An association between aging/longevity and cancer has long been suggested, yet the evolutionary and molecular links between these complicated traits remain elusive. Here, we analyze the relationship between longevity- and cancer-associated genes/proteins (LAGs/LAPs and CAGs/CAPs, respectively). Specifically, we address the following questions: (1) to what extent the CAGs and LAGs are evolutionary conserved and how they (or their orthologs) are related to each other in diverse species?
The naked mole rat (Heterocephalus glaber) is a strictly subterranean, extraordinarily long-lived eusocial mammal. Although it is the size of a mouse, its maximum lifespan exceeds 30 years, making this animal the longest-living rodent. Naked mole rats show negligible senescence, no age-related increase in mortality, and high fecundity until death. In addition to delayed ageing, they are resistant to both spontaneous cancer and experimentally induced tumorigenesis. Naked mole rats pose a challenge to the theories that link ageing, cancer and redox homeostasis.
Forkhead-box (FOX) family proteins, involved in cell growth and differentiation as well as embryogenesis and longevity, are DNA-binding proteins regulating transcription and DNA repair. The focus of this review is on the mechanisms of FOX-related human carcinogenesis. FOXA1 is overexpressed as a result of gene amplification in lung cancer, esophageal cancer, ER-positive breast cancer and anaplastic thyroid cancer and is point-mutated in prostate cancer. FOXA1 overexpression in breast cancer and prostate cancer is associated with good or poor prognosis, respectively.
Nutrigenomics refers to the complex effects of the nutritional environment on the genome, epigenome, and proteome of an organism. The diverse tissue- and organ-specific effects of diet include gene expression patterns, organization of the chromatin, and protein post-translational modifications. Long-term effects of diet range from obesity and associated diseases such as diabetes and cardiovascular disease to increased or decreased longevity.
Rapid progress is being made in our ability to modify the aging process. Rather than serving as a period of debility and decreasing health, for many people, the later years of life are becoming a period of continued productivity, independence and good health. Progress is also being made in increasing average lifespan. The leading causes of death (cardiovascular disease, cancer, lung disease, diabetes) are the end result of decades-long processes. With current knowledge, it is possible to delay the onset of these diseases.
The World Health Organization (WHO) assigns high priority to the prevention of non-communicable age-related diseases such as heart disease, cancer, diabetes, stroke and chronic lower respiratory diseases. They are now the leading causes of death, in both industrialised and developing countries, mostly due to increased life expectancy and urbanisation with associated changes in lifestyle and environment. Tobacco smoking, physical inactivity and resulting obesity are established risk factors for many chronic diseases.
This work is dedicated to the exploration of the role of epigenetic (epiG) factors in major psychosis. One of the key functions of epigenetic modification of the genome of eukaryotic cells is to suppress transcriptional activity of the retroelements. Examples of retroelements are endogenous retroviral sequences (ERVs), Alu's, and LINEs, among others, which as a rule are hypermethylated. There is evidence from schizophrenia (SCH) and other human complex diseases that some of the genomic retroelements become transcribed in the affected tissues.
INTRODUCTION: There is growing interest in the role of single genes in cognitive functions. Association studies are the most commonly applied method in this field. This method assumes that the genetic information affecting cognitive processes is "static" and unchanging. However, there is accumulating evidence that dynamic genomic and epigenetic alterations can modulate complex cognitive processes, and influence susceptibility to disorders associated with impaired cognitive functioning.