Table 1.

Exemplar hallmarks of molecular aging.

Hallmark	Description
Attrition of telomeres	Most mammalian somatic cells do not express telomerase, an enzyme that is responsible for replicating the terminal ends of linear DNA molecules. Therefore, the DNA sequences at the end of the chromosome progressively lose their telomere protection with each new cell division (López-Otín et al., 2013; Chang et al., 2019).
A decline in mitochondrial function and cellular energies	Declines in mitochondrial function and mutations in mitochondrial DNA appear to affect cellular energetics. Elevated levels of ROS resulting from mitochondrial dysfunction may decrease apoptosis and lead to resistance of chemotherapeutic agents thereby promoting breast cancer malignancy (López-Otín et al., 2013; Chang et al., 2019)
Genome Instability	Over time DNA damage accumulates in normal cells as the result of endogenous cellular activity such as DNA replication errors or DNA damage due to ROS (López-Otín et al., 2013; Chang et al., 2019). These damages not only lead to accelerated aging, but also make the cell vulnerable to cancer development.
Epigenetic Alterations	Epigenetic changes are alterations in gene expression that do affect the DNA sequence. These changes involve processes such as posttranslational histone modifications, DNA methylation patterns, and chromatin remodeling. Aging cells experience random DNA methylation drift creating mosaic aging stem cells that could lead to cancer (López-Otín et al., 2013; Aunan et al., 2016; Chang et al., 2019).
DNA damage that affects cellular senescence	Cellular senescence is by which a cell ceases to divide. The primary objective of senescence is to inhibit the proliferation of impaired cells and to mark the cells for destruction by the immune system. The process is associated with aging and age-related conditions. In older individuals, the widespread damage and poor clearance of senescence results in cell accumulation, which contributes to aging (López-Otín et al., 2013; Aunan et al., 2016; Chang et al., 2019).
Altered intracellular communication	As part of aging, inflammatory reactions increase leading to alterations in neurohormonal signaling. There is also a decrease in immunosurveillance against premalignant cells and pathogens and a change in the structure of both the extracellular and pericellular environments (López-Otín et al., 2013).