Diseases of the Nipple Diseases of the Nipple
Contents
12.1 Paget’s Disease . . . 352
12.1.1 Definition . . . 352
12.1.2 Macroscopic (Clinical) Features . . . 352
12.1.3 Microscopic Features . . . 352
12.1.4 Differential Diagnosis . . . 352
12.1.5 Additional Comments . . . 352
12.1.6 Further Reading . . . 353
12.2 Nipple Duct Adenoma . . . 353
12.2.1 Definition . . . 353
12.2.2 Synonyms . . . 353
12.2.3 Macroscopy . . . 353
12.2.4 Microscopic Features . . . 354
12.2.5 Immunoprofile . . . 354
12.2.6 Malignant Changes Associated with NDA . . . 354
12.2.7 Histopathology . . . 354
12.2.8 Further Reading . . . 354
12.3 (Infiltrating) Syringomatous Adenoma . . . 354
12.3.1 Definition . . . 354
12.3.2 Synonym . . . 354
12.3.3 Macroscopy . . . 354
12.3.4 Microscopic Features . . . 354
12.3.5 Differential Diagnosis . . . 355
12.3.6 Additional Comments . . . 355
12.3.7 Further Reading . . . 355
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12.1 Paget’s Disease
12.1.1 Definition
Presence of highly atypical, large cells with abundant cytoplasm and prominent nucleoli within the epidermis (mostly nipple), almost always associated with underlying ductal intraepithelial neoplasia (high-grade ductal intraepithelial neoplasia [DIN;
DCIS]).
12.1.2 Macroscopic (Clinical) Features
Often eczematoid itching and a unilateral change of the nipple, eventually associated with erosion. Ulceration, crusting, and serous or bloody discharge often occur in more advanced cases.
In about 50% of cases, a painless mass is palpable in the under- lying breast tissue. There is sometimes retraction of the nipple.
Occasionally, it may be bilateral [1, 4, 11, 15].
12.1.3 Microscopic Features (Fig. 86)
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Isolated cells or clusters of atypical round or oval cells are present within the squamous epithelium. The neoplastic cells show round, large, hyperchromatic nuclei; prominent nucle- oli; and clear pale, eosinophilic, or amphophilic cytoplasm.
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In the vast majority of cases (more than 95%), high-grade DIN (DCIS) within the lactiferous duct is present (intraepidermal spread of the tumor cells).
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A variant of Paget’s disease resembling Bowen’s disease with full-thickness epidermal atypia and severe nuclear atypia can occur.
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Intracytoplasmic mucin can be present.
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Paget’s disease can be associated with infiltrating carcinoma of various types (mostly infiltrating ductal carcinoma, NOS type).
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Very rarely, there is an association with infiltrating lobular carcinoma or lobular intraepithelial neoplasia (LIN, high- grade or pleomorphic variant).
12.1.4 Differential Diagnosis
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Clear cell changes of keratinocytes: Occasionally, normal squa- mous cells of the nipple show clear cytoplasm; the cells lack nuclear atypia and are smaller and uniform.
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Malignant melanoma: Often associated with clear-cut under- lying malignant melanoma. No underlying DIN (DCIS) or invasive carcinoma. The cells are typically cytokeratin (CK)- negative but HMB45-positive. One should keep in mind that some melanomas are devoid of pigment, while Paget cells can incorporate melanin from epidermal cells [19, 21].
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Bowen’s disease (squamous carcinoma in situ): The neoplastic cells usually involve the entire layers of epidermis, with mor- phological evidence of squamous cells usually lacking large clear or eosinophilic cytoplasm. There is no association with underlying breast carcinoma or DIN (DCIS) [8, 13, 23, 26]. The neoplastic cells in Bowen’s disease are typically positive for HMW-CK such as CK5/6 and CK34BE12. (See Table 12.1.)
Caution
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The most useful combination markers in difficult cases are low molecular weight cytokeratins (LMW-CKs) that are always positive in Paget’s disease (such as CK7 and CK8/18) and high molecular weight cytokeratins (HMW-CKs, either CK5/6 or CK34BE12) that are always negative in Paget’s dis- ease. MUC1 is another reliable marker that is always positive in Paget’s cells.
12.1.5 Additional Comments
Diagnostic problems particularly arise when fixation and tissue preparation are not optimal or when the biopsy was taken from a degenerative area. Poor fixation of the tissue makes it difficult to distinguish Paget cells from melanocytic cell population.
