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Morphometric assessment of nuclei in Bowen's disease and bowenoid papulosis.

BACKGROUND: Occasionally, Bowen's disease and bowenoid papulosis cannot be distinguished in microscopic finding. Their clinical presentations are quite different from one another. The purpose of this study was to evaluate the histological differences in Bowen's disease and bowenoid papulosis, by comparing the size and shape of nuclei, using image analysis system. METHODS: We performed morphometric assessment on 13 specimens of Bowen's disease and eight specimens of bowenoid papulosis using an image analysis system, and the following parameters were calculated, such as nuclear contour index (NCI), irregularities of nucleus (IN), form factor (form AR) and circulatory factor (form PE). RESULTS: For NCI, there were significant differences between the Bowen's disease and bowenoid papulosis, and IN also shows significant differences between these two dis-eases, showing that Bowen's disease has more corrugated or indented nucleus contour than bowenoid papulosis. In the parameter of form PE, there were significant differences between the two diseases, indicating that Bowen's disease has more oval-shaped nuclei than bowenoid papulosis. There were no significant differences in form factor between Bowen's disease and bowenoid pupulosis. CONCLUSIONS: Significant differences were found in the morphometric evaluation between Bowen's disease and bowenoid papulosis. The nuclei were larger, more oval and more irregular margins in Bowen's disease than bowenoid papulosis.

Adult↗

Photodynamic therapy in the treatment of Bowen's disease.

BACKGROUND: The treatment of Bowen's disease in anatomically difficult areas or especially large lesions can challenge accepted modalities of treatment. OBJECTIVE: The purpose of this study was to illustrate the effectiveness of photodynamic therapy in the treatment of Bowen's disease. In addition, photodynamic therapy may be used as adjuvant therapy for difficult lesions. METHODS: Six patients with Bowen's disease in various anatomic sites were treated with photodynamic therapy. Four were in a difficult anatomic site, or were especially large, or both. Photofrin, 1.0 mg/kg, was administered intravenously and laser treatment was given approximately 48 hours later with the argon dye laser. Light was administered at a wavelength of 630 nm and the light dose ranged from 185 to 250 joules/cm2. Treatment was given by surface radiation only. RESULTS: Eight lesions were treated. All showed a complete response at 3 months (100%) and continue to show a complete response at 6 and 12 months. Morbidity was low; the most significant side effects were moderate pain and edema. Healing time varied depending on the size of the lesion. CONCLUSION: Photodynamic therapy is an effective and useful alternative for Bowen's disease, especially those lesions in anatomically difficult areas or those that are especially large.

Adult↗

Topical treatment of Bowen's disease with 5-Fluorouracil.

BACKGROUND: Bowen's disease is a common skin cancer. There are many different therapeutic approaches to treatment. Topical 5-Fluorouracil (5-FU) cream has been used for many years and there are many published papers attesting to its effectiveness. However, no papers have presented long-term followup results with biopsy confirmation of cure. OBJECTIVES: The purpose of this article is to present the long-term findings following the use of this cream in the treatment of Bowen's disease. METHODS: Twenty-four patients with 26 biopsy-confirmed lesions of Bowen's disease were treated with topical 5-Fluorouracil cream and were followed for periods of up to 10 years. Posttreatment biopsies were performed in most cases. RESULTS: Two of the 26 lesions treated topically recurred at some point. The rest were apparently cured. CONCLUSION: The results presented in this article confirm that treatment of Bowen's disease with topical 5-Fluorouracil cream is safe and effective treatment.

Aged↗

Expression of E-cadherin in skin carcinomas.

In this study, we investigated the expression of E-cadherin in 31 cases of human skin carcinoma including basal cell carcinoma (BCC), squamous cell carcinoma (SCC), Paget's disease, Bowen's disease (invasive type), and trichilemmal carcinoma, by immunohistochemical staining using a monoclonal antibody specific for E-cadherin. Similar to the E-cadherin expression in normal epidermis, E-cadherin was strongly expressed in all samples of BCC on the cell borders, whereas marked decrease or loss of E-cadherin expression was found in the tumor cells of SCC, Paget's disease, and Bowen's disease (invasive type). On the other hand, E-cadherin expression of trichilemmal carcinoma was slightly reduced. Considering the clinical and histological features of these skin carcinoma, the reduction of E-cadherin expression is considered to be associated with the invasion and metastasis of human skin carcinoma.

