Condition

Squamous Cell Carcinoma

Squamous cell carcinoma is the second most common skin cancer. It usually appears as a rough, scaly or crusted bump on skin that has had years of sun, and it often looks like a sore that will not heal. Found early it is removed and cured. Left alone it grows deeper, and a small share spread.
Dr. Schwarz, MD · Board-certified dermatologistLast reviewed September 8, 2026
16:9 hero for Squamous Cell Carcinoma. Never cropped: the tone strip and the corner logo depend on the full frame.

Start here

A spot that has not healed in a month needs to be looked at - not watched, looked at. Squamous cell carcinoma almost never announces itself, and what turns up in clinic is a rough patch that bleeds when you shave, a scab that keeps returning in the same place, a tender bump on the ear. People are not ignoring something dramatic, they are being reasonable about something minor-looking, and that is the problem. A biopsy is small - a few minutes, some numbing, a stitch or two - while the surgery after a delayed diagnosis is not, and almost every large, complicated removal I have been part of started as something the patient had been keeping an eye on for a year.

— Dr. Schwarz, Board Certified Dermatologist

Key Facts

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How commonThe second most common skin cancer, after basal cell carcinoma. Hundreds of thousands of cases are treated in the United States each year
Who gets itMost often adults over 50 with years of accumulated sun exposure. Risk is much higher for people taking medicines that suppress the immune system, including organ transplant recipients
Curable or managedCurable in the large majority of cases when it is found and removed early. It does not go away on its own and it is not something to watch and wait on
Prescription neededIt is diagnosed by biopsy and treated with a procedure rather than a cream. Some very early forms can be treated with a prescription cream
Time to improveThe spot is usually removed in a single visit, and the wound takes about two to four weeks to heal

What It Is

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Squamous cell carcinoma is a cancer of the flat cells that make up the outer layer of skin, called squamous cells or keratinocytes. It is the second most common skin cancer, after basal cell carcinoma.

It usually looks like a firm, rough, scaly bump or a thickened patch, often pink or red on lighter skin and brown, gray or violet on deeper skin tones. It may have a central crust, a hard horn-like plug of keratin, or an open sore, and it bleeds easily. Two features recur: it does not heal, and it returns in exactly the same place after seeming to scab over.

Most appear where sun lands for decades - face, ears, lips, scalp on people with thinning hair, neck, backs of the hands, forearms and lower legs. They are often tender, which separates them from a harmless growth.

There is a path leading up to it. Years of sun damage produce actinic keratoses, rough precancerous patches. Some progress to squamous cell carcinoma in situ, also called Bowen disease, where abnormal cells fill the top layer but have not broken through. When they break into the deeper layer, it is invasive. Not every one follows that sequence, but many do, which is why the earlier steps are worth treating.

A fast-growing variant, keratoacanthoma, comes up over weeks as a dome-shaped bump with a central plug. It can shrink on its own, but it is treated as a squamous cell carcinoma because it cannot reliably be told apart from one.

Most stay where they started and are cured by removal. A small percentage spread, usually first to a nearby lymph node. The risk is higher for tumors that are large, deep, on the ear or lip, growing back after treatment, or in someone immunosuppressed. The cancer is common enough that this small percentage adds up to a meaningful number of deaths each year.

Symptoms

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A rough patch that will not heal

Scaly Red Patch

A persistent scaly, red or brown patch that flakes, cracks or bleeds and does not settle over weeks. It usually sits on sun-exposed skin such as the face, ears, scalp, forearms or hands. Anything that has not healed in a month deserves attention.
A hard growing lump

Firm Nodule

A firm, raised lump that grows over weeks to months, often tender, sometimes with a crusted or ulcerated top. It can grow quickly. Rapid growth is a reason to be seen sooner rather than later.
An ulcer that comes back

Sore That Keeps Returning

An open sore that scabs, appears to heal and then breaks down again in the same place. Long-standing scars, burns and chronic wounds are higher-risk sites. Repeat breakdown in one spot is the pattern to watch for.

Where It Shows Up

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Front view of a head with red marks across the scalp and forehead, on both ears, on the nose, on both cheeks, on the lower lip and on the neck.
Face, ears, lip and a thinning scalp
It turns up where sun has landed for decades: the face, the ears, the lower lip, the nose, a scalp with thinning hair and the neck. The ear and the lip are the two that matter most, because tumors there behave more aggressively than the same thing on a cheek.
Front view of a whole body with red marks on the backs of both hands, on both forearms, down both shins and on both feet.
Backs of the hands, forearms and lower legs
The backs of the hands and the forearms come next. On deeper skin tones the pattern is different: it appears more often on the legs and feet, and inside old burn scars, ulcers and wounds that have never healed, rather than on sun-exposed skin.