Paget cells are very often negative for estrogen receptors and progesterone receptors. Androgen receptors, however, are com- monly positive in Paget cells [14].
HER2/neu is almost always positive in mammary Paget’s dis- ease [5, 10, 14].
The Paget cells are usually negative for S100 and HMB45.
Table 12.1.
Immunohistochemical profile of Paget’s disease (PD), malignant melanoma (MM), and Bowen’s disease (BD)
PD MM BD
LMW-CK (CK8/18) + – –
HMW-CK (CK34BE12) – – +
HMW-CK (CK5/6) – – +
CK7 + – –
EMA + – –
CEA + (polyclonal) – –
– (monoclonal)
MUC1 + – –
The glandular nature of the neoplastic cells in Paget’s disease is confirmed by electron microscopic features. Immunohisto- chemical studies have confirmed that Paget cells have the same phenotype as the underlying DIN (DCIS). However, a few reports suggest that a minority of cases of Paget’s disease develop inde- pendently from the underlying carcinoma (primary intraepider- mal neoplasia of glandular type) [17].
12.1.6 Further Reading
1. Ashikari R, Park K, Huvos AG, et al. Paget’s disease of the breast.
Cancer 1970;26:680–685.
2. Banerjee SN, Estabrook A, Schnabel FR. surgical treatment of Paget’s disease. In: Silverstein MJ (ed). Ductal carcinoma in situ of the breast. Williams & Wilkins, Baltimore, 1997, pp. 551–554.
3. Bussolati G, Pich A. Mammary and extramammary Paget’s disease:
an immunohistochemical study. Am J Pathol 1975;80:117–128.
4. Dixon AR, Galea MH, Ellis IO, et al. Paget’s disease of the nipple. Br J Surg 1991;78:722.
5. Haerslev T, Krag Jacobsen G. Expression of cytokeratin and erbB2 oncoprotein in Paget’s disease of the nipple. An immunohistochem- ical study. APMIS 1992;100:1041–1047.
6. Hitchcock A, Topham S, Bell J, et al. Routine diagnosis of mammary Paget’s disease. A modern approach. Am J Surg Pathol 1992;16:
58–61.
7. Jones RR, Saul J, Gusterson B. The histogenesis of mammary and ex- tramammary Paget’s disease. Histopathology 1989;14:409–416.
8. Kariniemi AL, Ramaekers F, Lehto VP, et al. Paget’s cells express cytokeratin typical of glandular epithelia. Br J Dermatol 1985;112:
179–183.
9. Kawase K, Dimaio DJ, Tucker SL, et al. Paget’s disease of the breast:
there is a role for breast-conserving therapy. Ann Surg Oncol 2005;
12:391–397.
10. Keatings L, Sinclair J, Wright, et al. C-erbB2 oncoprotein expression in mammary and extramammary Paget’s disease: an immunohisto- chemical study. Histopathology 1990;17:243–247.
11. Kollmorgen DR, Varanasi JS, Edge SB. Paget’s disease of the breast: a 33-year experience. J Am Coll Surg 1998;187:171–177.
12. Kuan SF, Montag AG, Hart J, et al. Differential expression of mucin genes in mammary and extramammary Paget’s disease. Am J Surg Pathol 2001;25:1469–1477.
13. Lau J, Kohler S. Keratin profile of intraepidermal cells in Paget’s dis- ease, extramammary Paget’s disease, and pagetoid squamous cell carcinoma in situ. J Cutan Pathol 2003;30:449–454.
14. Liegl B, Horn LC, Moinfar F. Androgen receptors are frequently expressed in mammary and extramammary Paget’s disease. Mod Pathol 2005;18:1283–1288.
15. LIoyd J, Flanagan AM. Mammary and extramammary Paget’s dis- ease. J Clin Pathol 2000;53:742–749.
16. Marcus E. The management of Paget’s disease of the breast. Curr Treat Options Oncol 2004;5:153–160.
17. Morandi L, Pession A, Marucci GL, et al. Intraepidermal cells of Paget’s carcinoma of the breast can be genetically different from those of the underlying carcinoma. Hum Pathol 2003;34:1321–1330.
18. Paget J. On disease of mammary areola preceding cancer of the mammary gland. St Barth Hosp Rep 1874;10:87–89.
19. Pizzichetta MA, Canzonieri V, Massarut S, et al. Pigmented mamma- ry Paget’s disease mimicking melanoma. Melanoma Res 2004;14:
S13–15.
