Relationships between cancer and aging: a multilevel approach

  title={Relationships between cancer and aging: a multilevel approach},
  author={Vladimir Anisimov and Ewa Sikora and Graham Pawelec},
The incidence of cancer increases with age in humans and in laboratory animals alike. There are different patterns of age-related distribution of tumors in different organs and tissues. Aging may increase or decrease the susceptibility of various tissues to initiation of carcinogenesis and usually facilitates promotion and progression of carcinogenesis. Aging may predispose to cancer in two ways: tissue accumulation of cells in late stages of carcinogenesis and alterations in internal… 
Chronologic aging decreases tumor angiogenesis and metastasis in a mouse model of head and neck cancer.
The results indicate that host response to angiogenic factors inhibit tumor growth and metastasis of head and neck cancer.
Aging and cancer: Is glucose a mediator between them?
The new evidence adds to the concepts that have been being developed starting from mid-1970ies to suggest that age-related shifts in glucose and lipid metabolism increase the risk of cancer and compromise prognoses for cancer patients and to propose antidiabetic biguanides, including metformin, for cancer prevention and as an adjuvant means of cancer treatment aimed at the metabolic rehabilitation of patients.
Aging and Cancer: The IGF-I Connection
The IGFs are nutritionally dependent and are therefore modifiable risk-factors and understanding more about these links may facilitate new opportunities for treating and preventing cancer and ensuring a long healthy lifespan.
Age and Space Irradiation Modulate Tumor Progression: Implications for Carcinogenesis Risk
A reduced capacity of middle-aged hosts to support the progression phase of carcinogenesis is demonstrated and molecular factors that contribute to HZE radiation modulation of tumor progression as a function of age are identified.
Evaluating the physiological reserves of older patients with cancer: the value of potential biomarkers of aging?
Cell senescence and aging in carcinogenesis and liver repopulation
A model of orthotopic cell transplantation was used to explore the basic question as to whether the contribution of aging to the risk of cancer is, at least in part, related to alterations in the tissue microenvironment, and it was found that exposure to RS is a powerful inducer of cell senescence in hepatocytes in vivo.
Polyphenols and aging.
While the mechanisms by which these effects occur are yet to be fully understood, it is evident that further investigation may yield a potential use for polyphenols as pharmacological interventions against specific age-associated diseases.
The Epigenetic Link between Polyphenols, Aging and Age-Related Diseases
This review summarizes recent advancements linking epigenetics, polyphenols and aging as well as critical findings related to the various dietarypolyphenols in different fruits and vegetables.
Phylogeny, regeneration, ageing and cancer: role of microenvironment and possibility of its therapeutic manipulation.
The probable role of micro environment in all the discussed phenomena such as healing/regeneration, inflammation, and cancer is discussed and targeting of microenvironment is consequently predicted as a possible therapeutic target where controlled manipulation may represent a new approach to the treatment of cancer patients.


The relationship between aging and carcinogenesis: a critical appraisal.
  • V. Anisimov
  • Medicine, Biology
    Critical reviews in oncology/hematology
  • 2003
Gerontology as oncology. Research on aging as the key to the understanding of cancer
This review considers two possible explanations for the exponential increase in most neoplasms in the elderly, arguing in favor of the idea that tumor progression proceeds at faster rates in older mice and older persons than in younger mice and younger persons.
The age of cancer
Experimental data indicate that the aged, cancer-prone phenotype might represent the combined pathogenetic effects of mutation load, epigenetic regulation, telomere dysfunction and altered stromal milieu.
Effect of host age on tumor growth rate in rodents.
  • V. Anisimov
  • Medicine
    Frontiers in bioscience : a journal and virtual library
  • 2006
Experimental data on the effect of aging on the growth of transplanted tumors are discussed, finding that age-associated changes in both humoral and local host factors are critical to the behavior and progression of transplants tumors in the old host.
Immunity, ageing and cancer
An overview of the impact of age on human immune competence is provided, emphasizing T-cell-dependent adaptive immunity, which is the most sensitive to ageing, and will pave the way for rational interventions to maintain or restore appropriate immune function not only in the elderly but also in the cancer patient.
On the role of aging in carcinogenesis.
It is suggested that "Age 1/2" is determined by host genes that may vary among tissues of tumor origin but are common to all people and is independent of the determinant of age-standardized rates.
Insulin: a novel factor in carcinogenesis.
The role of newer drugs that restore sensitivity to insulin, thereby reducing hyperinsulinemia, is an exciting potential area of cancer prevention and the potential role of insulin as a tumor growth factor is discussed.
Handbook of the Biology of Aging
Lower Organisms: Identification of Longevity, Neurobiological Correlates of Age-Related Cognitive Decline: Animal Models, and Mechanisms Controlling in Vitro Cellular Senescene.
Lesion biomarkers of aging in B6C3F1 hybrid mice.
This study suggests strongly that the prevalence of many individual lesions, the total lesion burden, and the total types of lesions are good biomarkers of aging because they increase with age and reflect the effect of CR in slowing the aging process.
Age-dependent regulation of the tumorigenic potential of neoplastically transformed rat liver epithelial cells by the liver microenvironment.
It is suggested that progressive alterations in the hepatic parenchyma with increasing age enabled tumor formation by providing a less suppressive microenvironment for expression of the tumorigenic phenotype.