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| Illustration of cell | source: National Cancer Institute/unsplash |
I wrote this article following a surprising news report that researchers in South Korea have discovered a new method for treating cancer. This is undoubtedly a promising development, and I believe further advancement is needed in cancer treatment through more targeted therapeutic approaches. However, the question that crossed my mind was: is cancer really caused by external factors, or has it always been within us?
Therefore, before discussing cancer treatment theories from a biotechnology perspective, I felt compelled to share some insights about cancer itself.
What is Cancer?
Cancer is a disorder where certain body cells undergo uncontrolled proliferation and become toxic. Cancer cells can invade healthy cells, leading to abnormal cell division and spreading throughout the body via blood vessels in a process known as metastasis. Hence, the medical field categorizes cancer into stages 0 to IV, depending on its severity and spread.
Stage 0, also called carcinoma in situ, is the initial phase where abnormal cells begin to form but remain localized and treatable. Stage I indicates localized growth. Stages II and III suggest larger growth, with stage III showing invasive spread, possibly affecting lymph nodes. Stage IV marks metastasis, meaning the cancer has spread to distant parts of the body.
Given that cancer stems from abnormal cell growth, the key question is: what triggers this abnormal growth? Can it occur spontaneously or be caused by something external?
The Presence of Cancer Potential in the Human Body
What’s interesting is that the human body inherently carries the potential for cancer. This doesn’t mean we're born with cancer, but we carry certain genes that, when mutated, can lead to cancer. Think of these genes as switches that control cell growth. When the switch malfunctions, cell division may proceed uncontrollably.
Every biological activity in our body is controlled by DNA, organized into functional units called genes. These genes regulate when and how cells divide, grow, and die. Under normal conditions, the body strictly maintains this balance. But when mutations occur in these genes, uncontrolled cell growth can happen—this is the origin of cancer.
There are two main gene groups involved: oncogenes and tumor suppressor genes. Proto-oncogenes are normal genes that support cell growth. When mutated or overactive, they become oncogenes, continuously signaling cells to divide—like a car with a stuck accelerator.
In contrast, tumor suppressor genes act like brakes, preventing the growth of abnormal cells. One key suppressor gene is TP53, which produces the p53 protein. This protein can detect DNA damage and either halt the cell cycle to allow repair or trigger apoptosis if the damage is too severe.
If genes like TP53 are mutated and lose function, damaged cells may grow unchecked. If oncogenes are simultaneously activated, this can lead to the formation of tumors and ultimately cancer.
Mutations may be inherited (hereditary) or acquired over a lifetime. Hereditary mutations, passed down from parents, are present from birth. For example, BRCA1 and BRCA2 mutations increase the risk of breast and ovarian cancer.
Acquired mutations, however, result from environmental or lifestyle factors (epigenetics), such as radiation exposure, carcinogens in tobacco, certain viral infections (like HPV), high-fat diets, stress, and physical inactivity.
Importantly, not all mutations cause cancer. Our bodies have sophisticated DNA repair systems that often correct damage before it becomes a problem. However, when mutations accumulate or the repair system itself fails (due to defects in genes like MLH1 or MSH2), cancer risk increases significantly.
According to the National Cancer Institute, only 5–10% of cancers are hereditary; the remaining 90–95% are acquired during our lifetime. This highlights the importance of healthy lifestyles and environmental protection in cancer prevention.
The Role of Epigenetics in Cancer
Recent developments in epigenetics reveal that cancer doesn't always stem from DNA mutations. Epigenetic changes—such as DNA methylation, histone modification, and regulation by non-coding RNA—can alter gene expression without changing DNA sequences. For example, hypermethylation of a tumor suppressor gene promoter can silence the gene, even if the DNA remains structurally intact. It’s like switching off a gene without cutting the wire.
Self-Awareness and Early Detection
Recognizing that cancer is rooted in genetic and regulatory changes has shifted modern medicine from merely killing cancer cells to restoring proper gene expression. This includes gene therapy, epigenetic drugs, and targeted molecular treatments. We are entering a new era of cancer therapy—more personalized, specific, and hopefully more effective.
Genetic testing is also gaining importance, especially for those with a family history of cancer. It helps identify whether someone carries mutations that increase cancer risk, allowing early preventive actions.
So, cancer-related genes do exist in our bodies—in their normal form. They only become dangerous when DNA structure changes due to mutations or epigenetic modifications, making them dysfunctional. These changes can trigger uncontrolled cell growth, the hallmark of cancer.