Adult↗

Secondary localized cutaneous amyloid in Bowen's disease.

A case of Bowen's disease is described in which striking quantities of amyloid were detected in the papillary dermis visualized easily by routine haematoxylin and eosin staining. The material showed positive labelling with an antikeratin monoclonal antibody consistent with the proposed origin of the amyloid as degenerate keratinocytes. The pathobiology of amyloid associated with dysplastic squamous lesions is discussed.

Amyloid↗

Bowen's disease concealed by purpura.

Bowen's disease (BD) is a squamous cell carcinoma in situ characterized by a well-demarcated scaly erythematous thin plaque with an irregular outline. Clinically, BD is frequently misdiagnosed as superficial basal cell carcinoma, patches of dermatitis, psoriasis, lichen planus, actinic keratosis, benign lichenoid keratosis, irritated seborrheic keratosis, viral warts, amelanotic melanoma or melanoma. However, angiosarcoma has not usually been mentioned in the differential diagnosis of BD before. Herein, we describe two cases of BD presenting as purpura on the scalp of the elderly with an initial clinical suspicion of angiosarcoma.

Aged↗

High frequency of DNA aneuploidy detected by DNA flow cytometry in Bowen's disease.

To detect DNA aneuploidy in Bowen's disease, we investigated DNA flow cytometric analysis. Single cell suspensions were prepared from 18 fresh samples histopathologically diagnosed as solitary Bowen's disease and analyzed by DNA flow cytometry. In 16 (89%) of 18 lesions, DNA aneuploidy was demonstrated with a single aneuploid peak. DNA indices ranged from 1.29 to 1.74. The incidence of DNA aneuploidy in Bowen's disease is higher than those of cutaneous squamous cell carcinoma, which was 25-80% in the previous reports. Therefore, in Bowen's disease. DNA aneuploidy may not imply a good marker for characteristics of non-melanoma skin cancer. A single aneuploid peak commonly observed in Bowen's disease suggests that this disease consists of the monoclonal proliferation of keratinocytes containing abnormal DNA content.

Aged↗

[Expression of keratin 16 in normal and lesional skin of solitary and multiple Bowen's disease using monoclonal antibody Ks 8.12 staining].

Bowen's disease is an intraepidermal squamous cell carcinoma usually consisting of a solitary lesion. However, multiple Bowen's lesions are one of the characteristics of arsenicalism in endemic areas where people drink deep well water containing high concentrations of arsenic along the southwest coast of Taiwan. This work seeks to clarify the differences between multiple Bowen's disease in the blackfoot disease endemic area, and solitary Bowen's disease in a non-endemic area by means of Ks 8.12 monoclonal cytokeratin antibody staining. Ks 8.12 may be regarded as a specific antibody for Keratin 16 in the skin and is used as a marker for hyperproliferation. Our results show that Ks 8.12 staining of normal skin in patients with a solitary Bowen's lesion is patchy and always restricted to the basal cell layer. By contrast, the normal skin of patients with multiple Bowen's lesions shows diffuse Ks 8.12 staining of the basal cell layer and various degrees of staining of the suprabasal layers. Similar results were observed in both solitary and multiple Bowen's lesions showing diffuse Ks 8.12 staining of the epidermis. Our results revealed clear differences in keratin expression between the clinically normal skin of patients with solitary Bowen's disease and that of patients with chronic arsenicalism. Finally the clinically normal skin of patients with multipole Bowen's disease showed characteristic changes in the expression of Keratin 16 in the suprabasal layers.

Aged↗

Bowen's disease of the plantar arch.

Bowen's disease has previously been associated with the development of other malignancies particularly in patients with a history of arsenic exposure. A review of the literature is combined with a discussion of current theories regarding arsenic exposure, lesion differentiation, and prognostic implications. This report of a bowenoid lesion of the plantar arch emphasizes the importance of close follow-up of patients with Bowen's disease, especially on unexposed surfaces.

Arsenic↗

[A case of coexistence of Bowen's disease of the vulva with pre-invasive cancer of the cervix uteri].

