Squamous cell carcinoma: the skin cancer that plays by different rules

July 19, 2026 · William S. Farmer, MD

Squamous cell carcinoma is the second of the three skin cancers people are usually told about, and it tends to get explained as a middle case: worse than basal cell carcinoma, not as bad as melanoma. That framing is not exactly wrong, but it misses what actually makes this diagnosis different, and it leaves out the two measurements that matter most.

Here is the honest version.

It is more common than most people assume

The usual teaching is that basal cell carcinoma is several times more common than squamous cell carcinoma. That holds up across the whole population, but it stops being true as skin gets older. In a nationwide analysis of Medicare data, basal cell and squamous cell carcinomas were treated at essentially identical rates, roughly 3,280 versus 3,278 procedures per 100,000 beneficiaries, a ratio of almost exactly one to one. [1]

So if you are older and sun-damaged, this is not the rarer diagnosis. It is a coin flip.

Where it comes from, and what “precancer” actually means

Most squamous cell carcinomas arise out of sun-damaged skin, often in or near an actinic keratosis: the rough, scaly, sandpapery spots that show up on scalps, ears, faces, forearms, and the backs of hands. Patients are told these are precancers, then told not to worry much about any individual one, and both statements are true at once in a way that is genuinely confusing.

Here is how I would put it. Most actinic keratoses go away on their own, and any single one has a low probability of turning into a skin cancer. But as soon as you have more than one, that probability starts to climb, and it keeps climbing with every additional spot. [3]

Two things go wrong when patients hear only the first half of that.

The first is a math error I hear constantly. The low probability belongs to each spot, not to you. Someone with two hundred actinic keratoses does not carry the risk of one actinic keratosis. They carry two hundred small risks running at the same time, which is a completely different situation.

The second is that almost nobody knows how many they have. When I hand a patient a mirror and point out what an actinic keratosis looks like, they can usually find four or five on their own face. Then we start treating, and thirty spots later we are not yet halfway done. This is not a failure of attention. These spots are easier to feel than to see, and they hide in plain sight on skin you have looked at every day for seventy years. It is also why I often recommend a cream that treats the whole sun-damaged area rather than freezing them one at a time: not because any single spot is dangerous, but because there are almost always far more of them than anyone expects.

What it looks like

• A scaly, crusted, or rough patch that may look like a stubborn dry spot but keeps returning after it flakes off.
• A firm nodule, sometimes with a hard central plug, that can grow noticeably over weeks rather than years.
• A sore that will not heal, on the lip, ear, scalp, forearm, or back of the hand.
• Tenderness. Basal cell carcinomas are often painless. Squamous cell carcinomas are frequently sore.

As with basal cell carcinoma, none of this is a mole, so the ugly duckling sign will not find it. Comparing your moles to each other tells you nothing about a scaly patch on your ear.

Three things that mean come in now

I want to be blunt about this section, because it is the part that changes outcomes.

• If a spot on your skin is tender, go and be seen. Do not wait. It does not matter if it is the smallest spot on your body, the flattest, or barely pink at all. Tender skin is not normal skin. Consider that an instruction rather than a suggestion.
• If a spot bleeds when you wash yourself, have it checked. Ordinary skin does not bleed during a shower.
• If a wound refuses to heal, have it checked, even when you know exactly what caused it.

That last point is where I lose the most time with patients, so let me explain the trap. Most people never notice a skin cancer until they catch it on a doorframe or a car door and it bleeds. The injury is what drew their attention, so the injury becomes the explanation. They arrive telling me, with complete sincerity, that it is only where they hurt themselves and not a skin cancer.

Those two things are not opposites. Skin cancers really can develop at the site of an injury, and the mechanism is straightforward: wounded skin has to heal, healing means cells dividing, and every cell division is another opportunity for a mistake that starts a cancer. It is also often true that the spot was already there and the injury is simply when you finally noticed it. Either way it needs looking at, so do not let the fact that you can explain it become the reason you stay home.

The two measurements that matter: depth and width

This is the real difference from basal cell carcinoma. Squamous cell carcinoma can spread to lymph nodes and beyond. The great majority never do, and what separates the two groups is not how alarming the spot looks. It is size, in both directions.

The way I explain it in the room:

• Basal cell carcinoma is the slow one that essentially does not spread.
• Melanoma is the frightening one, which starts attempting to spread once it grows beyond about a millimeter deep.
• Squamous cell carcinoma sits in between, and which one it resembles depends on its size. Under about 2 cm across, roughly three quarters of an inch, it tends to behave like a basal cell carcinoma. At around 2 cm and above, it starts behaving more like a melanoma, with a real probability of reaching a lymph node and of growing along nerves.

