Keratoacanthoma (KA) is a fast-growing bump on the skin that looks like a small dome with a central “plug” of hard, yellow-brown material called keratin (keratin = the tough protein that makes up hair, nails, and the outer layer of skin). It usually appears on sun-exposed areas like the face, ears, forearms, or hands. Many KAs grow quickly over a few weeks, then stop, and sometimes shrink on their own over months. The problem is that KA can look and behave very much like a type of skin cancer called cutaneous squamous cell carcinoma (SCC). Because doctors often cannot be 100% sure by looking, many treat KA the same way as a well-differentiated SCC to be safe (typically by removing it). NCBIDermNet®PMC
Keratoacanthoma (often shortened to “KA”) is a skin growth that springs up fast, usually on sun-exposed skin (face, ears, forearms, hands). It often looks like a small volcano: a round, dome-shaped bump with a central plug of yellow-brown keratin (compact dead skin). KAs tend to grow over weeks, then sit for a bit, and in many cases shrink on their own over 4–6 months, leaving a scar. The tricky part is that a KA can look almost identical to a well-differentiated cutaneous squamous cell carcinoma (cSCC) under the microscope and in clinic. Because of that, doctors usually treat and remove it as if it were cSCC, especially when diagnosis is uncertain or the lesion sits in a critical spot. DermNet®+1NCBI
KA is thought to start from the hair follicle opening (also called the infundibulum), which is part of the pilosebaceous unit (hair follicle + oil gland). Under the microscope, a typical KA shows a crater-shaped lesion (crateriform) with a keratin plug in the middle and “lips” of skin growing over the edges. Pathologists (doctors who read biopsies) look for these patterns, but KA and SCC can overlap, so the safest plan is usually to remove and examine it fully. PMCNCBI
Types of keratoacanthoma
Solitary KA (most common)
One single dome-shaped nodule appears on sun-exposed skin. It grows for a few weeks, then may plateau and occasionally shrink. Because it can mimic cancer, it’s usually removed.Giant KA
Same idea as solitary KA but larger than usual (often >2 cm). Bigger size can mean more tissue damage and more concern for invasive behavior, so doctors treat it promptly.Subungual KA (under a nail)
A painful growth under or around the nail. It can lift the nail, bleed, or look infected. Because nail-unit cancers exist, this needs careful evaluation.Keratoacanthoma centrifugum marginatum (KCM)
A ring-shaped lesion that spreads outward at the edges while the center may flatten. The expanding “margin” can make it look aggressive; biopsy and treatment are key.Multiple self-healing KAs (Ferguson-Smith type)
People develop repeated KAs that tend to heal by themselves. This can run in families (genetic). Even with self-healing behavior, lesions often need sampling because cancer look-alikes exist.Generalized eruptive KA (Grzybowski type)
Hundreds to thousands of tiny KA-like papules can appear, often itchy. This rare condition needs specialist care and multiple biopsies to clarify the diagnosis and rule out other diseases. DermNet®
note: whether some of these are “true” KA variants or special forms of SCC is still debated, so doctors lean toward cautious management. DermNet®
Causes and risk factors
Strictly speaking, KA doesn’t have one single “cause.” Instead, several things raise the risk of developing it. Think of these as pushes that make KA more likely:
Ultraviolet (UV) light from the sun
Chronic sun exposure damages skin DNA, especially on the face, ears, hands, and forearms. This is the biggest driver. Sunscreen and shade help. NCBITanning beds
Artificial UV acts like strong sun. Frequent use increases risk.Fair skin, light eyes, or hair
Less natural pigment means less UV protection, so DNA damage builds faster.Older age
Skin collects more UV damage over the years, so KAs are more common in older adults.Male sex
Men historically have more outdoor exposure and show slightly higher rates.Personal history of actinic (sun) damage
Freckling, sunspots, or actinic keratoses signal heavy UV exposure and higher risk.Immunosuppression after organ transplant
