Aging is integral to the causation of many cancers and also impacts on treatment response, prognosis, treatment allocation, and treatment tolerance. Aging interacts with cancer in a range of ways: some of the molecular pathways and causes of aging and the pathways and causes of cancer overlap significantly. Cancer is more common in older age groups with predictions of substantial increases in the next 15 years of approximately 50% in developed countries, (largely due to the increase in the older population), and even higher in developing and middle income countries. One such age-related condition is cancer. As a result almost 50% of over 75s have 2 or more chronic health conditions. Consequently, life-span has outpaced health-span, as the burden of chronic health conditions has increased in this older population. This increase in lifespan has been accompanied by an increase in rates of chronic disease. The oldest old group of over 85 year olds is also predicted to double over the same period, from 2 to 4%. Consequently, the global proportion of people over 65 is predicted to increase from 18% now to 26% in 2041. In the western world, life-expectancy has doubled in the past 200 years and, whilst most of the early gains were in childhood longevity, in the past 70 years the majority of gains have been in older people. This article provides a review of these issues. Senolytic drugs include quercetin, navitoclax, and fisetin and preclinical and early phase clinical data are emerging of their potential role in cancer treatments, although none are yet in routine use clinically. A new group of drugs, senotherapies, (drugs which interact with senescent cells to interfere with their pro-aging impacts by either selectively destroying senescent cells (senolytic drugs) or inhibiting their function (senostatic drugs)) are under active investigation to determine whether they can enhance the efficacy of cancer therapies and improve resilience to cancer treatments. However, senescence may contribute to reduced patient resilience to cancer therapies and may provide a pathway for disease recurrence after cancer therapy. It may also be a key effector mechanism of many types of anticancer therapies, such as chemotherapy, radiotherapy, and endocrine therapies, both directly and via bioactive molecules released by senescent cells that may stimulate an immune response.
Senescence is generally regarded as a tumour suppressive process, both by preventing cancer cell proliferation and suppressing malignant progression from pre-malignant to malignant disease.
Cellular senescence is a key component of human aging that can be induced by a range of stimuli, including DNA damage, cellular stress, telomere shortening, and the activation of oncogenes.
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