What Happens Inside the Body When Skin Cancer Develops?

When people think about skin cancer, they usually think about the sun. But skin cancer actually begins much deeper — inside our cells.

Our skin cells grow and divide in a very controlled way. Special genes act like instructions. Some tell cells when to grow, and others tell them when to stop. There are also “repair” genes that fix damaged DNA. One important gene is called p53. It checks if a cell’s DNA is damaged. If the damage is too serious, it tells the cell to destroy itself (Wang et al.). This prevents unhealthy cells from spreading.

Skin cancer can start when these control systems stop working properly. If genes like p53 become damaged, cells with mistakes in their DNA may continue to divide instead of being removed. Over time, more and more mutations build up. Eventually, the cells begin growing out of control — this is cancer.

In melanoma, a common mutation happens in a gene called BRAF. When this gene changes, it can send constant “grow” signals to the cell, even when the body doesn’t need new cells. This causes fast and uncontrolled cell growth. The immune system also plays an important role (Castellani et al.). Normally, immune cells can recognize and destroy abnormal cells. But cancer cells sometimes develop ways to hide from the immune system, allowing them to survive and spread.

Not all mutations come from sunlight. Sometimes DNA mistakes happen naturally when cells divide. Our bodies usually fix these errors, but if too many build up, cancer can develop. In simple terms, skin cancer happens when the body’s “stop” signals fail and damaged cells keep multiplying. Understanding what goes wrong inside the cell helps scientists create better treatments that target these specific problems.

Skin cancer isn’t just about damaged skin on the outside — it’s about tiny changes inside cells that slowly grow into something much bigger.

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Citations

Bieging, Kathryn T., et al. “Unravelling Mechanisms of P53-Mediated Tumour Suppression.” Nature Reviews Cancer, vol. 14, no. 5, 17 Apr. 2014, pp. 359–370, pmc.ncbi.nlm.nih.gov/articles/PMC4049238/, https://doi.org/10.1038/nrc3711. Accessed 21 Feb. 2026.

‌Ozaki, Toshinori, and Akira Nakagawara. “Role of P53 in Cell Death and Human Cancers.” Cancers, vol. 3, no. 1, 3 Mar. 2011, pp. 994–1013, pmc.ncbi.nlm.nih.gov/articles/PMC3756401/, https://doi.org/10.3390/cancers3010994. Accessed 22 Feb. 2026.

Wang, Haolan, et al. “Targeting P53 Pathways: Mechanisms, Structures and Advances in Therapy.” Signal Transduction and Targeted Therapy, vol. 8, no. 1, 1 Mar. 2023, www.nature.com/articles/s41392-023-01347-1, https://doi.org/10.1038/s41392-023-01347-1. Accessed 22 Feb. 2026.

MedlinePlus. “TP53 Gene: MedlinePlus Genetics.” Medlineplus.gov, 2018, medlineplus.gov/genetics/gene/tp53/. Accessed 22 Feb. 2026.

Castellani, Giorgia, et al. “BRAF Mutations in Melanoma: Biological Aspects, Therapeutic Implications, and Circulating Biomarkers.” Cancers, vol. 15, no. 16, 8 Aug. 2023, p. 4026, pmc.ncbi.nlm.nih.gov/articles/PMC10452867/, https://doi.org/10.3390/cancers15164026. Accessed 24 Feb. 2026.

‌Haghighi, Anna Smith. “What Does a BRAF Mutation in Melanoma Mean?” Medicalnewstoday.com, Medical News Today, 23 June 2022, www.medicalnewstoday.com/articles/braf-mutation-melanoma. Accessed 22 Feb. 2026.