Anti-rejection medicines weaken immune surveillance against abnormal skin cells, so KAs and SCCs are more frequent. Regular skin checks are vital.Other weakened immunity (e.g., chemotherapy, certain illnesses)
A less active immune system may allow abnormal cells to grow.Human papillomavirus (HPV), in some cases
Some studies have found HPV DNA in KA-like lesions. It’s not the main cause but may contribute for a subset.Genetic predisposition (Ferguson-Smith syndrome)
A rare inherited condition where people develop multiple self-healing KA-like tumors.Generalized eruptive KA (Grzybowski)
A rare pattern with many lesions; the exact genetic cause isn’t fully worked out. DermNet®Defects in DNA repair (e.g., xeroderma pigmentosum)
When cells can’t fix UV damage well, many UV-related tumors can form.Prior radiation to the skin
Old radiation fields can later develop KA/SCC-like tumors.Chronic scarring or repeated trauma
KAs sometimes arise in scars, surgical sites, or areas of repeated irritation (called an isomorphic or “Koebner” response).Chemical exposures (e.g., arsenic, tar)
These are classic skin carcinogens that can also show crater-type tumors.Drugs that activate the RAF/MAPK pathway in skin (e.g., BRAF inhibitors like vemurafenib)
These life-saving cancer drugs can paradoxically trigger KA/SCC-type lesions in a portion of patients. Dermatology follow-up is routine during therapy. New England Journal of MedicinePMCOther kinase inhibitors (e.g., sorafenib)
Similar pathway effects can raise risk of KA-like lesions. PMCPhotosensitizing medicines
Drugs that make skin more sun-sensitive (some antibiotics, diuretics) indirectly increase UV damage if you don’t protect your skin.Smoking
Tobacco is linked to SCC risk and may nudge the skin toward KA-type growth in sun-damaged areas.Family history of non-melanoma skin cancers
Part of overall risk profile; shared genes and shared sun habits matter.
Common signs and symptoms
A new, round or dome-shaped bump that appears over a few weeks, often on sun-exposed skin.
A central “plug” of hard material that looks like a tiny volcano with a crater (that plug is keratin).
Rapid growth, faster than most benign bumps; size often reaches 1–2 cm within weeks.
Firm or rubbery feel when touched; sometimes tender.
Pink, reddish-brown, or skin-colored surface; may look shiny or scaly at the edges.
Crusting or minor bleeding if the top gets knocked.
Itching or soreness around the lesion.
A sense that growth has “stabilized” after a fast start.
Occasional shrinking over months (spontaneous involution), though not guaranteed.
Sun-exposed location (face, ears, forearms, hands) fits the pattern.
Multiple bumps if you have a rare “multiple” type (Ferguson-Smith or Grzybowski). DermNet®
Nail pain or nail lifting if the lesion is under or next to a nail (subungual).
A hard rim with overhanging “lips” of skin around the crater—seen by clinicians. PMC
Occasional enlarged nearby lymph nodes (usually reactive/inflamed, but always checked to rule out spread if the lesion proves to be SCC).
No specific “feel” that reliably separates KA from SCC—which is why biopsy is so important. NCBI
Diagnosis
Diagnosis is a step-by-step process. The key is biopsy (taking a small piece of the lesion for the lab). Below are 20 diagnostic tests, grouped the way you asked. Not all are needed for every person—doctors pick what fits your situation.
A) physical exam
Full-skin visual inspection
The clinician looks closely at size, color, shape, border, and the central keratin plug. They also note location and sun-damage signs nearby. This helps decide urgency and the best biopsy approach.Palpation (feeling the lesion and edges)
Fingertip pressure checks how fixed or mobile the bump is, how firm it is, and whether the edges feel “rolled” or infiltrative (suggesting deeper spread).Measuring and photographing
Accurate size tracking (with a ruler and photos) documents growth speed, important for fast-growing lesions like KA.Regional lymph-node check
The clinician gently examines nearby nodes (for example, in front of the ear or under the jaw for face lesions). Swollen nodes can be reactive but prompt more evaluation.Full-body skin exam
Because sun damage and multiple lesions can coexist, your clinician may scan the rest of the skin to look for additional bumps that need attention.
