Keratoacanthoma: Causes, Symptoms, Diagnosis, and Treatment

What is Keratoacanthoma?

Keratoacanthoma (KA) is a rapidly growing, dome-shaped skin tumor that is generally classified as benign, meaning it does not typically spread to distant sites or behave with the aggressive malignant potential of most skin cancers. It typically measures between 1 and 2 centimeters in diameter at its largest extent and is characterized by a distinctive central crater filled with a keratin plug (a core of hardened, compacted keratin, the structural protein of the skin’s outer layer). This feature gives the lesion its pathognomonic crateriform or volcano-like appearance.

What makes keratoacanthoma particularly clinically important, despite its fundamentally benign nature, is its striking biological and histological resemblance to squamous cell carcinoma (SCC) (also known as spinocellular carcinoma). This is one of the most common and potentially dangerous forms of skin cancer. The two lesions can be virtually indistinguishable under the microscope, and even experienced pathologists sometimes find it difficult to make a definitive distinction. Some authorities in dermatopathology have gone so far as to classify keratoacanthoma as a well-differentiated, low-grade variant of SCC rather than a truly separate entity. This view has significant implications for how the lesion should be managed clinically.

Natural History

The biological behavior of keratoacanthoma follows a characteristic three-phase life cycle:

1. Rapid proliferative growth phase: The lesion appears and grows quickly, reaching its full size in about 6 to 8 weeks. This rapid growth would be deeply alarming in most skin lesions, making keratoacanthoma clinically striking.

2. Maturation (stable) phase: Following the initial rapid growth, the lesion enters a period of relative stability lasting several weeks to months, during which its size and appearance remain essentially unchanged.

3. Spontaneous involution (regression) phase: In many cases, though not all, keratoacanthoma may spontaneously regress. During this process, the central keratin plug is shed, and the lesion resolves. It typically leaves behind a depressed, atrophic (thin) scar.

Despite this potential for spontaneous resolution, the close resemblance to squamous cell carcinoma means that treatment and removal are generally recommended rather than watchful waiting, as it is not possible to reliably predict which lesions will regress and which may progress or be misclassified malignancies.

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Causes

The precise etiology of keratoacanthoma is not fully established, and it is likely that the condition represents the result of a variable combination of genetic predisposition and environmental triggering factors rather than a single, universal cause. The most widely supported hypotheses implicate the following:

Ultraviolet Radiation

UV radiation, from both natural sunlight and artificial sources, is the most consistently identified environmental risk factor for keratoacanthoma. UV light induces characteristic mutagenic DNA damage (cyclobutane pyrimidine dimers and 6-4 photoproducts) in keratinocytes (the predominant cells of the epidermis), driving the uncontrolled proliferation that produces the tumor. The strong predilection of keratoacanthomas for sun-exposed skin surfaces is consistent with a UV-mediated pathogenesis.

Importantly, PUVA therapy, a combination phototherapy using psoralen plus ultraviolet A light to treat skin conditions such as psoriasis, vitiligo, and eczema, is associated with an increased risk of keratoacanthoma development. This reflects the mutagenic potential of cumulative UVA exposure.

Chemical Carcinogens

Exposure to a range of chemical carcinogens has been associated with keratoacanthoma development, including:

• Tobacco smoke: The carcinogens in cigarette smoke may contribute to keratoacanthoma risk, either through direct mucosal contact (relevant for oral keratoacanthomas) or systemic effects.
• Industrial chemicals and occupational carcinogens: Including polycyclic aromatic hydrocarbons and other known chemical mutagens.
• Tar and pitch products: Historical and occupational exposure.

Immunosuppression

Immunocompromised individuals, such as solid organ transplant recipients on long-term immunosuppressive therapy, patients with HIV/AIDS, those with hematological malignancies, and people taking systemic immunosuppressive medications, face a significantly higher risk of developing keratoacanthoma. This is consistent with the understanding that an intact immune system plays a crucial role in identifying and eliminating aberrant keratinocytes before they develop into clinically apparent tumors. The impaired immune surveillance in immunocompromised states allows these aberrant clones to proliferate unchecked.

Drug-Induced Keratoacanthoma

Certain targeted oncological therapies have been specifically associated with the development of keratoacanthoma as a paradoxical side effect:

• BRAF inhibitors (vemurafenib, dabrafenib): Used in the treatment of BRAF V600E-mutated metastatic melanoma, these targeted agents paradoxically activate the MAPK/ERK signaling pathway in cells lacking a BRAF mutation, driving hyperproliferation of keratinocytes and a dramatically increased risk of keratoacanthoma and cutaneous squamous cell carcinoma development. This well-recognized side effect requires active dermatological monitoring throughout BRAF inhibitor therapy.

