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Vulvar toker cells: the long-awaited missing link: a proposal for an origin-based histogenetic classification of extramammary paget disease.

To the Editor: The histogenesis of extramammary Paget disease (EMPD) has long been a subject of debate and controversy. Nowadays, it is generally agreed that at least two forms of the disease can be delineated, namely primary and secondary, with the latter representing secondary involvement from an underlying carcinoma originating most commonly in the lower gastrointestinal or urinary tract. As for the primary disease, skin adnexa (eccrine or apocrine glands), ectopic mammary glands, or pluripotential germinative cells in the epidermis and other structures have been implicated as a possible source of neoplastic cells. The recent description of vulvar Toker cells in the Journal by Drs. Willman, Golitz, and Fitzpatrick offers an attractive analogy with the breast, where a similar condition is referred to as mammary Paget disease (MPD). In this location, over 95% of cases of MPD are associated with an underlying ductal carcinoma, and the rest is thought to arise from Toker cells described in 1970. The same seems to be true for rare cases of Paget disease involving ectopic breast adjacent to a supernumerary nipple. We wonder why the same approach could not be applied for the anogenital area and the vulva in particular. This anatomic site contains structures that were originally variously called ectopic breast tissue, supernumerary breast tissue, and most recently, interpreted as anogenital mammary-like glands (MLG). These have been shown to be a normal constituent of this area, and lesions involving these structures have been demonstrated to manifest a striking homology with those seen in the breast. In this regard, the following question arises: why should EMPD differ from MPD histogenetically, if all anatomic conditions are so similar? Below are some lines to support the analogy. It is known that primary EMPD (without underlying carcinoma of internal organs) affects most often vulvar and perianal areas, where anogenital MLG are found in highest concentrations. There have been several documented cases of EMPD with an underlying ductal carcinoma involving anogenital MLG, and this is also in accordance with our experience (Fig. 1). EMPD has a notorious propensity for recurrences, and this can be partly explained by the presence of neoplastic cells residing in anogenital