Cancer is so often a disease of older people that a whole medical field, “oncogeriatrics,” exists to address the topic. Deeper understanding of the links between cancer and aging could lead to better treatments. Here, our Curious Dr. George asks Cancer Commons Clinical Scientist Kaumudi Bhawe, PhD, about the relationship between cancer and aging processes that occur in individual cells in our bodies—throughout our lives.
Curious Dr. George: As a molecular biologist, you have worked with many forms and elements of cancer cells. Are there any similarities between the processes of cellular aging and the development of cancer?
Dr. Bhawe: Cancer is a disease of aging. According to the National Cancer Institute (NCI), cancer incidence increases dramatically after age 50, with the median age of people diagnosed with cancer in the United States being 66. While chronological age is definitely a cause of cellular aging, it is not the only cause. In fact, the process of cellular aging is known to happen in cells right from the time a human embryo is still developing. What then, exactly, is cellular aging, and what does it have to do with cancer? This is a timely question with the recent publication of a paper in the scientific journal Cancer Discovery entitled “Hallmarks of Cancer: New Dimensions.” This article highlights aging—or “senescent”—cells as one of the newly acknowledged enabling characteristics of all cancers.
Aging cells can be defined by accumulated damage to the macromolecules, such as DNA and proteins, that are important for the cells to maintain themselves, to grow, and to divide. Certain molecules in a cell, are involved in a mechanism that surveys and repairs DNA damage each time the cell undergoes division. If there is more damage than can be repaired, an aging cell either dies or cannot divide, and goes into what is called irreversible cell-cycle arrest. The above-mentioned mechanism ensures that cells with faulty macromolecules are not increasing in number, and in this sense, it is a disease-preventing mechanism. For a very detailed overview of the DNA-damage-response mechanism and its relevance to cancer, you can read this scientific review article that was published last year.
However, once an aging cell enters irreversible cell-cycle arrest, it can stay alive for quite some time; up to months, as demonstrated by lab-based research. Not only can it stay alive, it can also evolve based on the cues it is receiving from its environment, and importantly, it can alter the very environment it finds itself in. It has been discovered that such senescent cells have an abnormal metabolism and secrete hundreds of different signaling molecules including proteins and lipids. Readers interested in learning more about this exciting field of study can start with this article from the scientific journal Communications Biology and this video from the news site Technology Networks.
Some of the ways in which cells can be induced to undergo aging/senescence include the slow natural aging caused by going through multiple cell-cycles, leading to telomere shortening, exposure to toxic chemicals (including chemotherapy) and radiation, exposure to reactive oxygen species (ROS), and activation of cancer-causing genes (oncogenes). So, you can see that as a cancerous tumor is forming, or even during treatment, senescence mechanisms are at work in at least some of the cancer cells as well as some of the non-cancerous surrounding (stromal) cells, such as fibroblasts, blood-vessel-forming cells, and immune cells.
Three key common features shared between aging cells and cancer-developing cells are:
1) accumulation of DNA defects
2) altered metabolic activity, and
3) an increase in secretion of environment-modulating molecules.
The current challenge lies in discovering and cataloging the specific details of each of these three features in order to identify true molecular similarities, differences, antagonism, and cooperation between the processes of aging and cancer. The NCI funds initiatives for cancer and aging research at premier institutes across the U.S. in the hopes of addressing this challenge and developing new, better strategies for cancer prevention and treatment.
Dr. Bhawe can be reached at firstname.lastname@example.org.
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