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• W3016435331 abstract "To the Editor: Invasive lobular breast carcinoma (LBC) is one of the most common entities among special types of breast cancer, being characterized by discohesive growth pattern and immunohistochemical (IHC) loss of the cell adhesion protein E-cadherin.1,2 In classic LBC, the characteristic growth pattern features neoplastic cells infiltrating through the surrounding stroma in single units or single files, with minimal disturbance of the overall tissue architecture1; E-cadherin loss is thought to account for LBC discohesive phenotype.2 Despite typically exhibiting features known to be associated with good prognosis [ie, low histological grade and estrogen receptor (ER)-positivity], LBC may be aggressive in behavior with high propensity for metastatic spread.1 We hereby report the exceptional occurrence of cutaneous involvement by the pleomorphic variant of LBC (PLBC) in a male patient. An 80-year-old man with no significant medical history presented with an enlarging lesion around the right nipple; physical examination revealed a 3-cm wide erythematous plaque encircling the nipple, which was indurated on palpation. A punch biopsy of the lesion was performed under the clinical suspicion of basal cell carcinoma. Histology revealed extensive infiltration of the superficial and reticular dermis by atypical cells with round-to-oval, at times histiocytoid morphology (Fig. 1A). The infiltrate exhibited higher cellularity in the superficial dermis, in contrast to a more infiltrative and discohesive growth pattern in the lower layers of the dermis (Fig. 1B). Higher magnification revealed markedly atypical cytology, with enlarged pleomorphic nuclei and occasional mitoses (Fig. 1C). IHC evaluation of neoplastic cells revealed positivity for CK-7, ER, and progesterone receptor, with absent expression of p63, CK-20, and HER-2; proliferation rate (assessed by means of Ki-67 staining) was approximately 15% (Fig. 1D). Loss of normal membranous expression of E-cadherin (Fig. 1E) and beta-catenin (Fig. 1F) was observed on neoplastic cells. Based on available morphological and IHC findings, a diagnosis of cutaneous involvement by PLBC was rendered.FIGURE 1.: A, Extensive infiltration of the superficial and reticular dermis by neoplastic cell population, with higher cellularity in the superficial dermis, and a more infiltrative growth pattern in the lower layers of the dermis. B, Infiltrative and discohesive growth pattern in the reticular dermis. C, Marked cytological atypia of neoplastic cells, with variation of cell size and pleomorphic nuclei. D, Increased proliferation rate (15%) assessed by means of Ki-67 staining. E, Complete loss of E-cadherin expression, typical for LBC. F, Concomitant loss of beta-catenin membranous expression by neoplastic cells; vascular endothelium serves as positive internal control (A, hematoxylin and eosin, original magnification ×20; B, original magnification ×200; C, original magnification ×600; D, Ki-67, original magnification ×200; E, E-cadherin, original magnification ×100; F, beta-catenin, original magnification ×200).Carcinoma of the male breast is an uncommon occurrence, representing less than 2% of all breast cancers 1,3,4; infiltrating ductal breast carcinoma (DBC) constitutes the majority of cases of male breast carcinoma (75%–95%).1 LBC is exceptionally rare in the male population, representing approximately only 1% of breast carcinoma in males; by contrast, its relative incidence in females is higher (10%–15%).3,4 This sex-dependent difference in relative incidence of LBC seems to be related to the absent development of lobular and terminal duct epithelium in males because lobular neoplasia (at least in females) is thought to derive mammary gland lobules.1 Invasive LBC of the male breast was first reported by Sanchez et al5 in 1986 in a patient with Klinefelter syndrome; endogenous or exogenous estrogenic stimulation promotes formation of acini and lobules, explaining the increased risk of malignancy associated with imbalances in the estrogen/androgen hormonal ratio.1,4 Additional risk factors for LBC of the male breast include BRCA2 and CDH1 germline mutations, hyperestrogenism secondary to obesity, exogenous hormonal administration, or testicular dystrophy, exposure to environmental radiation, electromagnetic energy, or high temperatures, and ethnical factors including African or Ashkenazi Jewish ancestry.1,3,4 Clinical presentation of LBC in male patients is similar to that of DBC1: a palpable mass with or without nipple changes, which is often diagnosed at late stages, partially due to low patient and clinical suspicion.3 As also observed in the female population, most of the LBC cases in male patients (>75%) exhibit a hormone receptor-positive phenotype.3,4 On IHC evaluation, the majority of LBC cases are characterized by a specific finding: diffuse loss of E-cadherin staining, secondary to CDH1 deletion, mutation, or hypermethylation.2 Indeed, heterozygous loss of CDH1 on chromosome 16q is observed in almost 90% of LBC cases.1,2 The ensuing E-cadherin loss of function is paralleled by loss of beta-catenin expression, as well as p120-catenin cytoplasmic relocalization; these additional IHC features are regarded as useful diagnostic clues in rare cases of LBC with retained IHC expression of E-cadherin protein.2 PLBC was first described in women by Dixon et al6 in 1982. According to the World Health Organization classification of breast tumors, PLBC is defined as a variant of LBC characterized by greater degree of nuclear atypia and pleomorphism.7,8 Histologically, despite the typical discohesive and infiltrating pattern of classic LBC, PLBC shows greater cellularity and distinct cytological features: a plasmacytoid or histiocytoid appearance with apocrine differentiation, 2 or 3 times larger nuclei with irregular contours and hyperchromasia, prominent nucleoli, and increased mitotic activity.7,8 The molecular underpinnings of PLBC (gain of 1q and 16p, loss of 16q and 11q, as well as frequent inactivation of CDH1) prove that PLBC has a closer biological relation to classic LBC, rather than to high-grade DBC.7 Conflicting data are available in the literature regarding the prognostic value of pleomorphism in LBC; despite earlier reports supporting a more aggressive behavior in comparison with nonpleomorphic LBC, later studies have revealed that pleomorphism alone does not provide any additional prognostic information independent of histologic grade (which, also in PLBC, is mainly driven by mitotic score).7,8 PLBC of the male breast is extremely rare, ours being only the eighth case reported in the available literature.3,4 Cutaneous involvement by invasive LBC (including PLBC) in the male population should be distinguished from primary histiocytoid (apocrine) carcinoma of the skin, a rare neoplasm that generally affects elderly men, typically occurring on the eyelid or on the axilla.9,10 Primary cutaneous histiocytoid carcinoma exhibits histiocytoid or signet-ring cell cytology with apocrine differentiation, similar to LBC.9 Notwithstanding, most cases of histiocytoid carcinoma of the skin will stain positive with p63, supporting a primary cutaneous origin; in addition, expression of E-cadherin is usually retained in histiocytoid carcinoma of the skin, as well as in other apocrine carcinomas.9,10 PLBC should be also distinguished from metastases of signet-ring carcinomas from other primary sites (including the stomach), sclerosing epithelioid fibrosarcoma, myeloid sarcoma, and plasma cell dyscrasias.11 Ascertainment of the CK-7(+) CK-20(−) ER (+) immunophenotype will be decisive in rendering a diagnosis of PLBC. In sum, we reported the exceptional occurrence of cutaneous involvement by PLBC in a male patient; IHC staining for E-cadherin is essential for proper diagnostic framing." @default.
• W3016435331 created "2020-04-24" @default.
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• W3016435331 date "2020-04-17" @default.
• W3016435331 modified "2023-09-28" @default.
• W3016435331 title "Cutaneous Involvement by Pleomorphic Lobular Carcinoma of the Male Breast: An Exceptional Occurrence" @default.
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