DNA methylation, specifically the addition of methyl groups (–CH₃) to CpG islands (often found in gene promoters), can suppress gene expression. This is particularly critical when tumor suppressor gene promoters are hypermethylated. In such cases, even without mutations, the gene remains silent (Esteller, 2008; Costa et al., 2023), failing to produce the proteins needed to stop cancer development.
Fortunately, our bodies are equipped with natural mutation repair systems. But over time, with age and exposure to risk factors (smoking, stress, poor lifestyle), this system can degrade. The combination of accumulated mutations and failed monitoring systems leads to cancer.
Don’t Panic—Be Proactive
Despite being life-threatening, cancer doesn’t appear overnight. It takes years for mutations to build up and form malignant tumors. This is why early detection is crucial. Identifying abnormal cells early greatly improves treatment outcomes (Hanahan, 2022). This article aims to raise awareness and familiarize readers with the basics of cancer.
Thanks to technological advances, scientists can now sequence the entire genome of cancer cells to identify specific mutations. This precision medicine approach allows for tailored therapies based on the genetic profile of each patient. DNA sequencing, in this context, is like a philologist decoding ancient texts.
With DNA sequencing and genetic analysis, researchers can pinpoint specific mutation patterns. This enables targeted therapy, which uses drugs that act specifically on the defective pathways in a patient’s cancer (Yu et al., 2024). A prime example is imatinib, used for chronic myeloid leukemia, which targets the BCR-ABL fusion protein resulting from the Philadelphia chromosome abnormality (Druker et al., 2001).
Conclusion
Cancer doesn’t strike from nowhere—it results from internal failures in our cellular growth control systems. Genes like proto-oncogenes and tumor suppressor genes exist in all of us. They work like switches that turn on and off precisely. But when those switches are damaged by mutations or epigenetic interference, uncontrolled cell growth occurs.
Understanding cancer as a result of internal mechanisms opens huge possibilities in prevention, early detection, and treatment. It marks the path toward precision medicine, where therapies are tailored to each individual's genetic makeup.
References:
Capp, J.-P., Aliaga, B., & Pancaldi, V. (2024). Evidence of epigenetic oncogenesis: a turning point in cancer research. arXiv. https://arxiv.org/abs/2411.14130
Cercek, A., et al. (2025). A New Immune Treatment May Work Against Several Cancer Types. Time. https://time.com/7280610/cancer-immunotherapy-dostarlimab-andrea-cercek/
Costa, P. M. da S., et al. (2023). Epigenetic reprogramming in cancer: From diagnosis to treatment. Frontiers in Cell and Developmental Biology, 11, 1116805. https://doi.org/10.3389/fcell.2023.1116805
Druker, B. J., Talpaz, M., Resta, D. J., Peng, B., Buchdunger, E., Ford, J. M., ... & Sawyers, C. L. (2001). Efficacy and safety of a specific inhibitor of the BCR-ABL tyrosine kinase in chronic myeloid leukemia. New England Journal of Medicine, 344(14), 1031-1037. https://doi.org/10.1056/NEJM200104053441401
Esteller, M. (2008). Epigenetics in cancer. New England Journal of Medicine, 358(11), 1148-1159. https://doi.org/10.1056/NEJMra072067
Hanahan, D. (2022). Hallmarks of cancer: New dimensions. Cancer Discovery, 12(1), 31–46. https://doi.org/10.1158/2159-8290.CD-21-1059
Jin, N., et al. (2021). Advances in epigenetic therapeutics with focus on solid tumors. Clinical Epigenetics, 13(1), 83. https://doi.org/10.1186/s13148-021-01069-7
Keshari, S., Barrodia, P., & Singh, A. K. (2023). Epigenetic Perspective of Immunotherapy for Cancers. Cells, 12(3), 365. https://doi.org/10.3390/cells12030365
Levine, A. J. (1997). p53, the cellular gatekeeper for growth and division. Cell, 88(3), 323–331. https://doi.org/10.1016/S0092-8674(00)81871-1
Martin, C., & Zhang, Y. (2025). Epigenetic drugs in cancer therapy. Cancer and Metastasis Reviews. https://doi.org/10.1007/s10555-025-10253-7
Miki, Y., Swensen, J., Shattuck-Eidens, D., Futreal, P. A., Harshman, K., Tavtigian, S., ... & Skolnick, M. H. (1994). A strong candidate for the breast and ovarian cancer susceptibility gene BRCA1. Science, 266(5182), 66–71. https://doi.org/10.1126/science.7545954
Yu, X., et al. (2024). Cancer epigenetics: From laboratory studies and clinical trials to precision medicine. Cell Death Discovery, 10(1), 28. https://doi.org/10.1038/s41420-024-01803-z
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