Our meta-analysis suggested that GSTM1 null genotype might be associated with an increased risk of developing oral cancer in individuals from Mainland China.
Nimbolide, a neem limonoid inhibits cytoprotective autophagy to activate apoptosis via modulation of the PI3K/Akt/GSK-3β signalling pathway in oral cancer.
Tumor-derived supernatants may impair the function of tumor-infiltrating pDCs, which subsequently decreases the immune response of CD4<sup>+</sup> T cells in human oral cancer through TGF-β- and IL-10- dependent mechanisms.
The inflammatory mediators including nuclear factor kappa B, vascular endothelial growth factor, inflammatory cytokines, prostaglandin pathways, p53, reactive oxygen and nitrogen species, and microRNAs are major key players in the pathogenesis of oral cancer.
Gender specific association of TP53 polymorphisms (EX4 215G>C Arg72Pro, IVS3+40-41ins16, and IVS6+62G>A), with risk of oral cancer subtypes and overall survival of the patients.
Fluorescence microscopy, real-time PCR, Western blot analysis, and in vivo bioimaging of mice containing orthotopic xenograft tumors were used to examine the ability of the dual peptide carrier to mediate specific delivery of bioactive siRNAs into EGFR-overexpressing oral cancer cells/tissues.
CCND1 gene and its protein cyclin D1 are frequently altered by different molecular mechanisms, including amplification, chromosomal translocations, mutations, and activation of the pathways involved in cyclin D1 expression, alterations which appear to be essential in the development of human cancers, including oral carcinoma.
In conclusion, CMP and its ingredient cordycepin can inhibit tumor growth and malignant transformation in a mouse model for oral cancer via inhibition of EGFR- and IL-17RA-signaling and enhancement of anti-tumor immunity.
In this study, quantitative expression level of IL-6 and VEGF in CAF and Oral Cancer Cells (OCCs) examined through Real Time PCR and ELISA and western blot analysis.
The combination of vorinostat and AZD1775 inhibits tumor growth and angiogenesis <i>in vivo</i> in an orthotopic mouse model of oral cancer and prolongs animal survival.<b>Conclusions:</b> Vorinostat synergizes with AZD1775 in HNSCC cells with mutant p53 <i>in vitro</i> and <i>in vivo</i> A strategy combining HDAC and WEE1 inhibition deserves further clinical investigation in patients with advanced HNSCC.<i></i>.
With these data, we identified TNFα as a prominent mediator in oral cancer-induced nociception and inflammation, highlighting the need for further investigation in neural-immune communication in cancer pain.
Chromosomal region 11q13, including genes CCND1, Fas-associated death domain (FADD), and CTTN, is often amplified in oral cancer with nodal metastases.