• Hedgehog pathway inhibitors (vismodegib): Used in the treatment of advanced or metastatic basal cell carcinoma, vismodegib has been associated with the development of keratoacanthoma in some patients. This paradoxical effect is thought to involve dysregulation of keratinocyte proliferation through mechanisms independent of the Hedgehog pathway.

Human Papillomavirus (HPV)

Certain strains of human papillomavirus have been detected in a subset of keratoacanthoma lesions, suggesting a possible viral contribution to the pathogenesis in at least some cases. HPV is a well-established driver of epithelial proliferation. Although its role in keratoacanthoma has not been proven as a universal mechanism, the detection of HPV DNA in some KA tissue samples supports its potential involvement.

Trauma and Surgical Procedures

Local skin trauma, including prior surgical procedures, lacerations, burns, and injection sites, has been reported as a potential trigger for keratoacanthoma development at the site of injury. This phenomenon, known as the Koebner phenomenon or isomorphic response, occurs in several skin conditions and may reflect the triggering of abnormal keratinocyte proliferation by wound healing stimuli in genetically susceptible individuals.

Genetic Predisposition

A subset of keratoacanthoma cases occurs in the context of specific hereditary syndromes, suggesting an important genetic dimension to susceptibility:

• Muir-Torre syndrome: An autosomal dominant inherited cancer predisposition syndrome (caused by mutations in the DNA mismatch repair genes MLH1 and MSH2, the same genes implicated in hereditary non-polyposis colorectal cancer/Lynch syndrome) characterized by the development of sebaceous skin tumors (including sebaceous adenomas and carcinomas) and multiple keratoacanthomas in association with internal malignancies (particularly colorectal, endometrial, and urological cancers). The discovery of multiple keratoacanthomas in a single patient, especially when associated with sebaceous tumors, should prompt evaluation for Muir-Torre syndrome.

• Ferguson-Smith syndrome: A rare autosomal dominant condition caused by mutations in the TGFBR1 gene, characterized by multiple, self-healing keratoacanthomas that develop primarily during adolescence and early adulthood, predominantly on sun-exposed skin.

• Grzybowski syndrome: An extremely rare condition characterized by the development of thousands of generalized eruptive keratoacanthomas.

Epidemiology

• Age: Keratoacanthomas can develop at any age but are rare before the age of 20. The peak incidence occurs between 50 and 70 years of age, reflecting the cumulative effects of UV exposure and other mutagenic factors over a lifetime.
• Sex: Keratoacanthomas occur about twice as often in men as in women, with a male-to-female ratio of roughly 2:1. This difference likely reflects historically higher levels of outdoor UV exposure and occupational carcinogen exposure in men. However, this gap may shrink as patterns of outdoor and occupational exposure evolve.

Risk Factors

The principal individual risk factors for keratoacanthoma include:

• Fair skin (Fitzpatrick skin types I–II): Lighter skin contains less melanin, the natural UV-protective pigment, resulting in less protection against UV-induced DNA damage. Fair-skinned individuals, particularly those with light hair, blue or green eyes, and a tendency to burn rather than tan, are at substantially higher risk.

• Cumulative sun exposure: A lifetime history of significant sun exposure, whether from outdoor work, recreational activities, or residence in high-UV environments, is the most important modifiable risk factor.

• Immunosuppression: As discussed above, transplant recipients, HIV-positive individuals, and patients on long-term immunosuppressive medications are at significantly elevated risk.

• History of other skin cancers: A personal or family history of skin cancer, including basal cell carcinoma, squamous cell carcinoma, or melanoma, increases the likelihood of keratoacanthoma development. This reflects shared risk factors and possibly shared genetic vulnerabilities.

• Certain medications: BRAF inhibitors, Hedgehog pathway inhibitors, and potentially other targeted cancer therapies with known dermatological side effect profiles.

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Symptoms and Clinical Appearance

Keratoacanthoma most commonly develops on hair-bearing, sun-exposed skin. This pattern reflects both the UV-mediated pathogenesis and the follicular origin that has been proposed for the tumor. The most frequently affected sites include:

• Face: Particularly the nose, cheeks, lips, and ears.
• Scalp and neck.
• Dorsum (back) of the hands and forearms.
• Dorsum of the feet and lower legs.
• Trunk: Less commonly affected than the above sites.

