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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 10  |  Issue : 6  |  Page : 293-296

Microglandular adenosis of the breast: A case report and a highlight on main diagnosis and management aspects


1 Surgical Oncology Unit, Oncology Center Mansoura University, Mansoura, Egypt
2 Department of Radiology, Faculty of Medicine, Mansoura University, Mansoura, Egypt
3 Department of Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt

Date of Submission11-Nov-2020
Date of Acceptance17-Nov-2020
Date of Web Publication24-Dec-2020

Correspondence Address:
Dr. Omar Hamdy
Surgical Oncology Unit, Oncology Center Mansoura University, Mansoura
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/cmrp.cmrp_54_20

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  Abstract 


Microglandular adenosis (MA) is a basically benign–recently borderline-breast disease which mimics well differentiated breast carcinoma clinically and pathologically. The incidence of carcinoma associated with MA reaches up to 27%. In this manuscript, we present a 64-year-old female patient presented with a right breast swelling. Sonomammogram revealed a breast imaging, radiology, and data system IVa right breast architectural distortion. Breast magnetic resonance imaging showed a heterogeneous segmental non mass enhancement in the upper outer quadrant with less extension to lower outer quadrant. Core needle biopsy revealed small uniform glandular structures lined by single layer cuboidal cells with luminal eosinophilic secretions. The cells showed positivity for cytokeratin (CK) and S-100 while P63, smooth muscle actin and CK5/6 were negative. Wide local excision of the mass was done. Microscopic examination revealed proliferation of small glands surrounded by collagenous stroma, some of them infiltrated into the adipose tissue, these glands were lined by a single layer of epithelial cells that lacks a myoepithelial cell layer. They showed positive reaction for S100 and were negative for estrogen receptor, progesterone receptor, and human epidermal growth factor receptor 2. This led to the diagnosis of breast MA. MA should be considered as a precursor for malignancy rather than an innocent lesion. Adequate surgical excision is recommended.

Keywords: Benign, borderline, breast diseases, microglandular adenosis


How to cite this article:
Hamdy O, Elzeiny A, Saleh GA, Hassan A. Microglandular adenosis of the breast: A case report and a highlight on main diagnosis and management aspects. Curr Med Res Pract 2020;10:293-6

How to cite this URL:
Hamdy O, Elzeiny A, Saleh GA, Hassan A. Microglandular adenosis of the breast: A case report and a highlight on main diagnosis and management aspects. Curr Med Res Pract [serial online] 2020 [cited 2021 Jan 25];10:293-6. Available from: http://www.cmrp.org/text.asp?2020/10/6/293/304825




  Background Top


Microglandular adenosis (MA) of the breast is a very rare disease with a few case reports and series documented till now. MA shows characteristic pathological features such as usual negativity for estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2) and positivity for S100. It is the only benign breast neoplasm which lacks a myoepithelial layer. The progression of classic MA to atypical MA to cancer has been clinically, pathologically, and genetically proven.[1]


  Case Report Top


A 64-year-old female patient, type II diabetic and hypertensive presented to our center complaining from right breast swelling. Clinical examination revealed an ill-defined heterogeneous breast area at the site of the complaint at the upper outer quadrant (UOQ) of the right breast with no palpable axillary or supraclavicular lymph nodes. Bilateral breast soft-tissue mammogram [Figure 1] revealed an oval high-density right breast mass in the UOQ, no suspicious micro calcification. Ultrasound revealed a breast imaging, radiology, and data system (BIRADS) 4a area of architectural distortion at UOQ at 10 and 11 o'clock at zone B, no overlying skin thickening. Neither pathological axillary nor supraclavicular lymph nodes were detected. Post-contrast breast magnetic resonance imaging (MRI) was recommended. MRI [Figure 2] revealed a heterogeneous segmental non-mass enhancement in the UOQ with less extension to the lower outer quadrant measuring 8 cm × 3 cm. Diffusion-weighted images revealed unrestricted diffusion pattern. It was described as BIRADS 4. Core needle biopsy was performed. Microscopic examination of the specimen revealed proliferation of small uniform glandular structures lined by a single layer of cuboidal epithelial cells with luminal eosinophilic secretions. Immunohistochemical (IHC) staining for S-100 showed diffuse positive reaction is epithelial cells while P63, smooth muscle actin and cytokeratin 5/6 were negative. This led to the diagnosis of MA. Wide local excision of the mass under general anesthesia was done. The patient was discharged in the same day with uneventful postoperative course. The pathology laboratory received the specimen as a fibrofatty breast tissue measuring 7 cm × 6 cm × 5 cm covered by an ellipse of skin with grossly healthy margins. Dissection of the specimen revealed an ill-defined mass measuring 5.5 cm × 4 cm × 4 cm with a firm grayish cut surface. Microscopic examination [Figure 3] revealed haphazard proliferation of small round tubular structures; some of them contained luminal eosinophilic secretions. They were lined by cuboidal epithelial cells with round bland nuclei and clear to pale eosinophilic cytoplasm. The surrounding stroma was collagenous. Some of these glands infiltrated into the breast fat. The cells showed S100 positive reaction with complete loss of myoepithelial markers around them. They were negative for ER, PR and HER2 [Figure 4]. All surgical cut margins were free from involvement by the lesion. This led to the diagnosis of breast MA with free surgical margins. On follow-up, the patient had a clean healed wound with no postoperative complications.
Figure 1: Right breast mammogram CC and MLO views (a and b): Scattered areas of fibroglandular density (breast composition B). An oval high density right breast mass with indistinct margins was seen at the upper outer quadrant, no suspicious microcalcifications

