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Chemoprevention

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Preventing cancers by avoiding or minimizing exposures, especially occupational and societal (habit-related) exposures to known environmental carcinogens is by far the most cost-effective and sustainable strategy for reducing the mortality and disability related to cancer[5,55]. Overall there is very limited success achieved in elimination of carcinogen from the environment and minimizing the exposure due to lifestyle choices and modern developments. Additional cost effective and practical approaches in cancer prevention interventions include pursuing lifestyle or dietary changes, medical interventions (chemoprevention) and / or prophylactic resection of high-risk organs in certain germ-line mutation carriers[11,56,12]. One of these approaches …show more content…

• Preventive approaches have been found to be successful in other environmental diseases such as infectious diseases (vaccines) and cardiovascular events (treating risk factors with stents,statins,lifestyle changes). Interest has been further stimulated by successes in chemoprevention of skin, breast, prostate, cervical, and colon cancer by various prevention agents employed [56,59,12] (Table 1).
The aim of cancer chemoprevention is to delay or disrupt the multiple pathways and processes involved in three steps of cancer causation i.e. initiation, promotion, and progression. The concept of prevention is best defined in the context of levels called primary, secondary, and tertiary prevention. Primary prevention is meant for general population and those at increased risk of cancer development. Secondary chemoprevention is intended for patients with premalignant lesions that may progress to an invasive disease. Tertiary chemoprevention is targeted to prevent cancer recurrence (local invasion and / or distant metastasis) or second primary tumor among those who already have developed the …show more content…

These dietary phytochemicals have been demonstrated to modulate incidence and / or multiplicity and / or latency period of carcinogen / spontaneously-induced tumors at various organ sites in experimental rodent models (Table 2). Surrogate markers like cell proliferation and apoptosis and various detoxication pathways (xenobiotic enzyme inductions / inhibition, lipid peroxidation etc.) have also been successfully used for demonstrating protective action in in vivo system. Overall, the mechanisms implicated in the dietary phytochemical-mediated inhibition are diverse (Figure 2). The observed anti-initiating and anti-promoting activity of dietary phytochemicals in experimental models involve modulation of redox status, direct interaction with proteins and modulation of signaling kinases ultimately leading to effects on genes and cell signaling pathways at multiple levels(Figure

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