Among these 14 variants, 9 variants were reported to be significantly associated with the risk of oral cancer (CYP1A1-MspI, CYP2E1-RsaI/PstI, MTHFR-C677T, p73-G4C14-to-A4T14, XRCC1-Arg194Trp, CYP1A1-Ile462Val, GSTM1-±, and NAT2 slow vs rapid).
We have identified the potential combined XRCCs 1-4 SNPs with genotypes that were associated with oral cancer risk and may have an impact on identification of a high-risk population.
However, in stratified analyses based on cancer site, a significant association was found between the XRCC1Arg194Trp polymorphism and oral cancer under the allelic, heterozygote, and dominant models.
We used immunohistochemical analyses to investigate XBP-1 expression in 255 OSCC tissue specimens, as well as migration and invasion assays with XBP-1 siRNA transfection of oral cancer cell lines to confirm its role in OSCC.
In conclusion, genetic variants of WWOX contribute to the occurrence of oral cancer, and the findings regarding these biomarkers provided a prediction model for risk assessment.
Previously, we constructed a recombinant <i>Bifidobacterium longum</i> displaying a partial mouse Wilms' tumor 1 (WT1) protein (<i>B. longum</i> 420) as an oral cancer vaccine using a bacterial vector and demonstrated that oral administration of <i>B. longum</i> 420 significantly inhibited tumor growth compared with the Db126 WT1 peptide vaccine in the TRAMP-C2, mouse castration-resistant prostate cancer (CRPC) syngeneic tumor model.
Recently, we developed a WT1 oral cancer vaccine using a recombinant Bifidobacterium displaying WT1 protein, which can efficiently deliver WT1 protein to the gut immune system, and we demonstrated that this oral cancer vaccine had a significant anti-tumor effect in a C1498-WT1 murine leukemia syngeneic tumor model.
This case-control study evaluated the association of SNPs in IRF6 (rs642961), WNT3A (rs708111), GSK3β (rs9879992), 8q24 (rs987525) and WNT11 (rs1533767), representing regions consistently identified as of susceptibility for oral clefts, with oral cancer (oral squamous cell carcinoma) and breast cancer.
This case-control study evaluated the association of SNPs in IRF6 (rs642961), WNT3A (rs708111), GSK3β (rs9879992), 8q24 (rs987525) and WNT11 (rs1533767), representing regions consistently identified as of susceptibility for oral clefts, with oral cancer (oral squamous cell carcinoma) and breast cancer.
Our results show the promise of combination therapy of PEG-PEI-Ce6 nanoparticles for delivery of Wnt-1 siRNA along with PDT in the treatment of oral cancer.
We propose that the involvement of p65 in HPV infected oral cancer may be linked to improved differentiation and better prognosis of the disease when treated.
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>.
Databases including PubMed, EMbase, CNKI, VIP and WanFang Data were searched to identify case-control studies concerning the association between an XRCC3 gene polymorphism and the risk of oral cancer from the inception to June 2014.
In immunohistochemistry analysis, FaDu xenografts from AGG-treated mice showed decreased expression of Snail, SOX2, and vimentin and increased expression of p73 and E-cadherin compared with the control group, confirming EMT inhibition as part of its anticancer efficacy against oral cancer.