What Happens in the Skin

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This is what is going wrong under the skin, in the order it happens. Click a step to see it.

How Squamous Cell Carcinoma happens
Skin basics
BARRIEREPIDERMISDERMIS0NORMAL SKIN1UV LIGHT DAMAGES THE DNA2DAMAGED CELLS SURVIVE3THEY MULTIPLY INTO A TUMOR4IT GROWS DEEPER AND CAN SPREAD

The outer layer of skin is a stack of flat cells that divide, move up and are shed. Every new copy is checked, and a gene called p53 retires any cell whose DNA is too damaged to fix. The DNA inside those cells is intact, and a firm boundary line underneath holds the whole layer above the deeper skin.

Ultraviolet light, mostly UVB from the sun and from tanning beds, reaches the outer layer of the skin and damages the DNA inside the flat cells there. This happens on ordinary days, not only on sunny holidays, and it adds up over decades.

The body repairs most of that damage, and cells too damaged to repair are supposed to die off. Over years some of the damage lands on the genes that run repair and shutdown, p53 most often, and once those controls are broken the damaged cells stay alive.

The surviving cells divide. First they build up as a rough precancerous patch, an actinic keratosis. Then they can fill the whole thickness of the top layer of skin, which is carcinoma in situ. Everything so far is still held above the boundary line.

The cells break through the boundary into the deeper layer, and the tumor now has access to blood vessels and lymph channels. It grows down into fat, cartilage, nerve or bone, and a small share reach a lymph node. Almost everything on the lists below is pushing on this step, and how early it is removed decides how it goes.

The outer film of dead cells and oil. It holds water in and keeps irritants out, and it is thinner than a sheet of paper. Almost every dry, itchy, stinging skin problem starts here.

The outer layer, and the only one anything in a jar reaches. It renews itself constantly: a cell made at the bottom takes about a month to reach the surface and flake off. Most of what a skincare product does, it does here.

The living layer underneath, holding the blood vessels, the nerves and the collagen. It is where lasting change happens and it is hard to reach: most of what is sold for the skin never gets this far.

The sequence runs roughly like this. Ultraviolet light, mostly UVB from sun and tanning beds, damages DNA inside keratinocytes in the outer layer of skin. The body repairs most of it, and cells too damaged to repair are supposed to die off. Over years, some damage lands on the genes that run repair and shutdown, most often p53. Once those controls break, damaged cells survive when they should not.

Those cells multiply. First as a rough precancerous patch, an actinic keratosis. Then they can fill the whole thickness of the top layer, which is squamous cell carcinoma in situ. Finally they break through into the deeper layer, where the tumor reaches blood vessels and lymph channels. That is invasive squamous cell carcinoma.

Ultraviolet light is by far the biggest cause, not the only one. The same cancer can develop from long-term inflammation or injury in one place, such as a burn scar or a wound that never closed, and years after radiation treatment. Certain strains of human papillomavirus contribute to squamous cell carcinomas in the genital area and around the nails. Long-term arsenic exposure is recognized. And when the immune system is suppressed, the cells that would normally remove abnormal cells stop doing it, which is why transplant recipients develop these cancers so much more often and faster.

Risk Factors

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Most of what drives squamous cell carcinoma accumulates over decades, and some of it is nothing a person chose. The list tells you how closely your skin should be watched.

Sun exposure
Total lifetime sun exposure
The main one. Cumulative - every year added together.
Sun exposure
Outdoor work or outdoor hobbies
Farming, construction, fishing, sailing, golf or gardening add up in a way holidays do not.
Sun exposure
Tanning beds
A recognized cause. Use before 35 raises risk most.
Inherited & age
Fair skin that burns easily
Skin that freckles and burns rather than tans, with red or blond hair and light eyes.
Inherited & age
Age
Most cases appear after 50 - the damage takes decades.
Inherited & age
Inherited conditions
Xeroderma pigmentosum, albinism and some forms of epidermolysis bullosa carry a much higher risk from a young age.
Damaged skin
Actinic keratoses or previous skin cancer
Both mark skin damaged enough to produce cancer once, and both raise the chance of another.
Damaged skin
Chronic wounds and scars
Ulcers, burn scars and long-standing inflammation can develop this cancer decades later.
Damaged skin
Previous radiation treatment
Skin cancers can appear in a treated area years later.
Other health factors
A suppressed immune system
Transplant recipients have a much higher risk, with more aggressive tumors. Ask your doctor about surveillance.
Other health factors
Certain medicines
Voriconazole, BRAF inhibitors for melanoma and some blood pressure medicines have been linked. A conversation for your prescriber.
Other health factors
Human papillomavirus
Some strains contribute to squamous cell carcinomas around the genitals and under or beside the nails.
Other health factors
Smoking
Associated particularly with squamous cell carcinoma of the lip.