Less frequently, and often overlooked, keratoacanthoma can also develop on mucosal surfaces, including:

• The oral mucosa (inner cheeks, gums, hard palate, floor of mouth).
• The lips.
• Periungual (around the nails) and subungual (under the nails) regions.
• Perianal skin and buttocks.

Mucosal keratoacanthomas may present diagnostic challenges, as their clinical appearance can differ from the classic cutaneous form and they may more closely resemble other mucosal lesions.

The Three Stages of Development

Stage 1: Proliferative Phase (Weeks 1–8)

The initial lesion typically presents as a small, flesh-colored or pink, dome-shaped papule, which is a raised, pimple-like bump. At this early stage, it can be easily mistaken for other common skin lesions, such as cysts, lipomas, or even molluscum contagiosum. What distinguishes keratoacanthoma from the outset is the extraordinary speed of its growth. In just 6 to 8 weeks, the lesion expands dramatically, often reaching 1–2 cm in diameter. Some lesions, known as giant keratoacanthomas, may grow even larger, up to 3 cm or more. During this time, it evolves from a flat papule into a raised, dome-shaped nodule with a characteristic central crater or cup filled with a plug of keratin. This central keratin plug, which is pale yellow, firm, and compacted, serves as the hallmark of the mature keratoacanthoma lesion. The surrounding skin is often slightly reddish or inflamed.

The rapidity of this growth phase can be extremely alarming to patients. This concern is appropriate, since such rapid growth should always prompt urgent dermatological evaluation to exclude malignancy.

Stage 2: Maturation (Stable) Phase (Weeks to Months)

Following the initial explosive growth, the lesion enters a period of relative stability. Its size remains approximately constant, the dome-shaped architecture with the central keratin plug is maintained, and the surrounding inflammatory changes may partially subside. This phase can last from several weeks to several months.

Stage 3: Involution (Regression) Phase

In some cases, though not all, the keratoacanthoma starts to spontaneously involute. The central keratin plug is gradually extruded (shed), the lesion shrinks, and the nodule eventually resolves, typically leaving a depressed, atrophic, hypopigmented scar at the site. This capacity for spontaneous regression is one of the most distinctive features of keratoacanthoma and has historically been cited as evidence for its fundamentally benign nature. However:

• Not all keratoacanthomas involute: Some lesions remain stable or continue to grow without regression.
• The timeline is unpredictable: When involution does occur, it may take many months. During this period, the lesion can cause discomfort and cosmetic concern. In sensitive anatomical locations, it may also lead to functional impairment.
• Involuted lesions leave scars: The resulting atrophic scar may be cosmetically unacceptable, particularly on the face.
• The possibility of misclassified SCC: Given the histological overlap with squamous cell carcinoma, a “resolving” lesion that is not removed cannot be definitively confirmed as a true keratoacanthoma rather than an SCC.

These considerations collectively justify the standard recommendation for active treatment rather than watchful waiting in most patients.

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Complications

Despite its overall favorable prognosis when treated appropriately, keratoacanthoma is associated with several potential complications:

Local Tissue Destruction

Although keratoacanthoma does not typically invade blood vessels or lymphatics in the same aggressive manner as metastatic malignancy, locally advanced or poorly treated keratoacanthomas can cause significant local tissue destruction through their sheer size and expansive growth. This is particularly relevant:

• In the perinasal and periocular regions, where a rapidly growing nodule can erode cartilage, obstruct vision, or compromise the function of surrounding structures.
• On the lips, where large or ulcerated lesions may impair speech, eating, and mouth closure.
• On the fingers (subungual or periungual keratoacanthomas), where they can erode bone (phalanges) and cause permanent structural damage to the digit.

Ulceration and Bleeding

The central keratin plug may break down, which exposes the underlying crater to secondary infection, ulceration, and bleeding. These complications increase patient discomfort and can make the clinical picture harder to interpret.

Scarring

Both the natural involution of keratoacanthoma and the scarring from inadequately treated lesions can leave permanent, cosmetically significant atrophic scars, particularly on the face, hands, and other visible areas. Surgical excision with careful wound closure generally produces a better cosmetic outcome than the scar left by spontaneous involution.