The Bowen disease is rare, especially when the focus is located on the vulva. In each case of diagnosis of+ the disease, one should also examine the patient with respect of the coexistence of an additional neoplastic focus in the skin or other internal organs. In their teaching hospital the authors observed a patient in whom the Bowen disease coexisted with preinvasive cervical carcinoma.

Adult↗

P16(INK4A) expression in Bowen's disease and Bowenoid papulosis.

BACKGROUND: Bowen's disease (BD) is a skin carcinoma in situ occurring over the entire body surface. It shares similar histopathological features with Bowenoid papulosis (BP) of the genitalia, but differs in etiology and clinical course. Increased p16(INK4A) (p16) tumor suppressor protein expression has been demonstrated in relation to the progression of cutaneous squamous neoplasms. OBJECTIVE: To evaluate the difference in p16 expression between Bowen's disease and Bowenoid papulosis. MATERIAL AND METHOD: Biopsies of 46 cases of BD in the period 1994 - 2003 and 14 cases of BP during 1987 - 2003 in the Anatomical Pathology Unit, Department of Pathology, Faculty of Medicine, Prince of Songkla University, Thailand were studied by immunohistochemical methods using the P16 kit (CINTec Histology Kit, clone E6H4, Code-Nr. K5334, DakoCytomation, Denmark). Nuclear/cytoplasmic immunoreactivity in more than 10% of neoplastic cells was considered positive. RESULTS: P16 expression was positive in 37 of 46 BD cases (80.4%) which was higher than that of BP (6 of 14 cases or 42.9%) (p value < 0.05, Chi-square test). The expression among the three groups of BD: extragenital (28 of 35), chronic arsenical-related (7 of 8) and genital lesions (2 of 3) was not significantly different (p value = 0.734, Chi-square test). CONCLUSION: P16 expression was more frequent in BD than BP. This suggests a possible association between p16 expression and tumorigenesis of these lesions.

Adult↗

Bowen's disease: squamous cell carcinoma in situ.

Bowen's disease is a premalignant condition that clinically presents as an asymptomatic, scaly or crusted plaque on the skin. Since the morphology of the lesions can mimic that of other cutaneous disorders, Bowen's disease is often not recognized initially. The diagnosis of Bowen's disease should be considered and a skin biopsy performed when a patient presents with a persistent cutaneous lesion that is of uncertain diagnosis or that has been previously diagnosed as "atypical" or "steroid-nonresponsive" dermatitis.

Bowen's Disease↗

[DNA determination by cytophotometry in bowenoid papules in comparison with condylomata acuminata and Bowen's disease].

The relation between bowenoid papules and Bowen's disease is characterized by largely corresponding histological pictures and diverging clinical-epidemiological features. In bowenoid papules and Bowen's disease, 5 cases each, compared with 5 cases of common condylomata acuminata, we determined the DNA by means of Feulgen's cytophotometry in visible light after Feulgen's staining. The following results were obtained: The average DNA content in bowenoid papules equals that in Bowen's disease, but it is significantly higher than in condylomata acuminata. What is different between the two groups "bowenoid papules" and "Bowen's disease" is the distribution of DNA: In Bowen's disease, DNA spreads into higher ranges of polyploidy. If we take recent molecular biological/virological findings into account, this result can be interpreted as a transition towards carcinoma in situ.

Adult↗

Imiquimod 5% cream in the treatment of Bowen's disease.

BACKGROUND: Large-diameter lesions of Bowen's disease at sites such as the shin may be difficult to treat surgically and may require alternate treatment modalities. OBJECTIVE: We investigated whether imiquimod 5% cream, a topical immune response modifier that stimulates the production of interferon alfa and other cytokines, is an effective topical treatment for Bowen's disease. METHODS: This was a phase II, open-label study in 16 patients, treating a single biopsy-proven plaque of Bowen's disease that was 1 cm or larger in diameter, with once-daily self-application of imiquimod 5% cream for 16 weeks. A biopsy was performed on the treated area 6 weeks after the end of treatment, with patient follow-up at 3 and 6 months. Lymphocyte CD4/CD8 ratios were analyzed in pretreatment and posttreatment biopsy specimens by immunophenotyping the lymphocytic infiltrate. RESULTS: Sixteen patients with Bowen's disease lesions ranging from 1 to 5.4 cm in diameter (0.7-21.6 cm(2) in area) were treated. Fifteen of these lesions were on the legs, and one was on the shoulder. Fourteen of the 15 patients (93% per protocol analysis) had no residual tumor present in their 6-week posttreatment biopsy specimens. One patient died of unrelated intercurrent illness before a biopsy specimen could be obtained. The median CD4/CD8 lymphocyte ratio in pretreatment biopsy specimens was 2:1, and this was reversed to a median of 1:2.2 in the posttreatment specimens. Ten patients completed 16 weeks of treatment, but 6 patients ceased treatment early (between 4 and 8 weeks) because of local skin reactions. CONCLUSION: Imiquimod 5% cream appears to be an effective treatment for Bowen's disease on the lower limbs. The 93% positive treatment response in biopsy-proven cases (excludes patient who died from an intercurrent illness who did not undergo a posttreatment biopsy) compares favorably with other current treatment modalities. The dosing schedule and length of treatment for Bowen's disease require further evaluation.