20. Rayne SC, Santa Cruz DJ. Anaplastic Paget’s disease. Am J Surg Pathol 1992;16:1085–1091.
21. Requena L, Sangueza M, Sangueza OP, Kutzner H. Pigmented mam- mary Paget disease and pigmented epidermotropic metastases from breast carcinoma. Am J Dermatopathol 2002;24:189–198
22. Schelfhout VR, Coene ED, Delaey B, et al. Pathogenesis of Paget’s disease: epidermal heregulin-alpha, motility factor, and HER recep- tor family. J Natl Cancer Inst 2000;92:622–628.
23. Shah KD, Tabibzadeh SS, Gerber MA. Immunohistochemical dis- tinction of Paget’s disease from Bowen’s disease and superficial spreading melanoma with the use of monoclonal cytokeratin anti- bodies. Am J Clin Pathol 1987;88:689–695.
24. Tocker C. Some observations on Paget’s disease of the nipple. Can- cer 1961;14:653–672.
25. Van der Putte SC. Mammary Paget’s disease confined to the areola and associated with multifocal Tocker cell hyperplasia. Am J Der- matopathol 1995;17:487–493.
26. Viehl P, Validire P, Kheirallah S, et al. Paget’s disease of the nipple without clinically and radiologically detectable breast tumor: Histo- chemical and immunohistochemical study of 44 cases. Pathol Res Pract 1993;189:150–155.
12.2 Nipple Duct Adenoma
12.2.1 Definition
A benign tumor of the nipple with compact proliferation of small tubules lined by epithelial and myoepithelial cells, with or without intraepithelial proliferation, around the collecting ducts.
12.2.2 Synonyms
Nipple adenoma, adenoma of the nipple, florid papillomatosis of the nipple, subareolar duct papillomatosis, papillomatosis of the nipple.
12.2.3 Macroscopy
Nipple duct adenoma (NDA) is a solitary tumor with well-delin- eated margins and greyish-white cut surface. Cystic dilatation of the underlying ducts can be present. Erosion or ulceration of the epidermis in advanced disease can occur.
12.2.4 Microscopic Features (Fig. 87)
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Although grossly the tumor appears well circumscribed, his- tologically the margins are often ill defined.
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Compact aggregates of tubules proliferate within and replac- ing the nipple stroma.
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Often, there are prominent sclerotic changes of the stroma, causing distortion of the tubules (sclerosing adenosis pat- tern).
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Ducts usually exhibit florid ductal hyperplasia with or with- out a mild degree of cytologic atypia.
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Papillary structures are often present; these can be a promi- nent feature (papillomatosis pattern).
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The tubules, compressed glands, and papillary structures dis- play a two-cell layer of epithelial and myoepithelial cells.
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Necrosis as well as surface (epidermis) erosion can occur.
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Increased mitotic activity is a common finding in the epithe- lial cells.
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Squamous or apocrine metaplasia may occur.
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Some areas of the stroma may show edematous or myxoid
changes. Elastosis can also be present. Areas of the stroma can
be cellular (desmoplastic appearance).
Caution
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NDA can be mistaken for invasive carcinoma or Paget’s dis- ease clinically. The adenosis pattern with significant stromal sclerosing (pseudoinfiltrative pattern) can easily be misinter- preted as invasive carcinoma.The presence of a myoepithelial cell layer and the heterogeneity of cell population exclude the possibility of cancer.
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The epithelial cells may show nuclear enlargement, higher nuclear-cytoplasmic ratio, vesicular or hyperchromatic nuclei, and prominent nucleoli. These changes are mostly reactive.
One should always pay attention to the heterogeneity of cell population in the proliferating areas, a feature characteristic of florid intraductal hyperplasia (UDH).
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The presence of intraluminal necrosis, increased mitotic activity, or surface erosion should not lead to the diagnosis of cancer. If there is any doubt about the nature of the tumor, immunohistochemistry should be performed.
12.2.5 Immunoprofile
The presence of a myoepithelial cell layer can be confirmed by smooth muscle actin or other myoepithelial markers (such as p63, CD10, and calponin). The heterogeneity of the cell popula- tion can be demonstrated by staining for HMW-CK (CK5/6 or CK34BE12).
12.2.6 Malignant Changes Associated with NDA
Rarely, high-grade DIN (DCIS) can arise in the background of NDA. An invasive ductal carcinoma may rarely be associated with NDA.