Rare Metastases

While true metastatic spread of keratoacanthoma is generally considered rare, and some classification systems even take it as evidence that the lesion was actually a squamous cell carcinoma, metastases have been documented in a small number of cases. These typically occur in regional lymph nodes. This observation underscores the importance of:

• Histological examination of all removed keratoacanthoma specimens.
• Lymph node assessment during clinical examination.
• Ensuring that the clinical and histological diagnosis is robust before concluding that a given lesion is a “true” benign keratoacanthoma rather than a well-differentiated SCC.

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Diagnosis

The diagnosis of keratoacanthoma relies on a combination of clinical assessment, dermoscopic evaluation, and, most importantly, histopathological examination. No single clinical or imaging feature is specific enough to confirm the diagnosis without analyzing tissue samples.

Clinical Inspection

The starting point is a thorough visual inspection of the lesion, assessing:

• Morphology: The characteristic dome shape with a central keratin plug is strongly suggestive.
• Size and growth rate: Rapid growth (reaching 1–2 cm within 6–8 weeks) is a hallmark feature.
• Location: Sun-exposed, hair-bearing skin.
• Surrounding skin: Evidence of actinic damage (solar keratoses, solar lentigines, telangiectasias) as a marker of cumulative UV exposure.

Regional Lymph Node Examination

A complete physical examination must include palpation of the regional lymph nodes draining the anatomical site of the lesion (e.g., cervical and parotid lymph nodes for facial lesions; axillary lymph nodes for upper extremity lesions; inguinal lymph nodes for lower extremity lesions). The presence of lymphadenopathy should raise concern for nodal metastasis and prompt urgent investigation.

Dermoscopy

Dermoscopy (also called epiluminescence microscopy) involves examining a lesion with a specialized handheld device. This device combines optical magnification and either a polarized or non-polarized light source with a skin interface, offering additional diagnostic information. The dermoscopic features of keratoacanthoma include:

• A central keratin mass, which appears as a white or yellow structureless area.
• Peripheral hairpin vessels (looped, hairpin-shaped blood vessels at the periphery of the lesion), though these may also be seen in SCC.
• White circles (Menzies criterion).

However, it must be emphasized that dermoscopy cannot reliably distinguish keratoacanthoma from squamous cell carcinoma. This is an important limitation: while dermoscopy is useful for excluding other non-pigmented raised skin lesions, such as basal cell carcinoma or sebaceous hyperplasia, it cannot substitute for tissue biopsy. Dermoscopy is, however, very useful for excluding other differential diagnoses and for identifying additional lesions on the surrounding skin.

Biopsy and Histopathological Examination

Tissue biopsy with histopathological examination is the definitive diagnostic investigation and is essential in all cases. The biopsy approach is important:

• Shave biopsy: Generally not recommended, as it samples only the superficial portion of the lesion and may fail to capture the deep architecture necessary for distinguishing keratoacanthoma from invasive SCC.

• Punch biopsy: A circular skin punch through the full thickness of the lesion can provide better tissue, but may still miss the deep dermal components.

• Excisional biopsy: Surgical removal of the entire lesion is both the preferred diagnostic approach (providing the full lesion architecture for histological analysis) and the definitive treatment. This combined diagnostic-therapeutic approach is recommended in most cases.

Histopathological Features

Under the microscope, keratoacanthoma shows:

• A crater-shaped architecture with a central keratin-filled invagination.
• A glassy (ground-glass) cytoplasm in the proliferating keratinocytes, which is relatively characteristic of KA compared to SCC.
• A symmetrical, well-circumscribed lesion with a “shoulder” of normal epithelium on each side of the crater. Sometimes this appearance is described as the lesion being “cupped” by the surrounding epidermis.
• A pushing (rather than infiltrating) deep margin: the deep border of the lesion tends to push rather than irregularly infiltrate the surrounding dermis.
• A mixed inflammatory infiltrate in the dermis surrounding the lesion.

Despite these features, the histological distinction between keratoacanthoma and well-differentiated SCC can be extremely challenging. It requires careful assessment of the entire lesion architecture, which is why excisional rather than incisional biopsy is preferred.

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Treatment

Despite the generally benign nature of keratoacanthoma and its potential for spontaneous involution, active treatment is recommended in the vast majority of cases, primarily because:

1. The histological overlap with squamous cell carcinoma makes a definitive benign diagnosis uncertain without complete excision and histological review.
2. Spontaneous involution is unpredictable in timing and cannot be guaranteed.
3. When involution does occur, it leaves a scar.
4. Local tissue destruction can occur before involution.
5. A small but real risk of metastasis exists.

