Pagetoid Bowen's Disease Research Articles

Concurrent Bowen's Disease and Pagetoid Bowen's Disease on the Nipple-Areola Complex: A Case Report and Dermoscopic Findings.

Concurrent Bowen's Disease and Pagetoid Bowen's Disease on the Nipple-Areola Complex: A Case Report and Dermoscopic Findings.

Unusual lesion on the vulva of a postmenopausal woman

Unusual lesion on the vulva of a postmenopausal woman

Focal CK7 Positivity in Pagetoid Bowen's Disease: A Mimic of Extramammary Paget's Disease.

Focal CK7 Positivity in Pagetoid Bowen's Disease: A Mimic of Extramammary Paget's Disease.

Diagnostic Clues for Pagetoid Bowen's Disease.

Diagnostic Clues for Pagetoid Bowen's Disease.

Ki-67 and p16 Immunostaining Differentiates Pagetoid Bowen Disease From "Microclonal" Seborrheic Keratosis.

We observed keratoses with "clonal" nests present as numerous tiny collections, in which cells in "pagetoid" array are found, a configuration we termed microclonal seborrheic keratosis (MSK). To better distinguish MSK from pagetoid Bowen disease (PBD), we investigated use of immunohistochemical staining. Biopsy specimens of 26 MSKs, 17 PBDs, and 11 borderline cases were reviewed for histopathology and stained with p53, Ki-67, and p16. High expression of Ki-67 and p16 was observed in 12 (80%) of 15 PBDs and in one (4%) of 23 MSKs. Low expression of p16 and high expression of Ki-67 were observed in 16 (70%) of 23 MSKs and in two (13%) of 15 PBDs. Expression of p16 was elevated in 12 (80%) of 15 PBDs and in three (13%) of 23 MSKs (P < .0001). We describe a "microclonal" variant of seborrheic keratosis with morphology sometimes challenging to distinguish from PBD. High expression of p16 and Ki-67 or p16 alone favors the diagnosis of PBD over MSK.

Intraepidermal malignancy in breast skin: A tale of two tumours

Mammary Paget's disease most commonly affects the nipple areolar complex and is frequently associated with an underlying in-situ or invasive breast carcinoma. Pagetoid Bowen's disease of the breast is extremely rare and contains cells which morphologically resemble those of Paget's disease and may also express CK7 on immunohistochemistry. Here, we report two unusual cases of a 42-year-old Chinese woman with a recurrence of high grade ductal carcinoma in-situ presenting as mammary Paget's disease away from the nipple areolar complex, and a 65-year-old Chinese woman with pagetoid Bowen's disease of the breast skin. To our knowledge, there are only two case reports that are similar to the former and one to the latter.

A Case of Extramammary Paget's Disease with Bowenoid Features: Bowenoid Extramammary Paget's Disease and Pagetoid Bowen's Disease

A Case of Extramammary Paget's Disease with Bowenoid Features: Bowenoid Extramammary Paget's Disease and Pagetoid Bowen's Disease

How do I diagnose Pagetoid Bowen Disease

Bowen disease is a variant of squamous carcinoma in situ, which sometimes presents with a pagetoid growth pattern with cytologically atypical clear cells. In that case, the differencial diagnosis includes Paget disease and melanoma in situ, as well as less common entities. Here we describe a case where histological differenciation is difficult and immunohistochemical studies are necessary to make a diagnosis. Here we also highlight the heterogeneity of CK7 expression and the apparent specific expression of p63 in Pagetoid Bowen Disease.

Heterogeneity of cytokeratin 7 expression in pagetoid Bowen's disease

Heterogeneity of cytokeratin 7 expression in pagetoid Bowen's disease

Cytokeratin 10‐negative nested pattern enables sure distinction of clonal seborrheic keratosis from pagetoid Bowen's disease

