WebDoctor Encyclopedia

Keratinocyte carcinomas

Bowen Disease

Squamous cell carcinoma that is still confined to the top layer of skin. It usually looks like a slowly growing red, scaly patch on sun-exposed skin.

Medically reviewed Last reviewed August 27, 2026

What Is Bowen Disease

Bowen disease is a form of cutaneous squamous cell carcinoma in situ. The term in situ means that the malignant cells are confined to the epidermis, the outermost layer of skin, and have not yet breached the basement membrane that separates the epidermis from the deeper dermis. Because the basement membrane remains intact, the lesion cannot spread to lymph nodes or distant organs at this stage.

The condition was first described by the dermatologist John Templeton Bowen in 1912. It is also referred to as squamous cell carcinoma in situ, Bowen’s disease, or intraepidermal carcinoma. Although it is a neoplasm, it behaves like a precancerous lesion because it may progress to invasive squamous cell carcinoma if left untreated.

Clinical Appearance

Typical lesions appear as a slowly enlarging, well‑defined, erythematous (red) plaque with a scaly or crusted surface. The border is often irregular, and the surface may feel rough like sandpaper. Most lesions develop on sun‑exposed skin such as the face, scalp, ears, neck, forearms, and lower legs.

In the anogenital region, Bowen disease can be associated with human papillomavirus (HPV) infection, especially high‑risk types 16 and 18. These genital lesions may be pigmented, velvety, or ulcerated and are sometimes called erythroplasia of Queyrat when they affect the glans penis or vulva.

Lesions are usually asymptomatic, but some patients report mild itching, burning, or tenderness. The size at presentation varies from a few millimetres to several centimetres.

Risk Factors

Factor Details
Age Most common after 60 years; rare before 40 years.
Ultraviolet radiation Chronic sun exposure is the principal environmental cause for extragenital lesions.
Immunosuppression Organ‑transplant recipients, HIV‑positive individuals, and patients on long‑term corticosteroids have higher incidence.
Arsenic exposure Historical exposure to arsenic‑contaminated water or medicines predisposes to multiple lesions, often on palms and soles.
Human papillomavirus High‑risk HPV types drive anogenital and some periungual variants.
Chronic skin injury Scars, chronic ulcers, and radiation dermatitis can act as local promoters.
Genetic susceptibility Fair skin, light eyes, and a personal or family history of non‑melanoma skin cancer increase risk.

Diagnosis

Clinical examination often suggests the diagnosis, but definitive confirmation requires a skin biopsy. A shave or punch biopsy that includes the full thickness of the epidermis is preferred because it allows the pathologist to assess the basement membrane.

Histologically, Bowen disease shows full‑thickness epidermal atypia: keratinocytes display enlarged, hyperchromatic nuclei, abundant mitoses, and loss of normal maturation. The basement membrane remains intact, distinguishing it from invasive squamous cell carcinoma where tumour nests penetrate the dermis.

Dermoscopy may reveal a scaly surface with glomerular vessels (coiled capillaries) and a white‑yellowish scale, but it is not a substitute for histopathology.

Treatment Options

Modality Typical Use and Features
Surgical excision Gold standard for solitary lesions; provides histologic margins and lowest recurrence.
Curettage and electrodesiccation Quick office procedure for small, low‑risk lesions on trunk or extremities; higher recurrence on high‑tension sites.
Topical 5‑fluorouracil Applied once or twice daily for 4–6 weeks; useful for multiple or large field‑change areas; causes inflammation and erosion.
Topical imiquimod Immune‑response modifier applied 3–5 times per week for 6–16 weeks; effective for superficial lesions, especially on the face.
Photodynamic therapy Photosensitiser (e.g., methyl aminolevulinate) followed by red light; good cosmetic outcome for multiple facial lesions.
Radiotherapy Reserved for patients unfit for surgery, large lesions, or sites where surgery would cause functional impairment.
Laser ablation Carbon‑dioxide or erbium:YAG laser for selected small lesions; limited long‑term data.

Choice of therapy depends on lesion size, site, number, patient comorbidities, and cosmetic considerations. All modalities are curative in the majority of cases when applied appropriately.

Risk of Progression to Invasive Squamous Cell Carcinoma

The reported progression rate varies across studies, but a commonly cited figure is approximately 3–5 % of untreated lesions becoming invasive over several years. In immunosuppressed patients the risk may be higher, sometimes quoted up to 10 %. Early treatment reduces this risk to well below 1 %.

Progression is more likely in lesions that are large, ulcerated, or located on high‑risk sites such as the ear, lip, or genital mucosa. Histologic features like marked cytologic atypia or subclinical dermal invasion on deep biopsy also raise concern.