Surgical Excision

Surgical excision with histologically confirmed clear margins is the gold standard treatment for keratoacanthoma. The procedure involves:

• Complete removal of the lesion under local anesthesia with an appropriate surgical margin of surrounding normal-appearing skin.
• Submission of the entire specimen for histopathological examination is not optional, as it provides the only definitive confirmation of the diagnosis and exclusion of SCC.
• Wound closure with sutures often produces an excellent cosmetic result, generally better than the scar left by spontaneous involution.

Surgical excision is an outpatient (day procedure) operation in the vast majority of cases, typically performed under local anesthesia in a dermatology clinic or minor surgery suite.

Mohs Micrographic Surgery

For keratoacanthomas in cosmetically or functionally sensitive locations (periorbital, perinasal, periauricular, or on the lips), where maximal tissue conservation is important, Mohs micrographic surgery offers the advantage of complete margin examination with progressive layer-by-layer tissue removal under real-time microscopic control. This ensures the lowest recurrence rate while preserving the maximum amount of healthy surrounding tissue.

Alternative Ablative Procedures for Small Lesions

For sufficiently small keratoacanthomas, such as those measuring less than 1 cm, in locations where cosmetic outcome is less critical, or in patients for whom formal surgical excision is not feasible, the following less invasive alternatives may be considered:

• Cryosurgery (cryotherapy): Destruction of the lesion by application of liquid nitrogen, causing freeze-thaw injury to the tumor cells. Effective for small, superficial lesions. Does not provide tissue for histological analysis.

• Electrodesiccation and curettage (ED&C): The lesion is removed by scraping (curettage) with a dermatological curette, followed by destruction of the tumor base with an electrocautery device. As with cryotherapy, no intact tissue specimen is available for histological examination, which limits the ability to confirm the diagnosis and exclude SCC.

Both ablative approaches are associated with higher recurrence rates than surgical excision and do not provide histological confirmation of the diagnosis. This is a significant clinical disadvantage given the SCC overlap issue.

Pharmacological (Non-Surgical) Alternatives

In selected cases, particularly those where surgery is not feasible, in patients with multiple lesions (as in Grzybowski syndrome or in patients on BRAF inhibitors), or when lesions are in anatomically challenging locations, pharmacological treatment options may be considered:

• Imiquimod 5% cream (topical immune response modifier): Applied to the lesion surface, imiquimod stimulates innate and adaptive immune responses against the tumor through Toll-like receptor 7 activation, promoting cell-mediated anti-tumor immunity. It is typically applied several times per week for several weeks. Evidence is primarily from case reports and case series.

• 5-Fluorouracil (5-FU): Available both as a topical cream for superficial lesions and as a local intralesional injection for deeper or more resistant lesions. 5-FU is an antimetabolite that inhibits thymidylate synthase, blocking DNA synthesis in rapidly proliferating cells. Intralesional 5-FU injections have been reported to be effective for some keratoacanthomas, particularly in patients with multiple or surgically inaccessible lesions.

• Intralesional methotrexate injections: Methotrexate, a folate antagonist that inhibits dihydrofolate reductase and thereby impairs DNA synthesis, injected directly into the lesion has been reported as effective in some cases. This is particularly true for elderly patients or those with lesions in surgically challenging locations.

• Oral isotretinoin (13-cis-retinoic acid, a synthetic analog of vitamin A): Used systemically, isotretinoin promotes keratinocyte differentiation and apoptosis and has been used, often in combination with other treatments, for patients with multiple keratoacanthomas or those at high risk of recurrence (e.g., patients on BRAF inhibitors). Its significant teratogenicity and other systemic side effects mean that it must be used under careful medical supervision.

• Intralesional bleomycin or interferon: Reported in smaller case series; may be considered in specific circumstances.

Post-Treatment Monitoring and Sun Protection

Following successful treatment of keratoacanthoma, long-term dermatological follow-up is strongly recommended:

• Regular skin examinations: Patients who have developed one keratoacanthoma are at elevated risk of developing additional keratoacanthomas and other skin malignancies (basal cell carcinoma, squamous cell carcinoma). Regular dermatological surveillance, typically every 6 to 12 months, allows early detection and treatment of new lesions.

