Aging and Cancer: Converging Routes to Disease Prevention

Abstract

A ging is often associated with neurological and physical deterioration and the development of diseases, including Parkinson's, Alzheimer's, diabetes, cardiovascular diseases, and cancer. Cancer is one of the diseases that drastically diminish quality of life and life expectancy. Extensive research into the molecular mechanisms of both aging and cancer has demonstrated the interrelatedness of their biological pathways.The most important of these pathways are the ones activated by DNA damage, depletion of stem cells, oxidative stress, and psychological stress. These pathways initiate multiple cascades of molecular signals that crossreact with each other, thereby activating the regulators of aging and cancer. Of these, the most interesting are the regulators of metabolism that respond directly to nutrient and energy cues. It is now becoming possible to infer from this evidence that external factors have a direct role in regulating aging and cancer. These include diet, physical activity, and stress control. This article will assess recent evidence linking the mechanisms of aging and cancer as well as surveying research on the effectiveness of natural approaches affecting these mechanisms. Aging and Cancer: Converging Routes to Disease PreventionKatya Chobotova, DPhilAn integrative approach to the combined challenges of aging, cancer and stress is a necessary part of a global vision of wellness. Recent research into the mechanisms of aging, cancer and stress has established the biological links between these processes. Understanding these links is an important stepping-stone for developing approaches and therapies that ensure wellness throughout all stages of aging. This paper will consider the most recent developments in research into the molecular mechanisms common to aging and cancer and will discuss the effectiveness of natural approaches for preventing disease. Metabolic regulators as well as nutrient and energy sensors are involved in the processes of aging and cancer, and these are open to external manipulation and control. It is now becoming possible to demonstrate how nutrition, physical activity and stress control can lead to disease-free aging.

Age-related molecular genetic changes of murine bone marrow mesenchymal stem cells

“…These results may also be quite relevant to oncogenesis; an age-related loss of p53 may predispose these cells to oncogenic transformation, perhaps generating cancer stem cells [67]. Aging is a well-established risk factor for oncogenesis [68,69]. The relevance of Flt1 induction is not clear, however it has been reported that bone marrow derived hematopoietic progenitor cells that express high levels of Flt1 have an enhanced potential to home to tissues that express VEGF [70].…”

Antioxidant and genoprotective effects of spent coffee extracts in human cells

“…Free radicals, such as reactive oxygen species (ROS), damage macromolecules as proteins, lipids and DNA. DNA damage by ROS can contribute to the formation of single and double strand breaks (SBs), as well as to the oxidation of purine and pyrimidine bases, leading to genome instability and subsequent potential cancer development (Chobotova, 2009). The formation of 8-oxoguanine (8-oxoGua) by ROS oxidation of guanine is one of the most common DNA lesions.…”

A Major Role for Nonenzymatic Antioxidant Processes in the Radioresistance of Halobacterium salinarum

“…ROS include molecules such as hydrogen peroxide (H 2 O 2 ), superoxide (O 2 ⅐ Ϫ ), and hydroxyl radicals (HO ⅐ ), all of which can be derived from molecular oxygen in metabolically active cells (58). Damage from ROS has also been implicated in a variety of human conditions, including the neurological diseases Alzheimer's and Parkinson's (7), aging, and a wide range of cancers (9,55,57). In response to the danger of ROS, organisms have evolved numerous defense and repair mechanisms, including conserved detoxification enzymes (e.g., superoxide dismutases [SOD] and catalases), free radical scavenger systems, and mechanisms to repair DNA damage (28,30,58).…”