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Squamous Cell Carcinoma in situ (Bowen’s Disease)

Squamous Cell Carcinoma in situ (Bowen’s Disease)


Squamous cell carcinoma (SCC) in situ, also known as Bowen disease, is SCC confined to the epidermis and superficial adnexal epithelium, further characterised by full-thickness involvement of the epidermis by dysplastic squamous cells. The term “Bowen disease” was originally used specifically to describe SCC in-situ in sun-protected skin as a harbinger of internal malignancy, but the terms “Bowen disease” and “SCC in situ” are now used interchangeably to describe epidermal SCC in situ of both sun-dam-aged and sun-protected skin.


Intraepidermal carcinoma; Bowenoid papulosis; keratinocytic intraepidermal neoplasia (KIN Ill) Vulvar intraepithelial neoplasia (VIN Ill), penile intraepithelial neoplasia (PelN Ill), erythroplasia of Queyrat, and anal intraepithelial neoplasia (AIN Ill) are discussed in the relevant WHO classifications of tumours of the corresponding organ systems.


Most cases present in the sun exposed skin of elderly White patients with higher cumulative sun exposure, with a median age of presentation > 60 years. Specific populations at higher risk of SCC in situ include organ transplant recipients on immunosuppressive regimens and populations with long-term exposure to high levels of arsenic in drinking-water. Ultra-violet (UV) radiation exposure from tanning beds has resulted in an increased number of young people presenting with SCC in situ, but the finding of SCC in situ in a young person with minimal sun damage should prompt consideration of arsenic exposure.


Most cases of SCC in situ (Bowen disease) are caused by UV radiation expo-sure, including UVB and UVA radiation exposure from sunlight or tanning beds. Radiotherapy and photo chemotherapy are also etiological. High-risk (alphagenus) HPV infection is the major cause of SCC in situ involving the peri-ungual region and genital skin. The terms “VIN Ill” and “PelN Ill” are used for genital lesions. Beta genus papilloma viruses may have synergistic effects with UV radiation in the setting of immunosuppression due to organ transplant or HIV infection in causing some cutaneous SCCs in situ. Arsenic ingestion can play a role in SCC in situ in non sun exposed skin.


SCC in situ predominantly involves sun-exposed skin, but also occurs in non sun exposed skin. Typical sites of involvement include the lower limbs, head, neck, and hands. Less commonly affected regions include subungual, periungual, genital (VIN III, PelN III, and erythroplasia of Queyrat), and perianal (AIN III) sites.

Clinical features

SCC in situ usually presents as a solitary, slow-growing, scaly, erythematous patch or plaque, which can remain unchanged for many years. Clinical features include crusting, pigmentation, and a verrucous appearance.  Dermoscopic features include scale, glomerular vessels, yellow crust, haemorrhage, hypopigmentation, and linear irregular vessels.


UV radiation—induced mutations of TP53play a role in the development of many SCCs. SCC in situ in the context of arsenic exposure arises from oxidative stress, depletion of natural antioxidants, immune dysfunction, genotoxicity, impaired DNA repair, and disrupted signal transduction{1155}.

Genetic profile

UV radiation—induced mutations of the gene encoding p53, which is centrally involved in cellular apoptosis, proliferation, and DNA repair, are present in 40% of SCC in situ cases. Amplification and activating mutations of HRAS, NRAS, and KRAS, likely due to UVB radiation exposure, are common. Molecular and cytogenetic studies pro-vide supporting evidence that SCC in situ and actinic keratoses are precursors of invasive SCCs.

Prognosis and predictive factors

Approximately 3—5% of all SCC in situ lesions progress to invasive SCC; among erythroplasia of Queyrat lesions specifically, the proportion is 10%.


WHO classification of skin tumours, 4th edition (2018): 46-47.

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