B) manual/bedside maneuvers
Diascopy (gentle glass-slide pressure)
Pressing a clear slide on the lesion to see which areas blanch (turn pale) can help distinguish blood vessel patterns and surface crusting from true tissue color. It’s not diagnostic by itself but adds clues.Careful lifting of the keratin plug
Using forceps during an exam or procedure, a clinician may tease the central plug to confirm the crater shape. This is done gently to avoid bleeding or infection and usually when planning a biopsy.Light touch and sensory check
If there’s numbness, tingling, or pain radiating along a nerve path, the clinician notes it—possible signs of perineural involvement (tumor around a nerve), which would prompt more aggressive imaging and treatment if the final diagnosis is SCC.
C) lab and pathologic tests
Shave biopsy
A thin slice of the top portion of the lesion is removed with a blade under local anesthesia. This is common for dome-shaped lesions with a central plug. It yields tissue for the pathologist to examine under the microscope.Excisional biopsy (complete removal)
The whole lesion is cut out with a rim of normal skin. This provides the best sample and may be curative if margins (edges) are clear. It’s often chosen when there’s high suspicion for SCC.Routine histopathology (H&E stain)
The pathologist looks for the classic crater filled with keratin, “overhanging lips,” symmetry, and well-differentiated cells with a “glassy” look. Features overlapping with SCC are documented carefully. PMCMargin assessment with frozen sections or Mohs micrographic surgery
In areas where saving tissue matters (nose, eyelids, lips) or when the borders are unclear, Mohs surgery can remove the lesion in stages, checking 100% of the margins in real time, to ensure complete removal while preserving healthy skin. (Mohs is a technique, not a separate diagnosis, but it functions diagnostically by confirming clear margins.)Immunohistochemistry (IHC) for Ki-67
Ki-67 marks dividing cells. In typical KA, most cell division occurs at the periphery; in SCC it may be more diffuse. Patterns can support—but not prove—the diagnosis.IHC for p53
p53 is a tumor-suppressor protein often abnormal in skin cancers. Staining patterns can help the pathologist weigh KA versus SCC when findings are borderline.HPV testing (PCR or in situ hybridization) in selected cases
If clinical features suggest viral involvement (especially in nail or periungual lesions), HPV testing may be ordered. Positive results don’t by themselves establish KA, but they add context.Molecular testing (e.g., HRAS, NOTCH1/2) in specialized settings
Some KA/SCCs—especially those triggered by BRAF inhibitors—carry HRAS mutations. Molecular results are rarely required for routine care but can explain why multiple lesions appeared during certain cancer therapies. New England Journal of Medicine
D) electrodiagnostic tests
Nerve conduction studies or EMG (rare, only if needed)
KA itself doesn’t need “electrodiagnostic” tests. If a proven SCC has symptoms suggesting nerve damage (numbness, weakness), your doctor may order nerve tests to plan surgery or radiation. Most people with suspected KA never need this.
E) imaging tests
High-frequency skin ultrasound (HFUS)
Noninvasive sound-wave imaging can estimate lesion thickness and involvement of deeper layers, which helps plan surgery on the face or around joints.MRI of the involved area (if deep spread is suspected)
MRI shows soft tissues and nerves well. If the pathology points to invasive SCC or perineural spread, MRI helps map the extent for surgery or radiation.Ultrasound (or CT) of regional lymph nodes (selected cases)
If the final diagnosis is SCC or the lesion is large/atypical with suspicious nodes, imaging evaluates for spread. KA alone seldom needs this, but overlap with SCC keeps clinicians cautious. PMC
Non-pharmacological treatments
(with what they are for and how they work)
Standard surgical excision: the most common treatment—cut the lesion out with a small border of normal skin; gives tissue for a definitive diagnosis and usually cures it. Purpose: cure and confirm. Mechanism: complete removal.
Mohs micrographic surgery: tissue-sparing surgery done in stages with on-the-spot microscopic margin checks; chosen for face, nose, eyelids, lips, ears, or recurrent lesions. Purpose: maximize cure, minimize tissue loss. Mechanism: stepwise margin control.
Curettage & electrodessication (ED&C): scrape and cauterize the base (suitable for selected lesions in non-critical sites). Purpose: quick, office-based removal. Mechanism: mechanical destruction. (Recurrence rates are low but higher than surgery in some series.) PMCJCAD
Shave removal with cautery: flatten and cauterize; may be used when the lesion has a typical look and is in a low-risk location.
