Oral cancer (oral cavity and oropharynx) is a common and aggressive cancer that invades local tissue, can cause metastasis, and has a high mortality rate. Conventional treatment strategies, such as surgery and chemoradiotherapy, have improved over the past few decades; however, they remain far from optimal. Currently, cancer research is focused on improving cancer diagnosis and treatment methods (oral cavity and oropharynx) nanotechnology, which involves the design, characterization, production, and application of nanoscale drug delivery systems. In medicine, nanotechnologies, such as polymeric nanoparticles, solid lipid nanoparticles, nanostructured lipid carriers, gold nanoparticles, hydrogels, cyclodextrin complexes, and liquid crystals, are promising tools for diagnostic probes and therapeutic devices. The objective of this study is to present a systematic review of nanotechnology-based drug delivery systems for oral cancers.

https://www.dovepress.com/getfile.php?fileID=21123

Nanotechnology-based drug delivery systems for treatment of oral cancer: a review.

Immunohistochemical study of tumour angiogenesis in oral squamous cell carcinoma

Background and Objectives

It is recognized that hypoxic/ischemic conditions leading to production of reactive oxygen species (ROS) are an important mediator of angiogenesis in the wound-healing process. Recently, low level light irradiation at 635 nm, which is used in many clinical fields, was found to decrease intracellular ROS levels, and consequently alleviate oxidative stress. The purpose of the present study was to investigate the effects of 635 nm light-emitting diode (LED) irradiation on angiogenesis in human umbilical vein endothelial cells, in an in vitro CoCl2-induced severe hypoxia model.



Study Design/Materials and Methods

The effects were assessed on cell viability, tube formation, hypoxia-inducible factor-1, vascular endothelial growth factor (VEGF), VEGF-1 and -2 protein expression, mitogen-activated protein kinase (MAPK) phosphorylation, and ROS dissociation.



Results

The results showed that, under hypoxic/ischemic conditions, irradiation with 635 leads to reduced production and increased scavenging of intracellular ROS, which results in alleviation of VEGFR-1 suppression, enhanced VEGF expression and ERK MAPK activation, and subsequent acceleration of angiogenesis with improved cell viability and tube formation.



Conclusion

Taken together, irradiation with 635 nm was shown to reduce intracellular ROS production, which results in increased angiogenesis. Thus, we suggest that irradiation with 635 nm accelerate angiogenesis under hypoxic/ischemic conditions, and may prove to be a useful alternative tool in wound healing. Lasers Surg. Med. 43:344–352, 2011. © 2011 Wiley-Liss, Inc.

Effects of 635nm light-emitting diode irradiation on angiogenesis in CoCl(2) -exposed HUVECs.

The objective of this study was to evaluate lymphangiogenesis in oral squamous cell carcinoma and in the associated lymph nodes and podoplanin expression in neoplastic cells at the invasive front. In addition, the association of the above parameters with lymph node metastasis was also investigated. We used immunohistochemistry to examine primary tumors and lymph nodes, regardless of metastasis. Lymphatic vessel density (LVD) and microvessel density (MVD) were assessed by antibodies D2-40 and CD105, respectively, in intratumoral and peritumoral areas and in lymph node regions. Vascular endothelial growth factor-C and vascular endothelial growth factor receptor-3 expression was evaluated in tumor cells and D2-40 (podoplanin) expression in parenchymal cells found at the invasive front. The majority of cases with nodal involvement presented a high peritumoral LVD. In addition, a strong association of LVD with size and site of primary tumors could also be identified. MVD was statistically associated with metastasis, and a significant association between the lymphangiogenic factors and the density of vessels in the intratumoral region was also seen. The well-differentiated tumors did not express podoplanin. LVD and MVD were higher in metastatic lymph nodes than in nonmetastatic lymph nodes. The enhanced vascular network in metastatic lymph nodes reinforces the previous reports of lymphangiogenesis occurrence in lymph nodes. Moreover, the expression of podoplanin by more undifferentiated tumor cells suggests that this protein could be an indicator of tumor aggressiveness.

Lymphangiogenesis and Podoplanin Expression in Oral Squamous Cell Carcinoma and the Associated Lymph Nodes

Signaling pathways promoting epithelial mesenchymal transition in oral submucous fibrosis and oral squamous cell carcinoma.

Oral cancer is an important cause of worldwide morbidity and mortality, with substantial economic, physiological, and psychosocial impacts due to its treatment modality and a great risk for recurrences and second primary oral squamous cell carcinomas (OSCC) development. Therefore, it is very important to understand the underlying cell biology of such tumors. It is now a well-accepted fact that angiogenesis is essential for the growth and metastasis of solid tumors, including head and neck squamous cell carcinoma. The main factor responsible for angiogenesis is VEGF and its receptors. It has been demonstrated that VEGFRs are also present on tumor cells themselves and other cells from the tumor microenvironment, in addition to tumoral endothelial cells (ECs). Therefore between these cells take place numerous and different interactions mediated via paracrine/autocrine pathways that promote angiogenesis, uncontrolled tumor proliferation and metastasation. In consequence, estimation of VEGF expression and its receptors became a reliable prognostic tool in OSCCS, predicting the poor disease-free survival, poor overall survival, and metastatic disease. Understanding the distribution and role of VEGF and its receptors in the progression of OSCC will be essential to the development and design of new therapeutic strategies.

VEGF and VEGFRs expression in oral squamous cell carcinoma.

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VEGF and VEGFRs expression in oral squamous cell carcinoma.