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Figure 2: Post-contrast right breast dynamic magnetic resonance imaging: Axial T2- fat-suppressed image (a): Large area of moderate signal intensity was seen at right breast upper outer quadrant and to less extent lower outer quadrant. Axial Dynamic magnetic resonance image with subtraction (b): Revealed heterogeneous segmental non-mass enhancement, no pathological axillary LNs. Axial diffusion-weighted image and corresponding ADC map (c and d): Revealed free diffusion with high ADC value 1.521 × 10−3 mm2/s

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Figure 3: Microscopic examination of the specimen: (a and b): Haphazard proliferation of small round tubular structures, some of them contain eosinophilic secretions (H and E, ×40 and × 200, respectively). (c): The lining cells are cuboidal with bland nuclear features and clear to pale eosinophilic cytoplasm. Intraluminal eosinophilic secretions also present (H and E, ×400)

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Figure 4: Immunohistochemical staining results (a): Strong positive nuclear and cytoplasmic reaction for S100 (S100, ×200) (b and c): Negative nuclear reaction for estrogen receptor and progesterone receptor, respectively, in the small glandular structures compared to normal nearby breast duct (estrogen receptor and progesterone receptor, ×200). (d): Negative membranous reaction for human epidermal growth factor receptor 2 (human epidermal growth factor receptor 2, ×200) (e): Complete loss of myoepithelial cell layer compared to nearby normal breast duct (smooth muscle actin, ×200)

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  Discussion Top


MA is a basically benign–recently borderline-breast glandular proliferation which occupies the breast stroma and adipose tissue without destruction of the normal glands.[2],[3] It was first reported in 1968.[4],[5] It affects females only with the age range from 28 to 82, with high incidence of multifocality.[2] Clinical presentation may be similar to breast cancer or it may be presented with an ill-defined swelling or a thickening, but axillary nodal involvement and distant metastasis have not been reported for classic MA.[6],[7] Our patient was presented by an ill-defined right breast swelling with no nodal involvement.

Mammogram may show calcifications or a hyperdense area simulating carcinoma and presenting with a radiologically suspicious appearance.[6],[7] The lesion in our patient was detected as a hyperdense area in the mammogram in comparison to the contralateral breast.

On the histopathological level, MA shows the proliferation of small uniform epithelial lined tubular structures in non-organoid fashion. Those structures invade the breast stroma and fatty tissue surrounds the normal ducts but do not alter or compress them. The tubules are lined by a single layer of cuboidal and occasionally flat cells. They lack a myoepithelial layer. The cells have a clear–occasionally granular-cytoplasm and rounded to ovoid nuclei with scarce nucleoli and very rare mitosis[2],[6] IHC studies usually show negativity for ER, PR, HER-2, gross cyst disease fluid protein-15 and epithelial membrane antigen. They usually show positivity for S-100 protein and pancytokeratin.[2],[6],[8] Some authors consider MA and atypical MA as low-grade triple-negative breast neoplasms.[9] In our patient, the tumor was negative for ER, PR, and HER2 and positive for S100.

Differential diagnosis of MA includes a variety of benign and malignant lesions such as tubular carcinoma, acinic cell carcinoma, and adenomyoepithelial (apocrine) adenosis.[2]

Despite its benign nature, a wide spectrum of lesions, including classic MA, atypical MA, and carcinoma arising on top of MA has been described. Atypical MA has a more pleomorphic structure, more dense and irregular glands, as well as more atypical cells in the form of scattered mitotic figures, hyperchromatic nuclei and prominent nucleoli.[6],[7],[9] The transition of MA to atypical MA and then to cancer has been documented more commonly to triple-negative breast cancer through the occurrence of additional genetic alterations. The rate of coexisting carcinoma equals 20%–30%[3],[7],[10],[11] The p53 and Ki-67 index values show a gradual increase from classic to atypical to MA associated with carcinoma.[12] The transition into many malignant subtypes has been documented.[10] Those subtypes include ductal carcinoma in situ, invasive duct carcinoma not otherwise specified,[13] adenoid cystic carcinoma,[14] spindle cell carcinoma, matrix-producing carcinoma,[3],[12] and acinic cell carcinoma.[9] Accordingly, MA is gaining an agreement to be considered as a cancer precursor rather than a simple innocent benign lesion.[10],[15]