12.2.7 Histopathology
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Infiltrating glands and solid aggregates of tumor cells without a myoepithelial cell component.
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The DIN (DCIS) or invasive carcinoma is typically composed of a homogeneous epithelial cell population negative for HMW-CK (such as CK5/6).
Caution
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It is always best to be conservative when the diagnosis of malignancy is in any doubt, particularly when the considera- tion is DCIS arising in NDA. Necrosis in ductal hyperplasia may occur and should not lead to the diagnosis of in situ ductal carcinoma. In a difficult case, immunohistochemistry for CK5/6 and myoepithelial markers can be very helpful.
12.2.8 Further Reading
1. Bhagavan BS, Patchefsky A, Koss LG. Florid subareolar duct papillo- matosis (nipple adenoma) and mammary carcinoma: report of three cases. Hum Pathol 1973;4:289–295.
2. Brownstein MH, Phelps RG, Magnin PH. Papillary adenoma of the nipple: analysis of fifteen new cases. J Am Acad Dermatol 1985;12:707–715.
3. Diaz NM, Palmer JO, Wick MR. Erosive adenomatosis of the nipple:
histology, immunohistology, and differential diagnosis. Mod Pathol 1992;5:179–184.
4. Fornage BD, Faroux MJ, Pluot M, et al. Nipple adenoma simulating carcinoma: misleading clinical, mammographic, sonographic, and cytologic findings. J Ultrasound Med 1991;10:55–57.
5. Gobbi H, Simpson JF, Jensen RA, et al. Metaplastic spindle cell breast tumors arising within papillomas, complex sclerosing lesions, and nipple adenomas. Mod Pathol 2003;16:893–901.
6. Goldman RL, Cooperman H. Adenoma of the nipple. A benign le- sion simulating carcinoma clinically and pathologically. Am J Surg 1970;119:322–325.
7. Jones DB. Florid papillomatosis of the nipple ducts. Cancer 1955;8:
315–319.
8. Jones MW, Tavassoli FA. Coexistence of nipple duct adenoma and breast carcinoma: a clinicopathologic study of five cases and review the literature. Mod Pathol 1995;8:633–636.
9. Mazzara PF, Flint A, Naylor B. Adenoma of the nipple. Cytopatholog- ic features. Acta Cytol 1989;33:188–190.
10. Montemarano AD, Sau P, James WD. Superficial papillary adeno- matosis of the nipple: a case report and review of the literature. J Am Acad Dermatol 1995;33:871–875.
11. Myers JL, Mazur MT, Urist mm, et al. Florid papillomatosis of the nipple: immunohistochemical and flow cytometric analysis of two cases. Mod Pathol 1990;3:288–293.
12. Pinto RG, Mandreker S. Fine needle aspiration cytology of adenoma of the nipple: a case report. Acta Cytol 1996;40:789–791.
13. Rosen PP, Caicco JA. Florid papillomatosis of the nipple. A study of 51 patients, including nine with mammary carcinoma. Am J Surg Pathol 1986;10:87–101.
14. Scott P, Kissin MW, Collins C, et al. Florid papillomatosis of the nipple: a clinico-pathological surgical problem. Eur J Surg Oncol 1991;17:211–213.
15. Zeng Z, Melamed J, Symmans PJ, et al. Benign proliferative nipple duct lesions frequently contain CAM 5.2 and anti-cytokeratin 7 im- munoreactive cells in the overlying epidermis. Am J Surg Pathol 1999;23:1349–1355.
12.3 (Infiltrating) Syringomatous Adenoma
12.3.1 Definition
A rare, nonmetastasizing, locally infiltrative tumor of the nipple/
areolar region showing some sweat duct differentiation.
12.3.2 Synonym
Infiltrating syringomatous adenoma
12.3.3 Macroscopy
A firm greyish-white mass usually with ill-defined borders sim- ulating an invasive carcinoma.
12.3.4 Microscopic Features (Fig. 88)
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Angulated or small curved (comma-like) tubules are evident.
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Compressed, cordlike glands or strands are present.
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The tubules (glands) show haphazard and infiltrating arrangements with permeation of the nipple stroma.
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The tubules and compressed glands are lined by two cell layers: a luminal layer of epithelial cells and a basally located myoepithelial cell layer.
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As a rule, there is no nuclear atypia or increased mitotic activ- ity.