The histopathologic pattern of clonal seborrheic keratosis (SK) is quite similar to the nested pattern of pagetoid Bowen's disease [squamous cell carcinoma in situ (SCCIS)], and differentiation between the two can be challenging, especially when only small pieces are available for interpretation. Eleven examples of clonal SK and 13 examples of pagetoid SCCIS were examined histopathologically (tabulating necrotic keratinocytes, suprabasal mitoses, infiltrate, parakeratosis housing plump nuclei, crowding of nuclei) and immunohistochemically (using Ki-67, bcl-2, cytokeratin 7 and cytokeratin 10). Sensitivity, specificity, p-values (Fisher's exact test, two-tailed) and positive/negative likelihood ratios (+LR/-LR) were calculated. Significant differences were seen with regard to crowding (p = 0.0009) and mitoses (p = 0.0006); however, only complete absence of necrotic keratinocytes or of crowding appeared to be diagnostically convincing for a diagnosis of clonal SK (-LR < 0.01). Significant differences were also seen with bcl-2 (p = 0.0005) and cytokeratin 10 antibodies (p < 0.00001). Both markers displayed a typical nested pattern in clonal SK, nests being bcl-2-positive and cytokeratin 10-negative. Cytokeratin 10-negative nests were the most convincing criterion for differentiation between clonal SK and pagetoid SCCIS (+LR > 10, -LR < 0.01). The most reliable marker to distinguish clonal SK from pagetoid SCCIS is cytokeratin 10 when it spares nests. Other criteria that assist in the differential diagnosis are bcl-2 expression, absence of crowding and of mitoses.

Clear Cells in Cutaneous Squamous Cell Carcinoma

Introduction Although few cases of squamous cell carcinoma (SCC) with clear cells have been published, we believe that these cells are often present in SCC. Material and methods We studied 249 SCCs, analyzing a number of clinical and histological variables. Various immunohistochemical techniques (immunoperoxidase method) were used to determine whether adnexal differentiation was present. Results There were 96 SCCs with a proportion of clear cells of over 25%. Advanced or established SCCs and SCCs associated with Bowen disease contained a larger proportion of clear cells. We defined 2 histological patterns: a) clear cells around the keratin pearls of SCCs arising from pre-existing actinic keratosis and with indirect signs of human papilloma virus infection in hair follicles; and b) clear cells that simulate adnexal differentiation in lesions arising on pre-existing Bowen disease lesions. There were also 19 carcinomas with true adnexal differentiation. Discussion Clear cells are frequently observed in SCC, though large numbers of clear cells are present only in certain SCCs. The appearance of clear cells in SCCs is progressive and they are only present in more advanced SCC. The presence of clear cells is suggestive of adnexal differentiation; however, in the majority of cases, their presence is due to infiltration of normal adnexal structures by the cells of pagetoid Bowen disease. True adnexal differentiation exists only in a small percentage of cases (7.6% in our study). The histological pattern described as clear cells around keratin pearls practically rules out this differentiation.

Las células claras en el carcinoma espinocelular cutáneo

IntroductionAlthough few cases of squamous cell carcinoma (SCC) with clear cells have been published, we believe that these cells are often present in SCC. Material and methodsWe studied 249 SCCs, analyzing a number of clinical and histological variables. Various immunohistochemical techniques (immunoperoxidase method) were used to determine whether adnexal differentiation was present. ResultsThere were 96 SCCs with a proportion of clear cells of over 25 %. Advanced or established SCCs and SCCs associated with Bowen disease contained a larger proportion of clear cells. We defined 2 histological patterns: a) clear cells around the keratin pearls of SCCs arising from pre-existing actinic keratosis and with indirect signs of human papilloma virus infection in hair follicles; and b) clear cells that simulate adnexal differentiation in lesions arising on pre-existing Bowen disease lesions. There were also 19 carcinomas with true adnexal differentiation. DiscussionClear cells are frequently observed in SCC, though large numbers of clear cells are present only in certain SCCs. The appearance of clear cells in SCCs is progressive and they are only present in more advanced SCC. The presence of clear cells is suggestive of adnexal differentiation; however, in the majority of cases, their presence is due to infiltration of normal adnexal structures by the cells of pagetoid Bowen disease. True adnexal differentiation exists only in a small percentage of cases (7.6 % in our study). The histological pattern described as clear cells around keratin pearls practically rules out this differentiation.