Depth. A prospective study of 615 patients found that tumors 2.0 mm thick or less did not metastasize at all in that cohort; between 2.1 and 6.0 mm about 4 percent did; and above 6.0 mm, 16 percent did. Immunosuppression, location on the ear, and larger surface size were the other independent risk factors. [2]

Width. The 2 cm threshold is not a rule of thumb, it is built into the staging systems used to grade these tumors, including the AJCC and the Brigham and Women’s Hospital system. [5] Crossing it moves a tumor into a higher-risk category, and the difference is visible in outcomes: in a large pooled analysis, squamous cell carcinomas larger than 2 cm recurred at 25.2 percent after Mohs surgery versus 41.7 percent after other treatments, compared with roughly 3 percent versus 11 percent for ordinary primary tumors. [4] Growth along nerves, called perineural invasion, is another feature that changes the plan substantially.

I include the actual numbers because they reframe the diagnosis. The question is not “does squamous cell carcinoma spread?” It is “was yours caught while it was still small?” For most people the answer is yes, and a thin, small, promptly treated squamous cell carcinoma has an excellent outlook. It also explains why waiting is the one genuinely costly decision here. These grow in both directions over months, and both directions count against you.

Who gets squamous cell carcinoma

Ultraviolet radiation. That is the answer, and it is not a close contest. Cumulative lifetime sun exposure is the reason these appear on scalps, ears, lips, forearms, and the backs of hands, and the reason they cluster in people who worked outdoors, lived in sunny places, or used tanning beds. If you have been told you have a lot of sun damage, that is the risk factor, and it is the one that produced the tumor.

Fair skin, age, prior radiation therapy, and certain chemical exposures add to that. So does a suppressed immune system, and it is worth explaining that one carefully, because it causes two opposite misunderstandings.

People on long-term immunosuppression, particularly organ transplant recipients, do have a substantially higher risk, and in that group squamous cell carcinoma predominates over basal cell rather than the other way around. It is not purely a matter of a weakened immune system either: some of the drugs involved appear to interfere directly with p53 signaling and DNA repair, which helps explain why this specific cancer is the one that surges. [6] If you take immunosuppressive medication for any reason, whether for a transplant, an autoimmune condition, or cancer treatment, say so explicitly at your visit. It usually means being seen every three to six months rather than annually.

But if that does not describe you, please do not read this section either of the two wrong ways. A normal immune system does not protect you from squamous cell carcinoma, and the great majority of the people I treat have one. Equally, being diagnosed with a squamous cell carcinoma is not evidence that something is wrong with your immune system and does not mean you need it investigated. Most of these tumors are the result of ordinary sun exposure accumulated over an ordinary life.

The treatment options, side by side

The options mirror those for basal cell carcinoma, with one important difference noted in the table: creams have a much narrower role here.

Option	What it actually is	Mainly used for	Recurrence	Scar
ED&C (electrodesiccation and curettage, or “scrape and burn”)	The spot is scraped out and the base burned, usually repeated a few times in one visit. No stitches.	Primarily superficial, low-risk tumors, usually somewhere other than the face	Higher than surgery	A wide, round, burn-like scar, noticeably larger than the original spot.
Prescription topical cream	A cream you apply at home over weeks. No cutting.	Actinic keratoses and squamous cell carcinoma in situ only. Not appropriate for invasive squamous cell carcinoma.	Not applicable to invasive tumors	No cut. See the warning below.
Standard excision (wide local excision, WLE)	The tumor is cut out with a margin of normal skin. The specimen goes to a lab and margins are reported days later.	Many tumors in lower-risk locations	About 11% for primary tumors of the skin and lip	Larger than Mohs, because extra normal skin is deliberately removed.
Mohs micrographic surgery	Removed one thin layer at a time, with 100% of the margin read on site during the visit.	Face, ears, lips, hands; large or recurrent tumors; perineural invasion; immunosuppressed patients	About 3% for primary tumors of the skin and lip	The smallest, because very little normal skin is taken.
Radiation	Repeated treatments, commonly 30 or more visits over roughly six to eight weeks.	People who genuinely cannot have surgery, and in some cases after surgery for high-risk tumors	Varies with tumor and technique	Wide, and it continues to change over years.
Doing nothing (active monitoring)	Watch it. Treat only if it starts to cause a problem.	A narrower option than in basal cell carcinoma, because these can spread. Considered mainly for frail patients with limited life expectancy.	Not applicable	None

Why you cannot just try the gentle option first

The same warning applies here as with basal cell carcinoma, and it applies more sharply, because this is a cancer that can spread.