• Rigorous photoprotection: Sun avoidance and comprehensive sun protection measures are essential for all patients with a history of keratoacanthoma:

  • Daily use of broad-spectrum (UVA and UVB) sunscreen with SPF 50+ on all sun-exposed skin, reapplied every 2 hours during outdoor exposure.
  • Wearing protective clothing (long-sleeved shirts, wide-brimmed hats, UV-protective sunglasses).
  • Avoiding peak UV radiation hours (10 AM to 4 PM).
  • Avoiding tanning beds and UV-emitting recreational devices.

• Discontinuation or modification of causative medications: When keratoacanthoma is related to BRAF inhibitor or other targeted therapy, the dermatologist and oncologist should collaborate to assess the risk-benefit balance of continuing, dose-reducing, or switching the causative agent.

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Frequently Asked Questions

Is keratoacanthoma dangerous?

Keratoacanthoma is classified as a benign tumor and, when treated promptly and completely, has an excellent prognosis with very low risk of recurrence or spread. However, it is not entirely without risk: it can cause local tissue destruction if left untreated, rarely metastasizes, and, most importantly, is histologically very similar to squamous cell carcinoma. This makes it impossible to definitively exclude malignancy without complete tissue removal and pathological examination. For these reasons, it should be taken seriously and treated rather than ignored or observed.

Can keratoacanthoma disappear on its own?

Yes, spontaneous involution (self-resolution) is a recognized feature of keratoacanthoma that distinguishes it from most other skin tumors. However, not all keratoacanthomas involute, the timing is unpredictable (often many months), the lesion may cause significant local damage before involuting, and the resulting scar may be cosmetically unacceptable. Furthermore, it is not possible to definitively rule out squamous cell carcinoma without removing and histologically examining the lesion. For all these reasons, active treatment is generally recommended rather than watchful waiting.

How quickly does keratoacanthoma grow?

One of the most alarming features of keratoacanthoma, and an important distinguishing characteristic, is its exceptional speed of growth. From its initial appearance as a small papule, it can reach 1–2 cm within just 6 to 8 weeks. Any rapidly growing dome-shaped skin lesion with a central keratin plug should prompt urgent dermatological evaluation.

What does a keratoacanthoma look like?

A typical keratoacanthoma is a dome-shaped, firm, flesh-colored or pink nodule with a central crater or cup filled with a hardened yellowish plug of keratin. It may appear volcano-like or crateriform. The surrounding skin is often slightly reddened or inflamed. It is most commonly found on sun-exposed skin of the face (nose, cheeks, lips, ears), scalp, neck, and backs of the hands.

Can keratoacanthoma come back after treatment?

After complete surgical excision with clear histological margins, recurrence rates are low, though not zero. Patients who have had one keratoacanthoma are at elevated lifetime risk of developing additional keratoacanthomas and other keratinocyte skin cancers (basal cell carcinoma, squamous cell carcinoma), reflecting shared underlying risk factors (particularly UV damage and immune status). Regular dermatological follow-up and rigorous photoprotection are therefore essential components of long-term management.

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References and Bibliography

• Keratoacanthoma - Patrick M. Zito; Richard Scharf. StatPearls, National Center for Biotechnology Information (NCBI).
• Schwartz RA. Keratoacanthoma: a clinico-pathologic enigma. Dermatologic Surgery. 2004;30(2 Part 2):326–333.
• Hodak E, Jones RE, Ackerman AB. Solitary keratoacanthoma is a squamous-cell carcinoma: three examples with metastases. American Journal of Dermatopathology. 1993;15(4):332–342.
• Kwiek B, Schwartz RA. Keratoacanthoma (KA): an update and review. Journal of the American Academy of Dermatology. 2016;74(6):1220–1233.
• Lien MH, Sondak VK. Nonsurgical treatment alternatives for basal cell carcinoma and squamous cell carcinoma. Journal of Skin Cancer. 2011;2011:571734.
• Dubas LE, Ingraffea A. Nonmelanoma skin cancer. Facial Plastic Surgery Clinics of North America. 2013;21(1):43–53.
• Cañueto J, Cardeñoso E, García-Hernández JL, et al. Epidermal growth factor receptor expression in keratoacanthoma and squamous cell carcinoma: a study of 43 cases. Acta Dermato-Venereologica. 2012;92(6):676–677.
• Feldman SR, Fleischer AB Jr, McConnell RC. Most common dermatologic problems identified by internists, 1990-1994. Archives of Internal Medicine. 1998;158(7):726–730.