A foreign invader—virus, infection—all might pose formidable threats to the human body, but a self-destructive threat might be lurking closer to home: cancer. Cancer often develops as the result of a buildup of genetic mutations that can cause healthy cells to turn aberrant. Aberrant cells tend to divide and proliferate rapidly, disregarding the body’s natural checkpoints for controlled cell growth.
A Genetic Problem?
An accumulation of genetic mutations can set off cancer in the body, but how do such mutations even start? Exposure to outside carcinogens or cancer-causing substances, cancer-causing viruses and even errors in DNA replication and cellular processes can all lead to genetic mutations. Common carcinogens include UV light, asbestos, and tobacco smoke. As much of a risk as exposure to carcinogens presents, an equal or greater risk is posed by errors in the body’s cellular processes (Hutter, 2024). The body has inherent checks in place for errors that occur in DNA replication, however, sometimes these go unnoticed. For example, when DNA is not replicated properly it can lead to mutations in important genes necessary for maintaining healthy cells.
Errors in DNA replication can range from small mistakes like missense mutations that consist of single nucleotide changes or larger mistakes like nonsense mutations that result in premature signaling that stops protein production. Researchers for years have been studying mutations in the p53 tumor suppressor gene that correlates with the development of many common cancers. TP53 is a gene on chromosome 17 that plays an important role in regulating cell division and regulates the production of the p53 protein (National Cancer Institute, 2011). Therefore, mutations in the TP53 gene often lead to uncontrolled cellular proliferation. Mutations in p53 have been observed in so many types of cancers that it has established itself as a key hallmark of cancer.
Confronting Cancer
We know some of the underlying causes of cancer, and now what can we do to treat it? In studying the causes of genetic mutations, researchers have come to understand more about the mechanisms behind cancer development. Taking p53 as an example, researchers have come to learn its role in cancer development and its role in preventing and even treating cancers. Currently, researchers are working on developing gene therapies that target the damaged TP53 gene and work to restore its normal function.
Cancer research has come a long way since it had originally taken root, yet there is still much more to learn and explore. By harnessing the power of the human genome, one day, cancer will be defeated.
References
Hutter, C. M. (2024, August 10). Carcinogen. Genome.gov. https://www.genome.gov/genetics-glossary/Carcinogen#:~:text=Definition
National Cancer Institute. (2011, February 2). https://www.cancer.gov/publications/dictionaries/cancer-terms/def/tp53-gene. Www.cancer.gov. https://www.cancer.gov/publications/dictionaries/cancer-terms/def/tp53-gene