Surface treatments treat the surface. If a tumor has depth and it is treated as though it does not, the skin on top heals over and looks entirely normal while the part that was never reached keeps growing underneath. There is nothing to see and no reason to come back, which is exactly why this is more dangerous than a treatment that plainly fails. And with squamous cell carcinoma, the thing growing quietly under normal-looking skin is a tumor that gets more capable of reaching a lymph node as it gets bigger.

The distinction between in situ and invasive comes from your pathology report, which is worth learning to read. This is why the table draws a hard line at creams: they have a real role for actinic keratoses and for squamous cell carcinoma in situ, where the abnormal cells genuinely are confined to the surface, and no role at all for an invasive tumor.

Which of these is right for a given tumor turns on more than where it sits. I have set out what actually drives that choice in when Mohs surgery is the right choice.

What happens if there is a risk it has spread

For most squamous cell carcinomas, removal is the whole story and nothing further is needed. For a minority, the features above, meaning thickness, size over 2 cm, growth along nerves, location, or immunosuppression, put a tumor into a higher-risk category where more than skin needs to be considered.

When that happens, your skin specialist will bring in other cancer specialties: medical oncology, radiation oncology, surgical oncology, and sometimes others depending on where the tumor is and what it is near. If that happens to you, understand that it does not automatically mean the situation is dire. Sometimes those referrals are genuinely necessary, and sometimes they are an abundance of caution. Both are appropriate, and you are entitled to ask which one you are dealing with.

Which patients need which referral is set out in national guidelines that are revised frequently as evidence changes. Keeping current with them is part of your skin specialist’s job, and it is a real part of it: the thresholds move. Every patient and every tumor is different, and the decision has to account for all of the factors together rather than any single one.

After one

As with basal cell carcinoma, the strongest predictor of a future skin cancer is having had one. Surveillance every six months is typical after a first squamous cell carcinoma, and every three to six months if you are immunosuppressed. The skin that produced one tumor has the same history everywhere else, and treating the surrounding sun damage rather than only the tumor reduces what has to be dealt with later.

The bottom line

Squamous cell carcinoma can spread, which makes it more serious than basal cell carcinoma, and the great majority never do, which makes it far less frightening than the word “spread” suggests. Size is the hinge, in both depth and width, and size is a function of time.

Which makes the practical advice unglamorous and specific. A scaly patch that keeps coming back, a spot that is tender, a spot that bleeds in the shower, or a sore that has not healed in a month or two is worth showing someone. Not because it is likely to be dangerous, but because the entire difference between an easy version of this and a hard one is measured in millimeters, and those millimeters accumulate while you wait.

References

1. Rogers HW, Weinstock MA, Feldman SR, Coldiron BM. Incidence estimate of nonmelanoma skin cancer (keratinocyte carcinomas) in the U.S. population, 2012. JAMA Dermatol. 2015;151(10):1081-1086. doi:10.1001/jamadermatol.2015.1187
2. Brantsch KD, Meisner C, Schönfisch B, et al. Analysis of risk factors determining prognosis of cutaneous squamous-cell carcinoma: a prospective study. Lancet Oncol. 2008;9(8):713-720. doi:10.1016/S1470-2045(08)70178-5
3. Criscione VD, Weinstock MA, Naylor MF, et al. Actinic keratoses: natural history and risk of malignant transformation in the Veterans Affairs Topical Tretinoin Chemoprevention Trial. Cancer. 2009;115(11):2523-2530. doi:10.1002/cncr.24284
4. Rowe DE, Carroll RJ, Day CL Jr. Prognostic factors for local recurrence, metastasis, and survival rates in squamous cell carcinoma of the skin, ear, and lip. Implications for treatment modality selection. J Am Acad Dermatol. 1992;26(6):976-990. doi:10.1016/0190-9622(92)70144-5
5. Karia PS, Jambusaria-Pahlajani A, Harrington DP, Murphy GF, Qureshi AA, Schmults CD. Evaluation of American Joint Committee on Cancer, International Union Against Cancer, and Brigham and Women’s Hospital tumor staging for cutaneous squamous cell carcinoma. J Clin Oncol. 2014;32(4):327-334. doi:10.1200/JCO.2012.48.5326
6. Wheless L, Jacks S, Mooneyham Potter KA, Leach BC, Cook J. Skin cancer in organ transplant recipients: more than the immune system. J Am Acad Dermatol. 2014;71(2):359-365. doi:10.1016/j.jaad.2014.02.039

Magnolia Forge Dermatology is coming to Raleigh, North Carolina. We are not yet scheduling appointments.

Medical content: William S. Farmer, MD · Last reviewed: July 2026