Course

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Left alone, this follows a predictable path. It does not resolve, and the stages below take years, or weeks to months in immunosuppressed people. Most people are cured by removal, though new skin cancers are common afterward, so regular skin checks are part of the treatment.

Field damageYears of exposure
Nothing here is cancer yet

Sun-damaged skin develops rough patches, mottled color and broken vessels. The ground is prepared, no cancer yet.

Actinic keratosisPrecancer
A rough patch that comes and goes

A rough, scaly, sandpapery patch. Any single one is unlikely to become cancer, but they mark skin that can.

Carcinoma in situEarly cancer
Still held in the top layer

A persistent scaly red or darker patch that looks like eczema or psoriasis but never responds to creams. The cells are still confined to the top layer.

Lower leg
Invasive tumorWeeks to months
A sore that will not heal

A firm, tender bump or a sore that will not heal, often crusted, often bleeding when caught. It grows steadily. Untreated it grows into fat, cartilage, muscle or bone and can track along nerves. That turns a small removal into a large reconstruction.

SpreadUncommon but serious
A small percentage reach the lymph nodes

A small percentage spread to nearby lymph nodes and occasionally further. Higher risk with large or deep tumors, ear or lip sites, recurrence, and immunosuppression.

What Makes It Better & Worse

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Four steps - ultraviolet light damaging DNA, damaged cells surviving, those cells multiplying into a tumor, and the tumor growing deeper or spreading. The outcome is decided mostly by how early the tumor is removed, so a delay at step three or four turns a small problem into a large one.

What is driving yours?

FATBARRIEREPIDERMISDERMIS

Ultraviolet light, mostly UVB from the sun and from tanning beds, reaches the outer layer of the skin and damages the DNA inside the flat cells there. This happens on ordinary days, not only on sunny holidays, and it adds up over decades.

The body repairs most of that damage, and cells too damaged to repair are supposed to die off. Over years some of the damage lands on the genes that run repair and shutdown, p53 most often, and once those controls are broken the damaged cells stay alive.

The surviving cells divide. First they build up as a rough precancerous patch, an actinic keratosis. Then they can fill the whole thickness of the top layer of skin, which is carcinoma in situ. Everything so far is still held above the boundary line.

The cells break through the boundary into the deeper layer, and the tumor now has access to blood vessels and lymph channels. It grows down into fat, cartilage, nerve or bone, and a small share reach a lymph node. Almost everything on the lists below is pushing on this step, and how early it is removed decides how it goes.

What helps

  • Daily broad-spectrum sunscreen SPF 30 or higher on face, ears, neck and hands.
  • Clothing, hats and shade More than sunscreen alone, and no reapplication.
  • Nicotinamide 500 mg twice a day modestly reduces new skin cancers.

What makes it worse

  • Continuing unprotected sun exposure Each dose raises the next cancer's odds.
  • Tanning beds A recognized cause, pointless after a diagnosis.
  • Smoking Lip cancer, and poorer healing after removal.

What helps

  • Prescription creams for the earliest forms Fluorouracil and imiquimod treat in situ disease and actinic keratoses, not invasive tumors. If you are pregnant or breastfeeding, ask the doctor managing your pregnancy.
  • Treating actinic keratoses Fewer of these cancers later.
  • Talking to your transplant team Adjusting immune-suppressing medicine is sometimes possible.

What makes it worse

  • Ignoring actinic keratoses The step immediately before this cancer.
  • A suppressed immune system Faster, more aggressive tumors - ask your transplant team about surveillance, and never stop medication yourself.

What helps

  • A biopsy for anything unhealed in a month The highest-value action here.
  • Surgical removal Cutting it out with a margin cures most cases.
  • Mohs surgery Layers checked during the appointment - spares tissue, highest cure rate.
  • Curettage and electrodesiccation Small, low-risk tumors, not the face.
  • Radiation when surgery is not possible Also used after aggressive tumors.
  • Regular skin checks after treatment How the next one is caught small.

What makes it worse

  • Waiting on a spot that will not heal The biggest factor in outcome.
  • A steroid cream on a scaly patch Flattens redness, leaves the cancer.
  • Black salve and escharotic pastes Destroy the surface, leave tumor at depth.
  • Picking the crust off repeatedly Keeps it looking nearly healed.
  • Skipping follow-up appointments New cancers are common after the first.