P63 Constitutes a Useful Histochemical Marker for Differentiation of Pagetoid Bowen's Disease from Extramammary Paget's Disease

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The expression of CD23 in cutaneous non‐lymphoid neoplasms

Cluster designation 23 (CD23) is generally used as a lymphoid marker. Its utility in cutaneous epithelial tumors has never been studied. In our routine practice, we observed that CD23 reacted strongly with eccrine and apocrine secretory coils. Immunohistochemical staining of CD23 was performed in a total of 131 cases of apocrine, eccrine, follicular and other cutaneous non-lymphoid tumors. CD23 expression was detected in all benign apocrine tumors and in half of benign eccrine tumors, particularly those derived from secretory coils. CD23 staining was seen in 42% (8/19) of microcystic adnexal carcinoma (MAC), while no staining was observed in tumor cells of desmoplastic trichoepithelioma, morpheaform basal cell carcinoma and syringoma. All mammary and extramammary Paget's disease were labeled with CD23. In comparison, pagetoid Bowen's disease, melanoma in situ and sebaceous carcinoma exhibited negative staining. In addition, CD23 reacted diffusely with cutaneous mucinous eccrine carcinoma in a manner similar to breast or colonic adenocarcinoma. CD23 appears to be a reliable immunohistochemical marker of the eccrine/apocrine secretory coil and helpful in identifying sweat gland tumors of such origin. It is of ancillary value in differentiating MAC from its mimicker. CD23 is a useful addition to the diagnostic immunohistochemical panels for Paget's disease.

Cluster designation 5 staining of normal and non‐lymphoid neoplastic skin*

Immunohistochemical staining for cluster designation 5 (CD5) has been found to label a variety of non-lymphoid tumors. A variety of eccrine, apocrine, follicular, epithelial, and pagetoid lesions were selected and stained with an anti-CD5 monoclonal antibody (Novocastra Labs, Newcastle upon Tyne, UK, clone 4C7) by immunohistochemistry. The intensity of positive cytoplasmic staining was graded semiquantitatively (1+ weak staining, 2+ strong staining). Additionally, the percentage of positive lesional cells was placed in one of four categories: >75%, 25-75%, 1-25%, and <1%. Within normal skin, CD5 labeled lymphocytes, apocrine glands, deep dermal eccrine glands, and smooth muscle (weak). The majority of benign and malignant apocrine lesions demonstrated strong focal (36%, n=11)-to-diffuse (64%, n=16) staining. In contrast, labeling of benign eccrine tumors was more focal, tending to localize around ducts (79%, n=19). Microcystic adnexal carcinoma demonstrated focal staining of deeper ductal structures (71%, n=7), whereas desmoplastic trichoepithelioma and basal cell carcinoma showed only rare positive cells. All cases of mammary (n=7) and extramammary (n=8) Paget's disease labeled diffusely for CD5. Pagetoid Bowen's disease (n=6), intraepidermal sebaceous carcinoma (n=3), nor melanoma in situ (n=6) showed any CD5 staining. Immunohistochemical staining for CD5 is extremely useful in the differential diagnosis of pagetoid epidermal lesions and will mark mammary and extramammary Paget's disease, but not pagetoid Bowen's disease, melanoma in situ, or sebaceous carcinoma.

Immunolabeling pattern of syndecan‐1 expression may distinguish pagetoid Bowen's disease, extramammary Paget's disease, and pagetoid malignant melanoma in situ

The differential diagnosis of pagetoid cells within the epidermis rests primarily between pagetoid Bowen's disease (PBD), extramammary Paget's disease (EPD), and pagetoid malignant melanoma (MIS) in situ. Although morphologic clues are often helpful in differentiating these lesions, the use of immunohistochemistry is often necessary to arrive at the correct diagnosis. Syndecan-1 is a cell-surface proteoglycan that mediates adhesion between cells and the extracellular matrix, and between cells themselves. Twenty-two cases of PBD, four cases of intraepidermal EPD, and 13 cases of MIS were examined for syndecan-1 immunoreactivity. Cell-membrane syndecan-1 immunoreactivity was evident in PBD, cytoplasmic syndecan-1 immunoreactivity was evident in EPD, whereas immunoreactivity for syndecan-1 was not present in MIS. The patterns of syndecan-1 immunoreactivity in these lesions may be a useful adjunct in the differentiation of PBD, EPD, and MIS.

Pagetoid dyskeratosis is a frequent incidental finding in hemorrhoidal disease.

