SCC stands for squamous cell carcinoma, a type of cancer that develops in the flat, thin cells lining the outer layer of your skin and several internal organs. It’s the second most common skin cancer, accounting for roughly 20% of all skin cancers, and about 90% of non-melanoma skin cancers are linked to ultraviolet radiation exposure. While the skin version gets the most attention, SCCs also develop in the lungs, esophagus, head and neck, cervix, and other organs lined with squamous tissue.
Where SCC Starts in the Body
Squamous cells are flat, scale-like cells that make up the surface layer of your skin and the lining of many hollow organs. In your skin, the outermost layer (the epidermis) is built from these cells stacked in layers. At the bottom of that stack sit basal cells, which constantly divide to produce new squamous cells that migrate upward. SCC begins when these basal cells accumulate genetic mutations that cause them to grow uncontrollably instead of maturing normally.
This isn’t a single event. SCC develops through a multistep process where mutations pile up over time, first creating precancerous patches and eventually progressing to invasive cancer. The most commonly affected gene is p53, a tumor suppressor that normally stops damaged cells from multiplying. When UV light or other carcinogens knock out p53, cells lose that safety brake.
Though skin SCC is the most familiar form, the same basic process can happen wherever squamous tissue exists. Lung SCC is strongly tied to tobacco smoke. Esophageal SCC has distinct genetic patterns, particularly in Asian populations, where unique mutations not seen in other SCC types have been identified. Head and neck SCCs are frequently driven by HPV infection or a combination of smoking and alcohol use. Cervical SCC is almost entirely caused by HPV.
What Skin SCC Looks Like
Cutaneous SCC doesn’t have one signature appearance, which is part of what makes it tricky to spot. It can show up as a firm bump (nodule) that may be skin-colored, pink, red, brown, or black depending on your skin tone. It can also appear as a flat sore with a scaly, crusty surface, a rough patch on the lip that develops into an open sore, or a new raised area on an old scar. Some lesions look wartlike, particularly on the genitals or around the anus. Sores inside the mouth can also be SCC.
The common thread is that these spots don’t heal. A sore that crusts over, seems to improve, then returns, or a rough patch that persists for weeks, deserves attention. SCC most often appears on sun-exposed areas: the face, ears, scalp, backs of the hands, and forearms. But it can develop anywhere on the body, including areas that rarely see sunlight.
Causes and Risk Factors
Ultraviolet radiation is the dominant cause of skin SCC. UVB rays, which make up only 1 to 2% of the UV light reaching the earth’s surface, are the primary carcinogen. They damage DNA directly by creating abnormal bonds between DNA building blocks. When the cell’s repair machinery can’t fix these errors, the mutations become permanent and accumulate with each additional exposure. This is why SCC risk correlates so strongly with cumulative lifetime sun exposure, not just sunburns.
Fair skin, a history of frequent sunburns, and long-term outdoor work or tanning bed use all raise risk substantially. But the single biggest risk factor is a weakened immune system. Solid organ transplant recipients, who take medications to suppress their immune systems for life, face up to 200 times the risk of developing skin SCC compared to the general population. People with chronic lymphocytic leukemia have roughly a 3.7-fold increase, and those with HIV face about a 2.8-fold increase. The immune system normally detects and destroys cells with cancerous mutations, so when that surveillance is suppressed, SCC can develop faster and behave more aggressively.
Precancerous Patches: Actinic Keratosis
Most skin SCCs don’t appear out of nowhere. They often start as actinic keratoses, rough, scaly patches caused by years of sun damage. These are not yet cancer, but they sit on the path toward it. A secondary analysis of a randomized clinical trial found that the four-year risk of an actinic keratosis area progressing to invasive SCC was 3.7% overall. That number climbs dramatically with severity: for thick, advanced actinic keratoses, the four-year risk reached nearly 21%, and for severe cases that needed repeat treatment, it was as high as 33.5%.
This is why dermatologists treat actinic keratoses proactively with freezing, topical creams, or light-based therapies rather than waiting to see what happens. Catching and treating these precancerous spots is one of the most effective ways to prevent SCC from developing in the first place.
How SCC Is Treated
The good news is that most skin SCCs caught early are highly curable. The five-year relative survival rate for cutaneous SCC is about 93.5%, and for localized tumors that haven’t spread, outcomes are even better.
Standard treatment for most skin SCCs is surgical removal. For straightforward cases, the surgeon cuts out the tumor along with a margin of healthy tissue and sends it to a lab to confirm clear edges. For SCCs on the face, ears, or other areas where preserving tissue matters, or for tumors that have recurred, Mohs micrographic surgery is the preferred approach. During Mohs, the surgeon removes thin layers of tissue one at a time, examining each layer under a microscope immediately, and stops only when no cancer cells remain at the margins. This technique achieves cure rates greater than 94% for SCC while removing the least amount of healthy skin possible.
Small, superficial SCCs can sometimes be treated without traditional surgery, using methods like freezing, scraping, or topical medications. Radiation therapy is another option when surgery isn’t practical, such as for older patients or tumors in difficult locations.
When SCC Is Advanced
A small percentage of skin SCCs grow deep, spread to lymph nodes, or metastasize to distant organs. These advanced cases require systemic treatment. In 2018, the FDA approved the first immunotherapy specifically for advanced cutaneous SCC. This treatment is a checkpoint inhibitor, a type of drug that essentially removes a “don’t attack” signal that cancer cells use to hide from the immune system. Once that signal is blocked, the body’s own immune cells can recognize and fight the tumor.
Immunotherapy has changed the outlook for patients with advanced SCC who previously had limited options. It’s given intravenously and works best in patients whose tumors aren’t suitable for surgery or radiation. For SCC in other organs like the lungs or esophagus, treatment plans typically involve combinations of surgery, radiation, chemotherapy, and immunotherapy depending on the stage and location.
Who Gets SCC Most Often
SCC is significantly more common in men than women, with men developing it at roughly double the rate. This likely reflects historical differences in occupational sun exposure and sun protection habits. Incidence rises sharply with age, and the rates are climbing globally as populations age and cumulative UV exposure increases.
People who are immunosuppressed represent a uniquely vulnerable group. For organ transplant recipients specifically, SCC often behaves more aggressively, tends to recur more frequently, and is more likely to spread. These patients typically need more frequent skin checks, sometimes every three to six months, and more aggressive treatment of precancerous spots to stay ahead of the disease.