Aging and cancer: molecular facts and awareness for Turkey

Abstract

Aging is a complex process influenced by multiple factors including biology and behavior as well as physical, social, and cultural aspects of the human environment. Additionally, these factors interact with each other. Aging starts biologically and then the other dimensions come. Biological aging is a time-related increase in an organism's intrinsic morbidity and mortality (Kirkwood and Austad, 2000;Adams et al., 2004;Hipkiss, 2007). Aging is universal and progressive and represents a steady decrease in physiological ability (Adams et al., 2004). It usually occurs after reproductive maturation and results from diminishing energy to maintain molecular fitness (Hayflick, 2000;Carnes et al., 2008). Age-related changes occur at different levels, caused by molecular damage that slowly overwhelms the defense, repair, and maintenance systems of the body. The result is an increase in generalized vulnerability at all levels of organization (Hipkiss, 2007). Cellular senescence has been proposed to contribute to organismal aging (Heemst, 2009). Biological aging does not have a simple cause; instead, it is a very complex or multifactorial process. Mainly genetic and environmental factors influence the rate of biological aging (Adams et al., 2004;Carnes et al., 2008). Some cellular causes are telomere shortening, accumulation of mutations in nuclear DNA and mitochondrial DNA, effects of oxidants or free radicals (oxidative stress), glycation (cross links), excess damaged proteins, and inadequate degradation of waste or increase in lipofuction within cells. These pathologies may cause age-related diseases. However, there is interindividual variation in the rate and nature of aging-associated diseases (Sander et al., 2008). These age-related diseases are the leading cause of death in developed/developing countries (Fontana, 2009). Among these diseases, there are cardiovascular diseases, cancers, neurodegenerative diseases, decreased resistance to infections, diabetes mellitus, and some others (Anisimov, 2001). These are named as totally age-associated pathologies or age-associated diseases. However, the distinctions between senescence and disease are blurred sometimes in biogerontology and medicine. Senescence and disease have some overlapping biological consequences (Carnes et al., 2008). Aging is not a disease, but it accompanies the decline in organ and body functions and indicates an increasing susceptibility to diseases such as cancer. During aging, the accumulation of genetic and epigenetic changes, the diminishing of telomere length, the progressive disruption of mechanisms for DNA repair, glucose metabolism regulation, cell cycle control, and stem cell renewal lead to the induction of senescence or apoptosis and loss of replicative capacity. These cellular dysfunctional mechanisms characterizing the aging process have also been found to be involved in carcinogenesis (Bassi et al., 2009). Actually, cellular

Identification of bladder cancer prognostic biomarkers using an ageing gene-related competitive endogenous RNA network

“…One current theory posits that as aging occurs, mutations accumulate and long-term chronic inflammation persists, cancer-promoting DNA mutations increase and DNA-damage repair mechanisms weaken. Eventually, a compromised immune and repair system can no longer cope with long term exposure to carcinogens such as sunlight, radiation and environmental chemicals leading to onset of cancer [ 6 ]. Nonetheless, a complete understanding of the link between ageing and cancer remains poorly understood.…”