Extramammary Paget's Disease

Murrell, Thomas W.; McMULLAN, FRANCIS H.

doi:10.1001/archderm.1962.01590050030006

Cited by 52 publications

(22 citation statements)

References 9 publications

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“…The origin of these cells is uncertain, and several theories have been advocated. These include: ( 1 ) spontaneous and simultaneous development of carcinoma in both the squaCase Report mous epithelium of the epidermis and an underlying apo crine gland [11]; (2) metastasis of carcinoma cells to the epidermis [12]; (3) intra-epidermal migration of tumour cells from a primary site through the overlying epidermis [13], and (4) multifocal malignant transformation of histogenetically similar cells in the epidermis and underlying structures [14].…”

Section: Discussionmentioning

confidence: 99%

Paget's Disease of the Gians penis: An Unusual Urological Malignancy

Smith¹,

Hamdy²,

Evans³

et al. 1994

Eur Urol

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Section: Discussionmentioning

confidence: 99%

Paget's Disease of the Gians penis: An Unusual Urological Malignancy

Smith¹,

Hamdy²,

Evans³

et al. 1994

Eur Urol

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“…The pathogenesis and histogenesis of the extramammary form, by contrast, are far more controversial, because most of the cases have no underlying carcinomas and the origin of Paget's cells is unknown (Hart and Millman, 1977;Jones et al, 1979). A variety of cell types have been proposed as the progenitors of extramammary Paget's cells, including pluripotential germinative epidermal cells (Murrell Jr and McMullan, 1962;Jones et al, 1979), and cells of both eccrine and apocrine sweat glands (Demopoulos, 1971; Lee et al, 1977;Roth et al, 1977;Mazoujian et al, 1984;Hamm et al, 1986). Furthermore, extramammary Paget's disease may arise multicentrically within the anogenital area (Gunn and Gallager, 1980) or even in distant anatomical sites known as 'triple' extramammary Paget's disease in which genitalia and both sides of axillae are affected at the same time (Kawatsu and Miki, 1971 al, 1990) and c-erbB-2 proto-oncogene products (Keatings et al, 1990;Meissner et al, 1990;Wolber et al, 1991;Nishi et al, 1994), and altered expression of p53 tumour-suppressor protein (Wienecke et al, 1994;Nakamura et al, 1995).…”

mentioning

confidence: 99%

Tumour cells of extramammary Paget's disease do not show either p53 mutation or allelic loss at several selected loci implicated in other cancers

Takata

Hatta²,

Takehara³

1997

Br J Cancer

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Summary Extramammary Paget's disease is a particular form of skin cancer of unknown histogenesis. To look for the genetic defects underlying the pathogenesis of this tumour, we have examined loss of heterozygosity (LOH), p53 and human papillomavirus (HPV) status, and the expression of c-erbB-2 and bcl-2 proteins in 14 cases. Unexpectedly, no LOH was detected at several loci commonly lost in other human cancers (namely 3p, 9p, 9q, 13q, 16q, 17p, and 17q) in 12 tumours examined. Altered p53 protein expression was entirely or mostly negative in all 14 cases. Direct sequencing of exons 5-8 of the p53 gene in eight cases revealed no mutation. Polymerase chain reaction amplification of the Ll gene of human papillomavirus (HPV) did not detect the virus that could inactivate p53 and retinoblastoma tumoursuppressor gene products. As expected, c-erbB-2 proto-oncogene protein was overexpressed in six cases. The expression of bcl-2 was negative in all cases. The results presented in this study suggest that molecular events underlying extramammary Paget's disease differ from those of other common epithelial malignancies and that tumour-suppressor genes located in chromosome regions not examined in this study may be important.

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“…One hypothesis is that EMPD arises from the malignant transformation of pluripotent stem cells in the epidermis. 20,21 Another hypothesis is that EMPD cells are derived from, or differentiating along the lines of, apocrine glandular cells. 22 In any case, EMPD is of epithelial component origin, and the DLD-1 cells used in the identification of PIG genes 9 are derived from human colon cancer.…”

Section: Discussionmentioning

confidence: 99%

PIG7/LITAF gene mutation and overexpression of its gene product in extramammary Paget's disease

Matsumura

Nishigori

et al. 2004

Intl Journal of Cancer

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To identify cancer-related genes that are involved in the carcinogenesis of extramammary Paget's disease (EMPD), we compared mRNA expression profiles of EMPD lesions and corresponding normal skin using cDNA array. Sixtyeight genes were highly expressed (>5-fold) in EMPD lesions compared to normal skin, and 40 genes were expressed less than one-fifth in EMPD lesions. Among them, PIG7/LITAF mRNA was overexpressed in 3 of 4 EMPD cases. PIG7/LITAF transcription is induced by p53 expression and has been implicated in the p53-induced apoptotic pathway. Since expression of p53 mRNA and p53 protein was not high in any of the 3 EMPD samples compared to the intact skin of the same patient, we analyzed PIG7/LITAF cDNA mutations among 12 EMPD samples (including the former 4) by PCR-SSCP. Three samples showed shifted bands (2 had point mutations leading to amino acid substitutions and 1 had a silent mutation). One sample with amino acid substitution overexpressed PIG7/ LITAF mRNA in cDNA array analysis and RT-PCR. PIG7/LITAF mRNA expression is confined to tumor cells in in situ mRNA hybridization analysis. These results indicate that genetic disorder and overexpression of PIG7/LITAF may be involved in EMPD carcinogenesis.

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Extramammary Paget's Disease

Cited by 52 publications

References 9 publications

Paget's Disease of the Gians penis: An Unusual Urological Malignancy

Paget's Disease of the Gians penis: An Unusual Urological Malignancy

Tumour cells of extramammary Paget's disease do not show either p53 mutation or allelic loss at several selected loci implicated in other cancers

PIG7/LITAF gene mutation and overexpression of its gene product in extramammary Paget's disease

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