Follow‑Up and Prevention

  • Patients treated for Bowen disease should have a full skin examination at least annually because they are at increased risk for new keratinocyte cancers.
  • Sun protection measures — broad‑spectrum sunscreen (SPF 30+), protective clothing, hats, and avoidance of peak UV hours — are essential to prevent new lesions.
  • Immunosuppressed individuals may benefit from more frequent surveillance, e.g., every 6 months, and from systemic retinoid chemoprevention under specialist supervision.
  • HPV vaccination before sexual debut reduces the incidence of anogenital Bowen disease and other HPV‑related neoplasia.
  • Patients with a history of arsenic exposure should be monitored for internal malignancies as well as cutaneous lesions.

Differential Diagnosis

Condition Key Distinguishing Features
Actinic keratosis Usually multiple, smaller, rough papules on sun‑damaged skin; histology shows partial‑thickness atypia, not full‑thickness.
Eczema (nummular dermatitis) Itchy, coin‑shaped plaques with vesiculation; responds to topical steroids; no atypia on biopsy.
Psoriasis Well‑demarcated erythematous plaques with silvery scale, often symmetric; Auspitz sign; histology shows parakeratosis and Munro microabscesses.
Invasive squamous cell carcinoma Ulcerated or nodular growth; histology demonstrates dermal invasion beyond basement membrane.
Superficial basal cell carcinoma Pearly border, telangiectasia; histology shows basaloid nests with peripheral palisading.
Paget disease of the breast/extramammary Often unilateral, eczematous nipple or genital lesion; immunohistochemistry positive for CK7, GCDFP‑15.

Key Points

  • Bowen disease is squamous cell carcinoma confined to the epidermis (in situ).
  • It presents as a persistent, scaly, erythematous plaque, most often on sun‑exposed skin.
  • Major risk factors include chronic UV exposure, immunosuppression, arsenic, and high‑risk HPV.
  • Diagnosis is confirmed by full‑thickness skin biopsy showing full‑thickness epidermal atypia with an intact basement membrane.
  • Multiple effective treatments exist; surgical excision offers the lowest recurrence, while topical and light‑based therapies provide good cosmetic results for selected lesions.
  • Untreated lesions carry a 3–5 % risk of progressing to invasive squamous cell carcinoma; treatment reduces this risk dramatically.
  • Long‑term follow‑up, rigorous sun protection, and HPV vaccination are cornerstone preventive strategies.

References

  1. National Cancer Institute. Squamous Cell Carcinoma of the Skin Treatment (PDQ®) – Health Professional Version. 2023. Available at: https://www.cancer.gov/types/skin/hp/skin-treatment-pdq Accessed: 27 August 2026.
  2. American Cancer Society. Skin Cancer – Squamous Cell Carcinoma. 2022. Available at: https://www.cancer.org/cancer/skin-cancer/squamous-cell-carcinoma.html Accessed: 27 August 2026.
  3. American Academy of Dermatology. Bowen’s Disease (Squamous Cell Carcinoma In Situ). 2021. Available at: https://www.aad.org/public/diseases/skin-cancer/bowens-disease Accessed: 27 August 2026.
  4. World Health Organization / International Agency for Research on Cancer. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Volume 100D: Radiation. 2012. Available at: https://publications.iarc.fr/116 Accessed: 27 August 2026.
  5. National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology: Squamous Cell Skin Cancer. Version 2.2024. Available at: https://www.nccn.org/professionals/physician_gls/pdf/squamous.pdf Accessed: 27 August 2026.
  6. Rogers HW, Weinstock MA, Feldman SR, Coldiron BM. Incidence Estimate of Nonmelanoma Skin Cancer (Keratinocyte Carcinomas) in the U.S. Population, 2012. JAMA Dermatology. 2015;151(10):1081‑1086. doi:10.1001/jamadermatol.2015.1187.
  7. Karia PS, Han J, Schmults CD. Cutaneous Squamous Cell Carcinoma: Estimated Incidence of Disease, Nodal Metastasis, and Deaths from Disease in the United States, 2012. Journal of the American Academy of Dermatology. 2013;68(6):957‑966. doi:10.1016/j.jaad.2012.11.015.
  8. British Association of Dermatologists. Guidelines for the Management of Cutaneous Squamous Cell Carcinoma In Situ (Bowen’s Disease). 2020. Available at: https://www.bad.org.uk/healthcare-professionals/clinical-guidelines/bowens-disease Accessed: 27 August 2026.
  9. Moy RL, Lee MW, Zalka A. Bowen’s Disease: A Review of Current Treatment Options. Dermatologic Surgery. 2019;45(3):321‑332. doi:10.1097/DSS.0000000000001765.
  10. Karia PS, Jambusaria-Pahlajani A, Harrington DP, et al. Evaluation of American Joint Committee on Cancer, International Union Against Cancer, and Brigham and Women’s Hospital Tumor Staging for Cutaneous Squamous Cell Carcinoma. JAMA Dermatology. 2014;150(4):376‑382. doi:10.1001/jamadermatol.2013.6005.