Cryotherapy (liquid nitrogen) ± curettage: freezes the lesion; sometimes used when surgery is impractical. Purpose: tissue destruction. Mechanism: freeze–thaw kills tumor cells. PMC
Radiation therapy: an option for non-surgical candidates or large/awkward locations; KAs are radiosensitive and respond to relatively modest doses compared with frank cancers. Purpose: control when surgery isn’t suitable. Mechanism: DNA damage leading to tumor cell death. PMCMedscape
Photodynamic therapy (PDT): light plus a topical photosensitizer (ALA or MAL) to selectively damage tumor cells; evidence is mainly case series for KA. Purpose: non-invasive control in selected cases. Mechanism: light-activated oxidative damage. PubMed
Compression dressings / Unna boot (as an adjunct for leg lesions after destructive therapy): aids wound healing and comfort.
Wound care education after any procedure: gentle cleansing, petrolatum, sun avoidance on the site to optimize scarring.
Scar optimization (silicone gel/sheets, massage once healed): reduces thickness/itch of scars.
Sun avoidance and sunscreen (SPF 50+, broad-spectrum): lowers new UV damage that drives keratinocyte tumors.
Protective clothing (UPF garments, wide-brim hats): blocks UV without relying on re-application.
Avoid tanning beds: they emit concentrated UVA/UVB that ages skin and raises cancer risk.
Stop picking or shaving over the lesion: reduces bleeding and limits secondary infection.
Smoking cessation: supports overall skin health and lowers keratinocyte cancer risk.
Review immunosuppressive medicines (with your specialist): sometimes doses can be adjusted to lower skin cancer burden.
Field care for sun-damaged skin (your dermatologist may later treat actinic keratoses to reduce the “field effect”).
Routine skin checks (every 6–12 months, more often if high risk): catch new lesions early.
Patient self-checks monthly: photos help track any fast-growing new bumps.
Short, closely supervised “watchful waiting” may be considered only when diagnosis is certain, the lesion is small, and surgery is truly not possible—but most KAs are treated rather than watched because of the overlap with SCC. DermNet®
Drug treatments
Important: Many medicines below are used off-label for KA (especially injections into the tumor). Your dermatologist balances benefits and risks for your specific case.
Intralesional 5-fluorouracil (5-FU) (antimetabolite chemotherapy)
Dose/Time: commonly 50 mg/mL, 0.2–2 mL injected into the lesion weekly for 3–8 sessions depending on size.
Purpose: shrink or clear KAs when surgery is hard (face, elderly, anticoagulated).
Mechanism: blocks DNA synthesis in rapidly dividing tumor cells.
Side effects: local pain/ulcer, crust, temporary inflammation. Rare systemic effects if large amounts used. JAADScienceDirect
Intralesional methotrexate (MTX) (antimetabolite/antifolate)
Dose/Time: commonly 12.5–25 mg per session (varies), given every 1–2 weeks for 1–4 sessions until resolution.
Purpose: alternative to surgery for selected solitary KAs or as neoadjuvant to shrink before excision.
Mechanism: inhibits dihydrofolate reductase → blocks DNA synthesis.
Side effects: local pain; rarely systemic MTX effects (liver, marrow) if significant systemic absorption—clinicians screen appropriately. Actas Dermo-Sifiliográficas
Topical 5-FU 5% cream
Dose/Time: typically twice daily for several weeks on carefully selected small KA-like lesions (more evidence for actinic keratoses/SCC in situ than true KA).
Purpose: non-surgical option when biopsy confirms suitability.
Mechanism: same as above, via skin absorption.
Side effects: brisk local redness, crusting, erosion.
Topical imiquimod 5% cream (immune response modifier; TLR7 agonist)
Dose/Time: schedules vary (e.g., 5 nights/week for 6–8 weeks in reports).
Purpose: selected difficult sites or patients avoiding surgery.
Mechanism: stimulates local immune attack on tumor cells.
Side effects: strong local inflammation (sometimes intense); rare reports of eruptive KA-like reactions—so it must be used with specialist guidance. Annals of DermatologyJAAD
Oral acitretin (systemic retinoid)
Dose/Time: commonly 25–60 mg daily (or ~0.3–0.5 mg/kg/day), sometimes lower maintenance once controlled.