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Squamous metaplasia within the glands is a very common finding.
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Some of the glands may show usual ductal hyperplasia.
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Small keratinous cysts are often present.
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The stroma is either unaltered or, in some cases, can show reactive cellular areas (desmoplasia).
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Myxochondroid stromal changes may also occur.
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Invasion into the smooth muscle bundles of the nipple is com- mon.
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Perineural invasion can rarely be identified.
12.3.5 Differential Diagnosis
Well-differentiated ductal carcinoma or tubular carcinoma; well- differentiated adenosquamous carcinoma.
Caution
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The most important feature for distinguishing syringomatous adenoma from a well-differentiated ductal or tubular carcino- ma is the presence of epithelial and myoepithelial cells in the tubules of the syringomatous adenoma. While squamous metaplasia within the glands frequently occurs in syringoma- tous adenoma, it is not a feature of tubular carcinoma.
12.3.6 Additional Comments
Syringomatous adenoma also occurs deep within the breast proper.
All reported cases have been unilateral, and none has been associated with axillary lymph node metastasis. There is no hematogenic metastasis.
Because of its infiltrating pattern and local recurrences, this type of tumor has been considered by some dermatopathologists as microcystic adnexal carcinoma [2, 3] or sclerosing sweat duct (syringomatous) carcinoma. The reported recurrences are most likely because of incomplete excision of this frequently ill-de- fined tumor, which often extends beyond the grossly apparent margins.
Optimal treatment is complete excision with free margins [1, 5, 6, 8].
12.3.7 Further Reading
1. Carter E, Dyess DL. Infiltrating syringomatous adenoma of the nip- ple: a case report and 20-year retrospective review. Breast J 2004;10:
443–447.
2. Goldstein DJ, Barr RJ, Santa Cruz DJ. Microcystic adnexal carcino- ma. Cancer 1982;13:182–184.
3. Henner MS, Shapiro PE, Ritter JH, et al. Solitary syringoma. Report of five cases and clinicopathologic comparison with microcystic ad- nexal carcinoma of the skin. Am J Dermatopathol 1995;17:465–470.
4. Jones MW, Norris HJ, Snyder RC. Infiltrating syringomatous adeno- ma of the nipple. A clinical and pathological study of 11 cases. Am J Surg Pathol 1989;13:197–201.
5. Rosen PP. Syringomatous adenoma of the nipple. Am J Surg Pathol 1983;7:738–745.
6. Slaughter MS, Pomerantz RA, Murad T, et al. Infiltrating syringoma- tous adenoma of the nipple. Surgery 1992;111:711–713.
7. Suster S, Moran CA, Hurt MA. Syringomatous squamous tumors of the breast. Cancer 1991;67:2350–2355.
8. Tavassoli FA. Pathology of the breast, 2nd edn. Appleton & Lange, Stamford, CT, 1999, pp. 751–755.
9. Ward BE, Cooper PH, Subramony C. Syringomatous tumor of the nipple. Am J Clin Pathol 1989;92:692–696.
10. Yosepovich A, Perelman M, Ayalon S, et al. Syringomatous adenoma
of the nipple: a case report. Pathol Res Pract 2005;201:405–407.
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Fig. 86: Paget’s disease.
Case history: A 63-year-old woman presented with an itching, eczematoid nipple of her left breast.
Although there was a bloody nipple discharge, no palpable tumor could be identified in the breast.
Fig. 86.1: Clinical aspect of Paget’s disease shows a sharply demarcated eczematoid change of the nip- ple and areolar region. (Courtesy of Dr. G. Lushin, Graz, Austria.)
Fig. 86.2: Epidermis of the nipple showing isolated or small clusters of atypical cells. The atypical cells show hyperchromatic or vesicular nuclei.
Fig. 86.3: Highly atypical cells within the squamous epithelium of the nipple. The atypical cells reveal pale eosinophilic or amphophilic cytoplasm.
Fig. 86.4: Immunohistochemically, the tumor cells are characteristically positive for CK8/18 (low mo- lecular weight cytokeratin). The tumor cells are also typically positive for CK7 (not shown).
Fig. 86.5: The neoplastic epithelial cells in Paget’s disease are completely negative for high molecular weight cytokeratins such as CK34BE12 or CK5/6.
Fig. 86. 6: The tumor cells in Paget’s disease are very often negative for estrogen receptors and progesterone receptors.
