and chemotherapy resistance by a posttranscriptional regulation and also highlight the possibility of the application of let-7 targeting therapy against CRC.
When [p27.sup.kip1] is localized in the cytoplasm, Cdk2 is no longer inhibited and it is free to activate E2F1, resulting in cell cycle progression and tumorigenesis, [5,6,13].
This dosage has been proved to be of potent chemopreventive efficacy upon intestinal tumorigenesis, and our preliminary experiments certified its efficacy.
We can conclude that, although the two concepts of CO and CSC have been often used indiscriminately, it is pivotal to take into account precise definitions in order to better define the molecular mechanisms that drive tumorigenesis and cancer plasticity and improve the development of new targeted strategies.
The negative correlation between the use of anti-inflammatory drugs and cancer incidence proves that active inflammation supports carcinogenesis, and anti-inflammatory drugs can prevent inflammation-related tumorigenesis. (4,5) Inflammation leads to neoplastic transformation by altering gene expression levels of oncogenes and tumor suppressors.
EMP2 is a cancer promoting protein, highly expressed in epithelial malignancies and associated with tumorigenesis, with triple negative breast cancer highly prominent on that list.