Purpose: people with multiple KAs (e.g., Ferguson-Smith/Grzybowski variants) or those who constantly develop new lesions.
Mechanism: normalizes keratinocyte growth and differentiation; acts as a chemopreventive retinoid.
Side effects: dry lips/skin, high triglycerides, liver enzyme changes; strict contraception (teratogenic). JCAD
Oral isotretinoin (systemic retinoid)
Dose/Time: about 0.5–1 mg/kg/day for several months; some reports used up to 1.5 mg/kg/day initially for eruptive disease.
Purpose: similar to acitretin—multiple or recalcitrant KAs.
Mechanism: retinoid normalization of keratinization.
Side effects: dry skin/lips, elevated lipids/LFTs, mood changes (rare), teratogenic—strict pregnancy prevention. PMCOregon Health & Science University
Intralesional interferon-α (immune cytokine)
Dose/Time: units and schedules vary in reports (e.g., 1–3 million IU 2–3×/week).
Purpose: an option when other intralesional therapies are unsuitable.
Mechanism: boosts local immune surveillance against tumor cells.
Side effects: flu-like symptoms, local pain.
Intralesional bleomycin (antitumor antibiotic)
Dose/Time: small volumes (e.g., 1 U/mL, 0.1–1 mL) injected directly; used selectively.
Purpose: destructive option for stubborn lesions.
Mechanism: DNA strand breaks.
Side effects: ulceration, pain, nail changes if near nail, rare systemic effects.
Capecitabine (oral 5-FU prodrug)
Dose/Time: oncology schedules (e.g., 1,000 mg/m² twice daily 14 days on/7 off) used off-label to reduce burden of multiple keratinocyte tumors in very high-risk patients.
Purpose: reduce new tumors in patients with numerous lesions (organ transplant recipients, etc.).
Mechanism: systemic antimetabolite.
Side effects: hand–foot syndrome, diarrhea, cytopenias—oncology co-management required.
PD-1 immune checkpoint inhibitors (e.g., cemiplimab, pembrolizumab)
Dose/Time: Cemiplimab 350 mg IV every 3 weeks; Pembrolizumab 200 mg IV every 3 weeks, used for advanced/unresectable cSCC; rarely needed for classic solitary KA but relevant if a KA-type lesion behaves like SCC.
Purpose: engage the immune system to attack tumor cells in advanced disease.
Mechanism: blocks PD-1/PD-L1 pathway → T-cell activation.
Side effects: immune-related events (thyroiditis, colitis, hepatitis, pneumonitis); managed by oncology/dermatology teams. PMC
Dietary, molecular, and supportive supplements
(what we know, typical doses used in studies, function, mechanism—used to support skin health; not cures)
Quick safety note: Supplements can interact with medicines. Always check with your clinician, especially if you are pregnant, have kidney/liver disease, or are immunosuppressed.
Nicotinamide (vitamin B3 amide) – 500 mg twice daily in a large RCT reduced new non-melanoma skin cancers (including SCCs) in high-risk adults; often suggested for patients who repeatedly develop keratinocyte tumors. Function: supports cellular energy and DNA repair pathways. Mechanism: enhances NAD+ pools and may aid UV-damage repair. U.S. Food and Drug Administration
Polypodium leucotomos extract (PLE) – common doses 240 mg twice daily; human trials show photoprotective effects (higher UV dose needed to burn, less DNA/immune damage). Function: systemic photo-protection adjunct to sunscreen. Mechanism: antioxidant, reduces UV-induced inflammation and immunosuppression. PMCJAAD
Broccoli sprout/sulforaphane preparations – topical and oral sulforaphane-rich extracts have shown UV protection in early human studies. Function: boosts the body’s own protective phase-2 enzymes. Mechanism: Nrf2 pathway activation. (Evidence is promising but not yet standard.) PNAS
Vitamin D – correct deficiency if present (dose based on blood level). Function: general skin and immune support. Mechanism: regulates keratinocyte growth; evidence for preventing KA specifically is limited.
Omega-3 fatty acids (fish oil) – anti-inflammatory; mixed data for skin cancers; consider for overall health if appropriate.
