Triple Extramammary Paget's Disease

Kawatsu, Tomoyuki; Miki, Yoshiharu

doi:10.1001/archderm.1971.04000210090018

Cited by 54 publications

(14 citation statements)

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“…Extra-mammary Paget's disease may occur simultaneously in the genital area and, unilaterally or bilaterally, in the axillary region (1). Such cases have been reported as double or triple extra-mammary Paget's disease.…”

Section: Sirmentioning

confidence: 99%

Quadruple Extra-mammary Paget's disease

Abe¹,

Kabashima²,

Nishio³

et al. 2007

Acta Derm Venereol

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Section: Sirmentioning

confidence: 99%

Quadruple Extra-mammary Paget's disease

Abe¹,

Kabashima²,

Nishio³

et al. 2007

Acta Derm Venereol

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“…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). Because of its particular biological properties, we were interested in examining genetic changes in extramammary Paget's disease.…”

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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“…After the report by Kawatsu and Miki [3], only 6 cases with triple involvement of Paget's disease in genital and both axillary regions have been accumulated in the litera ture (table I) [3,[6][7][8][9], Therefore, this disor der is considered to be extremely rare.…”

Section: Discussionmentioning

confidence: 99%

“…In 1971, Kawatsu and Miki [3] reported a case who had three involve ments of Paget's disease in the genital and in both axillary regions, and they named the case triple extramammary Paget's disease. In this report, we describe another case of this type and also discuss the results of im munohistochemical studies for carcino embryonic antigen (CEA) and others.…”

mentioning

confidence: 99%