What helps

  • Immunotherapy for advanced disease For tumors that spread or cannot be removed.

What makes it worse

  • Tumors on the lip and ear Higher risk of spread.

How These Treatments Work

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Treatments for Squamous Cell Carcinoma do not all work in the same place. Tap one to see where it acts.

Pick a treatment
Skin basics
BARRIEREPIDERMISDERMISREMOVES ITFOR PRE-CANCERS ONLYFOR WHEN SURGERY CANNOTWATCHES FOR SPREADPREVENTS THE NEXT ONE

The main treatment, with a margin, because this one can grow deep.

These treat the damaged cells that come before it, not the tumor itself.

Also used after surgery for high-risk tumors.

This type can spread, which is why the checks continue after it is out.

The damage that made this one is still there.

The outer film of dead cells and oil. It holds water in and keeps irritants out, and it is thinner than a sheet of paper. Almost every dry, itchy, stinging skin problem starts here.

The outer layer, and the only one anything in a jar reaches. It renews itself constantly: a cell made at the bottom takes about a month to reach the surface and flake off. Most of what a skincare product does, it does here.

The living layer underneath, holding the blood vessels, the nerves and the collagen. It is where lasting change happens and it is hard to reach: most of what is sold for the skin never gets this far.

Over-the-Counter Products

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Everything here you can buy without seeing anyone.

No over-the-counter options listed yet.

Prescriptions

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These need a prescription.

No prescription treatments listed yet.

Procedures

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These are done in the office, usually over several visits.

16:9 hero for Skin Biopsy. Never cropped: the tone strip and the corner logo depend on the full frame.Diagram: how Skin Biopsy works in the skin
Always
Nothing else on this page happens without it. Even an experienced dermatologist with a dermatoscope cannot settle this by looking, and the report says far more than yes or no — how deep it goes, how aggressive the cells look, whether it is tracking along a nerve. Those details choose the treatment. It takes a few minutes under local anesthetic and leaves a small wound. A biopsy does not make cancer spread.
16:9 hero for Mohs Surgery. Never cropped: the tone strip and the corner logo depend on the full frame.Diagram: how Mohs Surgery works in the skin
Strong evidence
The tumor is removed a layer at a time and each layer is checked under the microscope during the same appointment, so the surgeon stops as soon as the edges are clear. It gives the highest cure rate and takes the least normal skin, which is why it is used on the face, ears, lips, hands, feet and genitals, and for large, recurrent or aggressive tumors. It is a long appointment rather than a difficult one.
16:9 hero for Surgical Excision. Never cropped: the tone strip and the corner logo depend on the full frame.Diagram: how Surgical Excision works in the skin
Strong evidence
The standard removal: the tumor is cut out with a margin of normal skin around it and the wound is stitched closed, usually in one visit under local anesthetic. It cures the large majority of straightforward tumors on the trunk, arms and legs. The margins are checked afterwards rather than during, so occasionally a second procedure is needed to clear an edge.
A gloved clinician treating a small dark spot on a patient's shoulder with a fine handheld instrument16:9 hero for Electrodesiccation and Curettage. Never cropped: the tone strip and the corner logo depend on the full frame.
Moderate evidence
The tumor is scraped out with a small loop and the base is sealed with an electric current, repeated a few times in one sitting. It is quick and effective for small, thin, low-risk tumors on the trunk and limbs. It is not used on the face, on large or recurrent tumors, or anywhere depth matters, because nothing is sent for margin checking and it leaves a round pale scar.
A rectangular LED panel in a white frame, angled on a white background, its face filled with a dense grid of several hundred small blue lights all lit, casting a blue glow onto the surface beneath it.Diagram: how Photodynamic Therapy works in the skin
Limited evidence
A light-activated cream treatment for the earliest forms only — actinic keratoses and some cases of carcinoma in situ. It treats a whole patch of sun-damaged skin at once and heals with a good cosmetic result. It has no role in an invasive tumor, and using it on one delays proper removal.
16:9 hero for Cryotherapy (Liquid Nitrogen). Never cropped: the tone strip and the corner logo depend on the full frame.Diagram: how Cryotherapy (Liquid Nitrogen) works in the skin
Limited evidence
A quick freeze in clinic, used for actinic keratoses and occasionally for a small patch of carcinoma in situ. It is a treatment for the step before this cancer, not for the cancer itself. Freezing an invasive tumor leaves cells behind at depth and hides what is happening under a healing crust.