Administration, Topical↗

Partial spontaneous regression of Bowen's disease.

BACKGROUND: Although the lesions of Bowen's disease often show conspiciously irregular configurations, there have been no studies performed to elucidate what these clinical features imply. Of 90 patients with Bowen's disease, 34 (group 1) had such irregular lesions with patches of normal-appearing interlesional skin. Their clinical backgrounds were compared with those of 56 patients without irregular lesions (group 2). Specimens of lesional, interlesional, and perilesional skin from 17 patients in group 1 were examined to evaluate the histopathologic evidences of regression. OBSERVATIONS: The lesions of group 1 patients were more commonly located on the trunk, larger in size, and of longer duration than those of group 2 patients. The specimens of lesional skin from the 17 group 1 patients revealed amyloid deposition (12 patients), melanophages (three patients), increased vascularity (15 patients), and inflammatory cell infiltrates (17 patients). The interlesional skin also exhibited amyloid deposition (12 patients), melanophages (six patients), increased vascularity (15 patients), dermal fibrosis (16 patients), inflammatory cell infiltrates (15 patients), and epidermal atrophy (eight patients). The perilesional skin showed no amyloid depositions, melanophages, or increased vascularity. CONCLUSION: These histopathologic findings in normal-appearing interlesional skin may represent partial spontaneous regression of Bowen's disease.

Adult↗

Perianal Bowen's disease.

Thirty-three patients with perianal Bowen's disease were treated at the Cleveland Clinic Foundation from 1954 to 1986. Twenty-one patients were women and 12 were men, ranging in age from 30 to 69 years (mean, 48 years). Twenty patients (61 percent) presented with symptomatic perianal disease, while 13 patients (39 percent) were noted as having perianal Bowen's disease upon pathologic examination of routine hemorrhoidectomy specimens. Ten of the patients (30 percent) had prior histories of unrelated cancer. Twenty-seven patients were managed by wide local excision, three patients by simple excision, three patients by fulguration, and one patient by an abdominoperineal resection. During a follow-up period averaging 3.7 years (range, 0.3 to 10 years), one patient developed a new invasive skin cancer while a second patient experienced a recurrence of perianal Bowen's disease. The characteristic gross appearance of this lesion and its failure to respond to conventional therapy should prompt the performance of a biopsy, which readily establishes the diagnosis. This experience confirms that wide local excision is adequate therapy for perianal Bowen's disease and that close clinical follow-up is necessary to identify disease recurrence or the development of a malignancy.

Adult↗

Cutaneous and pulmonary cancers associated with Bowen's disease.

Thirty-one patients with Bowen's disease were studied in a restricted district of Namikata and its neighborhood of Ehime, Japan. Nineteen were alive and 12 were dead; the youngest living patient was 52 years of age. Invasive skin cancers were found in 10 patients and internal malignancies in 10, including 7 patients with pulmonary cancers. Palmoplantar keratosis was present in 25 patients and raindrop-type pigment anomalies in 15. Neutron activation analysis of hair showed only slightly higher arsenic values in patients with Bowen's disease than those in normal controls, though the differences were statistically significant at p less than 0.05. A possible arsenic exposure 43 years previously was considered responsible for the occurrence of neoplasms, though the arsenic route and amount were not determined. Bowen's disease started within 10 years, invasive skin cancers after 20 years, and pulmonary cancers after 30 years following the suspected arsenic exposure.

Adolescent↗