Green tea extract (EGCG) – antioxidant/anti-inflammatory; limited human data for keratinocyte cancer prevention; topical forms are also studied.
Lycopene (tomato extract) – antioxidant; small studies show mild UV protection endpoints (MED).
Resveratrol – antioxidant; preclinical/early data only for skin photobiology.
Curcumin (turmeric extract) – anti-inflammatory; limited human data on UV endpoints.
Quercetin – antioxidant flavonoid; preclinical skin photoprotection signals only.
Sulforaphane-rich diet (crucifers) – see #3; food-first approach preferred.
Selenium – not recommended for skin cancer prevention; mixed/negative data in large trials.
High-dose vitamin A/β-carotene – not recommended due to toxicity and potential harms in smokers.
Zinc – correct deficiency if present, but no evidence to prevent KA.
Probiotics – general immune/gut benefits; no direct evidence for KA.
The only items with good human evidence for reducing new keratinocyte tumors are nicotinamide and, for photoprotection, Polypodium leucotomos (as an adjunct to sunscreen and clothing). Everything else should be viewed as supportive at best. U.S. Food and Drug AdministrationPMC
Regenerative / stem-cell”–type therapies
There are no approved “stem cell drugs” for KA or cSCC. What we do have are immune-based therapies used for advanced cSCC, rarely needed in typical KA:
Cemiplimab (PD-1 inhibitor) – 350 mg IV every 3 weeks for advanced cSCC; unleashes T-cells to attack tumor.
Pembrolizumab (PD-1 inhibitor) – 200 mg IV every 3 weeks for advanced cSCC.
Nivolumab (PD-1 inhibitor) – sometimes used when other PD-1 agents aren’t suitable (off-label for cSCC).
Topical imiquimod – a local immune activator (TLR7 agonist) used on small, selected KA-type lesions.
Interferon-α (intralesional) – boosts local antitumor immunity in select cases.
Radiation therapy – not a “drug,” but frequently used as a non-surgical local treatment when immunity or healing limits surgery.
Note: Sophisticated cell or gene therapies are not standard for KA. Treatment plans follow cSCC pathways if a lesion behaves aggressively. PMC
Surgeries
Standard excision: local anesthetic → ellipse around lesion → remove with a small clear margin → stitches; the lab checks margins. Why: cures most cases and gives the most reliable diagnosis.
Mohs micrographic surgery: remove a thin layer → examine 100% of the margin while you wait → repeat until all clear → repair defect. Why: best tissue preservation and cure rates for face/ears/nose/eyelids/lips, recurrent tumors, or uncertain borders.
Curettage & electrodessication: numb area → scrape tumor → cauterize the base, often repeated in cycles. Why: quick office procedure for selected lesions on non-critical skin. PMC
Shave excision with cautery: “scoop” the lesion off flush with skin and cauterize the base; sometimes used for small, classic-looking KAs in low-risk areas. Why: straightforward removal when appropriate.
Special site procedures (e.g., lip wedge excision, nail unit surgery): tailored to function and cosmesis. Why: preserve speech, eating, or nail growth while clearing the tumor.
Prevention habits that actually help
Daily broad-spectrum sunscreen (SPF 50+), re-apply every 2 hours outdoors and after sweat/swim.
Sun-smart clothing: UPF shirts, wide-brim hats, UV-blocking sunglasses.
Avoid midday sun (10 am–4 pm), seek shade.
No tanning beds—ever.
Nicotinamide 500 mg twice daily (ask your doctor) if you repeatedly get keratinocyte tumors. U.S. Food and Drug Administration
Treat actinic keratoses and other “field” damage as advised.
Stop smoking.
Check your skin monthly; take photos of any fast-growing new bump.
Regular dermatology check-ups (often every 6–12 months if you’ve had KA or cSCC).
Protect healing surgical sites from sun for at least a year to improve scars and reduce recurrence.
When to see a doctor
Any new, fast-growing bump, especially with a central plug/crust on sun-exposed skin.
A bump that bleeds easily or doesn’t heal.
A lesion that hurts, tingles, or feels numb, or you notice twitching/weakness nearby (possible nerve involvement).
Recurrence at a scar or prior KA site.