When to See a Dermatologist

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The rule here is one month: any spot that has not healed in a month should be examined, which catches most squamous cell carcinomas while they are still small and does not ask you to know what you are looking at. Make an appointment now for a scaly or crusted bump that keeps bleeding, a sore that scabs and breaks open in the same place, a rough patch growing, thickening or turning tender, a lump with a hard central plug that came up over weeks, a new firm bump on the ear, lip, nose or scalp, or a raised or ulcerated area inside an old scar, burn or long-standing wound. Ask to be seen sooner, and say why, if you have had a transplant or take immune-suppressing medicine, if you have had a skin cancer before, if the spot is on the lip or ear, or if it is growing fast. Seek urgent assessment for heavy bleeding, numbness or tingling around it, deep or shooting pain, or a firm lump in the neck, armpit or groin. Only a biopsy settles this, so if something has been there for months, do not accept reassurance based on appearance - ask whether it should be biopsied.

— Dr. Schwarz, Board Certified Dermatologist

Complications

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Lookalikes

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Actinic Keratosis

These are the step immediately before this cancer, so they sit on the same sun-damaged skin and feel like the same sandpaper. An actinic keratosis is flat or barely raised, comes in numbers rather than singly, and flakes off and returns. A squamous cell carcinoma is the one that thickens into a firm lump, becomes tender, bleeds, and stays. Any single rough patch that starts to grow up rather than sit flat is the one to have looked at.

Basal Cell Carcinoma

Both are common sun-driven cancers, both turn up on the face and ears, and both can present as a sore that will not heal. A basal cell carcinoma tends to look pearly or translucent, with a rolled shiny edge and fine threadlike vessels running across it, and it grows slowly over years. A squamous cell carcinoma is rougher, scalier, more often tender, and moves over weeks to months. Only the biopsy separates them reliably, and both are treated by removal.

Psoriasis

This is the mix-up that costs people the most time. Squamous cell carcinoma in situ on the lower leg is a persistent scaly red or darker patch, and it is regularly treated as psoriasis or eczema for months. Psoriasis is usually symmetrical, turns up on both shins, knees or elbows at once, and improves with the creams given for it. A single patch, on one leg only, that has never responded to those creams should be biopsied rather than treated again.

Myths

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  • "Skin cancer only matters if it is melanoma." Melanoma is more dangerous spot for spot, but squamous cell carcinoma is far more common, grows into cartilage, nerve and bone, and spreads in a small share of cases. Its numbers make it a significant cause of skin cancer deaths.
  • "If it does not hurt, it cannot be cancer." Many are tender, but plenty are painless. Pain is not the test. Failure to heal is.
  • "I do not sunbathe, so I cannot have skin cancer." Most of the ultraviolet exposure behind this is incidental - driving, walking, working outdoors, waiting for a bus - piled up over decades, not earned on a beach.
  • "People with deeper skin tones do not get skin cancer." It is the most common skin cancer in people with deeper skin tones. It appears more often on the legs or inside old scars, and it is found later.
  • "A biopsy makes cancer spread." It does not, and this belief causes some of the longest delays. A biopsy takes a small sample so the diagnosis can be made.
  • "It scabbed over, so it is healing." Squamous cell carcinomas characteristically crust, appear to heal, then break down again in the same place. That cycle is a warning, not reassurance.
  • "You can burn it off at home." Black salve and similar corrosive pastes destroy surface tissue and leave tumor at depth. The wound looks like healing while the cancer grows.

Questions Patients Ask

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Is squamous cell carcinoma serious?

It is a real cancer and treated as one. Most cases are cured by removal, which is why the emphasis is on early checks. Untreated, it grows into deeper structures and a small share reach lymph nodes. How serious it gets depends on how long it is left.

How fast does it grow?

Usually weeks to months rather than days or years. The keratoacanthoma variant can appear and enlarge within a few weeks. In immunosuppressed people growth can be much faster, which is why the advice for that group is more urgent.

Will I need Mohs surgery?

It depends on the site and how the tumor looks under the microscope. Mohs is generally used on the face, ears, lips, hands, feet and genitals, and for large, recurrent or aggressive tumors. Tumors on the trunk, arms and legs usually get a standard excision.

Can it come back after it is removed?

The treated one can recur, though that is uncommon when margins were clear. Far more common is a new skin cancer elsewhere, because the same damage runs through the rest of the skin. Hence follow-up after a cure.

Does having one mean I will get more?

It substantially raises the odds - many people who have one keratinocyte cancer develop another within a few years. Hence skin checks, daily sun protection and treating actinic keratoses.

Do I need a scan or a lymph node test?

Most people do not. Scans and node assessment are reserved for high-risk features - large size, deep invasion, growth along nerves, recurrence, immunosuppression - or an enlarged node. Your dermatologist decides from the pathology report and examination.

References

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