Molecular basis of cancer formation and

As discussed in sections Introduction and Molecular Basis of Cancer Formation and Development, the formation of cancer is very complex. Generally, the cyclic processes involving oxidation and inflammatory processes (Figs. 1 and 2) lead to the formation of cancer cells. These cancer cells survive if the host is immunocompromised which is generally the case under the conditions of severe oxidative stress [55,58,60]. This leads to the cancer cell proliferation and tumor formation [29]. Finally, due to immune exhaustion, the cancer growth overpowers immune response. Therefore, oxidative stress is the main cause of cancer formation and the subsequent immune exhaustion is the source of cancer growth. Hence, the chemotherapeutics for the treatment of cancer need to be efficient immunomodulators and antioxidants. It is important to note here that the plant polysaccharides with immunomodulatory properties concurrently possess antioxidant activity [5,85] and hence are the ideal candidates for the prevention and treatment of cancer. 

As discussed in the section on stmcture-function relationship of polysaccharides, p-D-glucans and protein bound p-o-glucans are potential candidates for chemotherapeutics for cancer because of their capacity to improve host immunity and hence improve immunosurveiUance. As discussed in section Molecular Basis of Cancer Formation and Development, the process of immunosurveiUance within the host immune system is responsible for the identification and destruction of cancer cells [8,65,72,115,116]. 

Other fundamental pathway to the discovery of anticancer chemotherapeu-tics is to identify the polysaccharides that counter the effects of mutated tumor suppressor gene p53. Mutated p53 gene is present in 50% of all human cancers studied in the literature [37-39]. This mutated gene will lose the ability to effectively bind to DNA. Therefore, the p21 protein cannot be produced and hence disturbs the process of controlled cell division that eventually leads to the formation of tumor [42] (see section Molecular Basis of Cancer Formation and Development ). It has already been demonstrated in the literature that PSP extracted from higher plants reduces cell proliferation by increasing... 

The protective effects of carotenoids against chronic diseases appear to be correlated to their antioxidant capacities. Indeed, oxidative stress and reactive oxygen species (ROS) formation are at the basis of oxidative processes occurring in cardiovascular incidents, cancers, and ocular diseases. Carotenoids are then able to scavenge free radicals such as singlet molecular oxygen ( O2) and peroxyl radicals particularly, and protect cellular systems from oxidation. 

Caffeic Acid Phenethyl Ester (CAPE). CAPE, a phenolic compound with antioxidant properties, is an active ingredient derived from honeybee propolis (52). CAPE has antiviral, anti-inflammatory and antiproliferative properties. The compound differentially suppresses the growth of numerous human cancer cells and also inhibits tumor promoter-mediated processes in transformed cells (53,54). In transformed cells, CAPE induces apoptosis and inhibits the expression of the malignant phenotype (55,56). In addition, CAPE treatment attenuates the formation of azoxymethane-induced aberrant crypts and the activities of ornithine decarboxylase (ODC), tyrosin protein kinase, and lipoxygenase activity (57). Although the molecular basis for these multiple chemopreventive effects of CAPE is not clear, recent studies have demonstrated that CAPE is a potent and specific inhibitor of the transcription factor NF-kB (58). CAPE inhibited the activity and expression of COX-2 in the carrageenan air pouch model of inflammation as well as in TPA-treated human oral epithelial cells (59). CAPE was able to reduce neointimal formation by inhibiting NF-kB activation in a model of endothelial injury of rat carotid artery (60). 

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