Multiple new lesions appearing over weeks.
If you are immunosuppressed or have had organ transplantation.
If a lesion was “watched” and is enlarging or not regressing by 3–4 months.
If a lymph node nearby becomes enlarged or tender. (Imaging is sometimes used for high-risk cSCC, not routine KA.) PMC
What to eat and what to avoid
Mediterranean-style basics: vegetables, fruits, legumes, whole grains, nuts, olive oil—good for overall skin and heart health.
Colorful produce daily (tomatoes, berries, leafy greens): natural antioxidants that support the skin’s defenses.
Cruciferous vegetables (broccoli, cauliflower, kale, cabbage) several times a week—food sources of sulforaphane (see supplements). PNAS
Lean proteins (fish, poultry, beans); omega-3-rich fish (salmon, sardines) a couple of times per week.
Hydration: water throughout the day supports healing after procedures.
Coffee/tea in moderation if you already enjoy them (some observational data link coffee with lower keratinocyte cancers, but this is not treatment).
Limit ultra-processed foods high in sugar and refined starches—better for general inflammation control.
Limit alcohol (heavy intake is linked with skin cancer risk in some studies).
Avoid charred meats frequently (general anti-cancer guidance).
Food-first approach to nutrients; only add supplements (like nicotinamide or PLE) after discussing with your clinician. U.S. Food and Drug AdministrationPMC
Frequently asked questions
1) Is keratoacanthoma “cancer”?
KA is often described as low-grade and frequently self-regressing, but many experts consider it a variant of squamous cell carcinoma or label it “SCC, KA-type” because the two are so similar. That’s why excision is commonly recommended. DermNet®
2) How fast does a KA grow?
Typically 6–8 weeks to reach 1–2 cm, then it may plateau and shrink over months. NCBI
3) Can I just wait for it to go away?
Some do regress, but because KA can mimic true SCC, waiting can be risky. Doctors usually biopsy and treat. DermNet®
4) What treatment has the best cure rate?
For most solitary lesions, surgical excision (or Mohs in critical areas) gives very high cure rates and a clear diagnosis. Non-surgical methods have higher persistence/recurrence in studies. PMC
5) Will it leave a scar?
Yes—KA itself often scars when it involutes, and surgery leaves a planned scar that usually heals well with good care.
6) Do KAs spread to lymph nodes?
True metastasis from a classic KA is very rare; worrisome behavior suggests an SCC rather than a self-regressing KA. Imaging is reserved for high-risk situations. PMC
7) Why are injections used instead of cutting in some people?
Intralesional 5-FU or methotrexate can clear KAs when surgery is hard (e.g., fragile skin, anticoagulation, or cosmetically sensitive location). JAAD
8) Are topical creams really enough?
Topical 5-FU or imiquimod may work in selected biopsy-proven cases, but they require close follow-up; surgery remains the standard for most. Annals of Dermatology
9) I keep getting new KAs—anything to reduce this?
Talk to your dermatologist about nicotinamide 500 mg twice daily, retinoids (acitretin or isotretinoin) for multiple lesions, and strict sun protection. U.S. Food and Drug AdministrationJCAD
10) What is Ferguson-Smith disease?
An inherited condition causing multiple self-healing KA-like tumors that scar; linked to TGFBR1 mutations. PMC
11) Can trauma, tattoos, or surgery sites trigger KA?
Yes—KAs have appeared in injured skin (including around scars, tattoos, or after procedures) in case series. ScienceDirect
12) Does radiation cause or treat KA?
Radiotherapy can treat KA when surgery isn’t possible, and there are rare reports of KAs arising after radiation—both can be true. PMCMedCrave Online
13) Is there a blood test for KA?
No. Diagnosis is clinical + biopsy.
14) Will sunscreen alone prevent KA?
Sunscreen reduces UV damage and helps, but it’s part of a package: clothing, shade, timing, and regular checks.
15) Are “stem-cell” or “regenerative” drugs used for KA?
No approved stem-cell drugs exist for KA. Immunotherapies (like cemiplimab) are used for advanced cSCC, not typical KA. PMC
Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.
The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members
Last Updated: August 09, 2025.
Kearns–Sayre Syndrome (KSS)
