Disease relevance of Bowen's Disease

• The percentages of hCDC47-positive cells were 65.4% in squamous-cell carcinomas, 60.9% in Bowen's disease, 12.6% in seborrheic keratosis and 3.9% in normal epidermis (n = 5 in all cases) [1].
• The frequency of 8-hydroxy-2'-deoxyguanosine positive cases was significantly higher in arsenic-related skin neoplasms (22 of 28; 78%) than in arsenic-unrelated Bowen's disease (one of 11; 9%) (p < 0.001 by chi2 test) [2].
• In seborrheic keratosis, a benign condition, cells with hCDC47-positive nuclei were located in the outermost layers of the tumor lobules, while in Bowen's disease, carcinomas in situ and squamous-cell carcinomas, they were present throughout the lesions [1].
• In premalignant actinic keratoses and Bowen's disease, 42% (11 out of 26) of samples exhibited telomerase activity [3].
• The increasing number of successful renal transplantations worldwide is producing a progressive increase in patients at risk for non-melanoma skin cancers, such as squamous cell carcinoma (SCC), basal cell carcinoma (BCC), and Bowen's disease (BD), and at significantly increased risk for metastatic SCC [4].

Psychiatry related information on Bowen's Disease

• The latency periods for the development of arsenical keratoses, Bowen's disease, and SCC were 28, 39, and 41 years, respectively [5].

High impact information on Bowen's Disease

• Epidemiologic studies demonstrated that long-term exposure to arsenic induces arsenical skin cancers, including Bowen's disease [6].
• The role of oxidative DNA damage in human arsenic carcinogenesis: detection of 8-hydroxy-2'-deoxyguanosine in arsenic-related Bowen's disease [2].
• p53 mutation spectrum in Japanese Bowen's disease suggests a role for mutagens other than ultraviolet light [7].
• This suggests that the Fragile Histidine Triad gene is not a common target for deletion in Bowen's disease and the cell lines HaCaT and A431 [8].
• In Bowen's disease, GST-pi positive, dysplastic cells existed throughout the epidermis [9].

Chemical compound and disease context of Bowen's Disease

• 8-Hydroxy-2'-deoxyguanosine was also detected in normal tissue adjacent to the arsenic-related Bowen's disease lesions [2].
• METHODS: Twenty-six patients with biopsy-proven Bowen's disease received eight 5-FU iontophoretic treatments in 4 weeks [10].
• The arsenic-induced increases in SCEs and HFCs were also consistently, but not statistically significantly, higher in arsenic-induced Bowen's disease patients than in matched controls at all arsenite treatment levels of 0.5, 1.0 and 2.0 microM [11].
• Carbon dioxide laser provides ease of surgery, excellent cosmesis, preservation of function, and effective treatment for patients with Bowen's disease of the digits [12].
• Treatment of multiple lesions of Bowen disease with isotretinoin and interferon alfa. Efficacy of combination chemotherapy [13].

Biological context of Bowen's Disease

• Histology showed that both cases were Bowen's disease, and subsequent treatment with 5-fluorouracil and cryotherapy led to complete resolution [14].
• PATIENTS AND METHODS: Allelic imbalance analysis was performed in 22 SCC and five Bowen's disease specimens [15].
• Mutational analysis was performed on exons 1alpha, 1beta and 2 of the CDKN2A locus in 22 SCC, five Bowen's disease and 39 BCC specimens [15].
• Cell surface carbohydrates in proliferative epidermal lesions. II. Masking of peanut agglutinin (PNA) binding sites in solar keratoses, Bowen's disease, and squamous cell carcinoma by neuraminic acid [16].
• We evaluated immunohistochemically the p53 phosphorylation state of Ser392 and Ser15 sites in 44 actinic keratoses (AKs), 62 squamous cell carcinomas (SCCs), 23 Bowen's disease (BDs) and 43 basal cell carcinomas (BCCs) [17].

Anatomical context of Bowen's Disease

• Survivin was also expressed in 19 premalignant lesions of Bowen's disease (SCC in situ) and hypertrophic actinic keratosis (HAK), suggesting that its appearance occurs early during keratinocyte transformation [18].
• Defective IL-2 receptor expression in lymphocytes of patients with arsenic-induced Bowen's disease [19].
• In SCC and Bowen's disease, 1-2B7B antigen was expressed not only along the interface of the tumor nest and stromal tissue, but also in the intercellular space of the desmosomes and other adhesion junction structures that lack associating tonofibrils [20].
• HPV DNA was found in 93% of common warts, 69% of squamous cell carcinomas (SCC), 52% of basal cell carcinomas (BCC), 41% of actinic keratoses, 31% of extragenital Bowen's disease, 22% of keratoacanthomas, 16% of normal skin tissues and 47% of hair follicles [21].
• No differences between Bowen's disease and bowenoid papulosis were found in terms of densities of S 100-positive dendritic cells and keratin pattern [22].

Gene context of Bowen's Disease

• The PCNA labelling index was 36.9 +/- 12.6% in Bowen's disease (n = 16), and 40.7 +/- 11.0% in Bowen's carcinoma (n = 3) [23].
• Normal adult skin, squamous cell carcinoma (SCC), senile keratosis, Bowen's disease, basal cell carcinoma (BCC), seborrhoeic keratosis and verruca vulgaris were stained immunohistochemically with a panel of monoclonal and polyclonal antibodies that recognize different epitopes of CEA and related molecules [24].
• The expression of CD9, CD81 and CD82 was markedly down-regulated in basal cell carcinoma but not in Bowen's disease [25].
• By contrast, differentiating epidermal tumours such as Bowen's disease, keratoacanthoma and squamous cell carcinoma expressed SPRR3 [26].
• All preneoplastic epidermal lesions showed p63 expression in all cell layers. p53 was found in seven of 10 cases of BCCs, all 10 cases of SCCs, and nine of 10 cases of Bowen's disease [27].

Analytical, diagnostic and therapeutic context of Bowen's Disease

• In immunohistochemistry analysis, p53 overexpression was found in 43.5% (10/23) of cases with Bowen's disease, 14% (1/7) of cases with BCC and 44% (4/9) of cases with SSC [28].
• Randomized comparison of photodynamic therapy with topical 5-fluorouracil in Bowen's disease [29].
• OBJECTIVE: We sought to determine whether iontophoresis of 5-FU is an effective therapy for Bowen's disease [10].
• Thus, we report these two cases to illustrate that CK 7 can be expressed by pagetoid Bowen disease and should not be a cause of confusion in the differential diagnosis [30].
• Mohs surgery has been reported in three previous publications as a successful treatment for local invasive vulvar SCC and Bowen's disease [31].

References