Fig. 86.7: In contrast to estrogen receptors and progesterone receptors, neoplastic cells in Paget’s disease frequently express androgen receptors.
Fig. 86.8: The neoplastic cells almost always over- express HER2/neu.
Fig. 86: Final remarks
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In a difficult case, the most useful markers in order to identify Paget’s cells are LMW-CK (CK8/18, CK7) in combination with high mo- lecular weight cytokeratin (CK34BE12, CK5/6).
While the tumor cells in Paget’s disease are
positive for LMW-CK, they are typically nega-
tive for high molecular weight cytokeratin.
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Fig. 87: Nipple duct adenoma.
Case history: A 50-year-old woman presented with bloody nipple discharge and a firm tumor located in the left nipple. The overlying skin was ulcerated.
The tumor was clinically and mammographically interpreted as malignant. A needle core biopsy of the tumor was performed, and the lesion was erro- neously interpreted as DCIS associated with foci of infiltrating ductal carcinoma. The patient was treat- ed by modified radical mastectomy.
Fig. 87.1: The cut surface of the mastectomy spec- imen shows a solid tumor, greyish-white to yellow in color, with well-defined margins.
Fig. 87.2: At low magnification, the tumor exhibits compact aggregates of tubules proliferating within and replacing the nipple stroma. Sclerotic changes of the stroma are also present, which cause distor- tion of the tubules.
Fig. 87.3: Some areas of the tumor with elongated and irregularly distributed tubules (sclerosing adenosis pattern).
Fig. 87.4: Several ducts reveal florid-type intraduc- tal proliferations with tufting growth pattern.
Fig. 87.5: Intraductal hyperplasia of usual type demonstrating several irregular and slit-like sec- ondary lumens.
Fig. 87.6: Higher magnification of the intraductal proliferating cells showing a heterogeneous cell population consisting of epithelial and modified myoepithelial (progenitor) cells. While the prolifer- ating epithelial cells show round nuclei, the modi- fied myoepithelial (progenitor) cells display a small spindle shaped or bipolar dark nuclei and scant cytoplasm. The cytology (cell population) and the architecture of the involved ducts are typical of usual ductal hyperplasia.
Figs. 87.7 and 87.8: Immunohistochemistry for CK5/6 showing the heterogeneous positive reac- tion of the proliferating cells (mosaic positive pat- tern) that is typical for usual ductal hyperplasia.
Fig. 87: Final remarks
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Nipple duct adenoma (or florid papillomatosis of the nipple) can easily be mistaken for inva- sive carcinoma or Paget’s disease, clinically.
As unfortunately happened in this case, nee-
dle core biopsy of the nipple duct adenoma
can be misinterpreted as carcinoma. Skin ero-
sion or ulceration, increased mitotic activity,
and luminal necrosis can occur in nipple duct
adenoma and should not mislead to the diag-
nosis of cancer. The morphologic (and even-
tually immunohistochemical) analysis of the
proliferating cells (recognition of epithelial
and modified myoepithelial cells) and identifi-
cation of basally located myoepithelial cells in
the glands with pseudoinvasion are the most
helpful clues for appropriately classifying this
rare, benign neoplasm.
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Fig. 88: (Infiltrating) syringomatous adenoma.
Case history: A 43-year-old woman presented with a firm tumor of the areolar region of the right breast. Clinical and mammographic examinations of the tumor revealed a tumor with ill-defined bor- ders, highly suspicious for malignancy.
Figs. 88.1 and 88.2: Excisional biopsy of the tumor showing numerous open glands or tubules with haphazard and infiltrating arrangements.
Figs. 88.3 and 88.4: Several angulated tubules
with irregular and infiltrating arrangements are
present.
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Fig. 88.5: In addition, several areas of the tumor show compressed, cordlike glands or strands.
Fig. 88.6: Infiltrating glands showing angulated tubules and cordlike compressed structures.
Figs. 88.7 and 88.8: At higher magnification, the tubules and cordlike structures clearly reveal a basally located myoepithelial cell layer.
Figs. 88.9 and 88.10: Angulated or small curved (comma-like) tubules with infiltrating growth pat- tern containing a myoepithelial cell layer.
Fig. 88: Final remarks
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The syringomatous adenoma of the nipple has a true infiltrating growth pattern with invasion into smooth muscle bundles of the nipple. The stroma can be either unaltered or, in some instances, can show reactive, cellular (desmoplastic) areas.
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