Pagetoid dyskeratosis is considered a selective keratinocytic response in which a small part of the normal population of keratinocytes is induced to proliferate. Pagetoid dyskeratosis has been found incidentally in the squamous epithelium of the skin in various locations and in the ectocervix in uterine prolapse. In cases in which these pale cells are conspicuous, there is a hazard of overdiagnosis. It has been suggested that friction is the most probable inductor of the lesion. To the best of our knowledge, pagetoid cells have not been reported in surgically resected hemorrhoids. We here describe the location of pagetoid dyskeratosis in the squamous epithelium of hemorrhoids and the incidence of this lesion in a group of 100 unselected patients surgically treated for hemorrhoidal disease. In addition to the conventional histologic method, special staining procedures and an immunohistochemical study of cytokeratins were performed in selected cases. Pagetoid dyskeratosis was found in 68 cases (68%) and was a prominent finding in 22 cases (22%). The cells of pagetoid dyskeratosis were strongly positive for high-molecular weight cytokeratin. These cells showed an immunohistochemical profile that was different from that of the surrounding squamous cells and indicative of premature keratinization. In hemorrhoidal disease, the cushions are susceptible to trauma as a result of prolapse. In this setting, friction may be the stimulus for the appearance of pagetoid dyskeratotic cells. These cells must be distinguished from the artifactual clear cells of the squamous epithelium, glycogen-rich cells, and koilocytes. The lesion must also be distinguished from extramammary Paget disease, pagetoid spread of carcinoma cells, pagetoid Bowen disease, and pagetoid melanoma. Pathologists should be familiar with the histologic features of pagetoid dyskeratosis in hemorrhoidectomy specimens to avoid misdiagnosis. Routine histologic study is usually adequate for recognizing this lesion.

Multiple pagetoid Bowen's disease

Multiple pagetoid Bowen's disease

Ｐａｇｅｔｏｉｄ Ｂｏｗｅｎ病の１例

A sixty-year-old male with pagetoid Bowen's disease is reported. A reddish-brown plaque of 35×40mm was noticed on his left lower leg about 3 years previously. Brown or black thick scales were present at the center of the plaque. Light microscopy of the biopsy lesion taken from the plaque by a practicing doctor revealed large pagetoid cells within the hypertrophic epidermis. The atypical and clear pagetoid cells suggested the diagnosis of extramammary Paget's disease, pagetoid melanoma or pagetoid Bowen's disease.Immunohistochemical studies; the pagetoid cells were positively stained with keratin but negatively stained with S-100 protein, or carcinoembryonic antigen. We therefore, diagnosed the lesion as pagetoid Bowen's disease. When examined the excised specimen, the center of the lesion showed the features of typical Bowen's disease. However, pagetoid cells were present at the margin of the lesion. Electron microscopically, aggregated tonofilaments were observed around the nuclei of the pagetoid cells: the cells showed the feature of atypical keratinization.

Capsule Dermatopathology: Pagetoid Bowen's Disease vs. Extramammary Paget's Disease

The Journal of Dermatologic Surgery and OncologyVolume 2, Issue 1 p. 24-25 Feature Capsule Dermatopathology: Pagetoid Bowen's Disease vs. Extramammary Paget's Disease Kenneth Raiten M.D., Kenneth Raiten M.D. Department of Dermatology, Skin and Cancer Unit, New York Univeristy Medical Center, New YorkSearch for more papers by this authorCleire Paniago-Pereira M.D., Cleire Paniago-Pereira M.D. Department of Dermatology, Skin and Cancer Unit, New York Univeristy Medical Center, New YorkSearch for more papers by this authorA. Bernard Ackerman M.D., A. Bernard Ackerman M.D. Department of Dermatology, Skin and Cancer Unit, New York Univeristy Medical Center, New YorkSearch for more papers by this author Kenneth Raiten M.D., Kenneth Raiten M.D. Department of Dermatology, Skin and Cancer Unit, New York Univeristy Medical Center, New YorkSearch for more papers by this authorCleire Paniago-Pereira M.D., Cleire Paniago-Pereira M.D. Department of Dermatology, Skin and Cancer Unit, New York Univeristy Medical Center, New YorkSearch for more papers by this authorA. Bernard Ackerman M.D., A. Bernard Ackerman M.D. Department of Dermatology, Skin and Cancer Unit, New York Univeristy Medical Center, New YorkSearch for more papers by this author First published: March 1976 https://doi.org/10.1111/j.1524-4725.1976.tb00139.xCitations: 17Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume2, Issue1March 1976Pages 24-25 RelatedInformation