AGEING The decline in organismal fitness that occurs with increasing age.
AGEING PHENOTYPES The specific physiological manifestations of ageing.
ANTAGONISTIC PLEIOTROPY The hypothesis that genes or processes that were selected to benefit the health and fitness of young organisms can have unselected deleterious effects that are manifest in older organisms and thereby contribute to ageing.
APOPTOSIS Ordered, genetically programmed cell death triggered by both physiological stimuli and cellular damage. Apoptosis avoids cell lysis and subsequent inflammation.
BASE EXCISION REPAIR A DNA-repair pathway that excises and replaces damaged DNA bases.
CARETAKERS Tumour-suppressor genes or proteins that act to protect the genome from damage or mutations. Many caretaker genes encode proteins that recognize or repair DNA damage.
CELLULAR SENESCENCE The essentially irreversible loss of cell division potential and the associated functional changes that are triggered by damage and other potential cancer-causing stimuli.
COMPLEX ORGANISMS Multicellular organisms that are composed of both post-mitotic and renewable (mitotic) somatic tissues.
GATEKEEPERS Tumour-suppressor genes or proteins that regulate cellular responses that prevent the survival or proliferation of potential cancer cells. These responses are known as apoptosis and cellular senescence, respectively.
HOMOLOGOUS RECOMBINATIONAL REPAIR A relatively error-free pathway that repairs DNA double-strand breaks using an undamaged sister chromatid or homologous chromosome as a template.
LONGEVITY Average or maximum lifespan of a cohort of organisms.
MISMATCH REPAIR A DNA-repair pathway that removes and replaces nucleotides that have been misrepaired by DNA polymerases during DNA replication.
NECROSIS Passive or unregulated cell death, in which cells lyse and deposit degradative and antigenic cell constituents into the surrounding tissue. Necrotic cell death, in contrast to apoptosis, often provokes an inflammation reaction.
NON-HOMOLOGOUS END-JOINING REPAIR A relatively error-prone pathway that repairs double-strand breaks by ligating non-homologous DNA ends.
NUCLEOTIDE EXCISION REPAIR A DNA-repair pathway that removes and replaces damaged nucleotides, particularly those that distort the DNA helix.
SIMPLE ORGANISMS Multicellular organisms that are composed entirely or largely of post-mitotic somatic cells.
TELOMERES The DNA–protein structure that stabilizes the ends of linear chromosomes and protects them from degradation or fusion. In vertebrates, telomeres are composed of several-kilobase pairs of the sequence TTTAGGG and several associated proteins.
XERODERMA PIGMENTOSUM A group of cancer-prone syndromes in humans that are caused by defects in the nucleotide excision repair genes.