Treatment options vary according to the risk features; they include observation, surgical excision as well as wide local excision. Thorough and careful pathological assessment of the excised specimen is necessary to exclude associated atypical or malignant component.[2],[6],[10],[16] If an associated carcinoma is discovered, the patient will be managed according to the carcinoma type and stage.[6]


  Conclusion Top


MA is a microscopically benign lesion with a transition potential mainly into basal-like breast cancer. It should be differentiated from other simulating breast neoplasms. Wide local excision with free margins should be the standard of the case of such rare disease.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understand that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Damron AT, Korhonen K, Zuckerman S, Tchou J, Dumoff KL, Bleiweiss IJ, et al. Microglandular adenosis: A possible non-obligate precursor to breast carcinoma with potential to either luminal-type or basal-type differentiation. Int J Surg Pathol 2019;27:781-7.  Back to cited text no. 1
    
2.
Foschini MP, Eusebi V. Microglandular adenosis of the breast: A deceptive and still mysterious benign lesion. Hum Pathol 2018;82:1-9.  Back to cited text no. 2
    
3.
Schwartz CJ, Dolgalev I, Yoon E, Osman I, Heguy A, de Miera EC, et al. Microglandular adenosis is an advanced precursor breast lesion with evidence of molecular progression to matrix-producing metaplastic carcinoma. Hum Pathol 2019;85:65-71.  Back to cited text no. 3
    
4.
Clement PB, Azzopardi JG. Microglandular adenosis of the breast-a lesion simulating tubular carcinoma. Histopathology 1983;7:169-80.  Back to cited text no. 4
    
5.
McDivitt RW, Stewart FW, Berg JW. Atlas of Tumor Pathology, Second Series, Fascicle 2, Tumors of the Breast. USA: Armed Forces Inst Pathol Washingt DC; 1968.  Back to cited text no. 5
    
6.
Kim DJ, Sun WY, Ryu DH, Park JW, Yun HY, Choi JW, et al. Microglandular adenosis. J Breast Cancer 2011;14:72-5.  Back to cited text no. 6
    
7.
Sahasrabudhe N, Brelsford K, Kumar S, Mene A. Atypical microglandular adenosis presenting as a breast lump. Diagnostic Histopathol 2011;17:36-9.  Back to cited text no. 7
    
8.
Popper HH, Gallagher JV, Ralph G, Lenard PD, Tavassoli FA. Breast carcinoma arising in microglandular adenosis: A tumor expressing S-100 immunoreactivity. Report of five cases. Breast J 1996;2:154-9.  Back to cited text no. 8
    
9.
Geyer FC, Berman SH, Marchiò C, Burke KA, Guerini-Rocco E, Piscuoglio S, et al. Genetic analysis of microglandular adenosis and acinic cell carcinomas of the breast provides evidence for the existence of a low-grade triple-negative breast neoplasia family. Mod Pathol 2017;30:69-84.  Back to cited text no. 9
    
10.
Tsang JY, Tse GM. Microglandular adenosis: A prime suspect in triple-negative breast cancer development. J Pathol 2016;239:129-32.  Back to cited text no. 10
    
11.
Shin SJ, Simpson PT, Da Silva L, Jayanthan J, Reid L, Lakhani SR, et al. Molecular evidence for progression of microglandular adenosis (MGA) to invasive carcinoma. Am J Surg Pathol 2009;33:496-504.  Back to cited text no. 11
    
12.
Khalifeh IM, Albarracin C, Diaz LK, Symmans FW, Edgerton ME, Hwang RF, et al. Clinical, histopathologic, and immunohistochemical features of microglandular adenosis and transition into in situ and invasive carcinoma. Am J Surg Pathol 2008;32:544-52.  Back to cited text no. 12
    
13.
Koenig C, Dadmanesh F, Bratthauer GL, Tavassoli FA. Carcinoma arising in microglandular adenosis: An immunohistochemical analysis of 20 intraepithelial and invasive neoplasms. Int J Surg Pathol 2000;8:303-15.  Back to cited text no. 13
    
14.
Acs G, Simpson JF, Bleiweiss IJ, Hugh J, Reynolds C, Olson S, et al. Microglandular adenosis with transition into adenoid cystic carcinoma of the breast. Am J Surg Pathol 2003;27:1052-60.  Back to cited text no. 14
    
15.
Zhong F, Bi R, Yu B, Cheng Y, Xu X, Shui R, et al. Carcinoma arising in microglandular adenosis of the breast: Triple negative phenotype with variable morphology. Int J Clin Exp Pathol 2014;7:6149-56.  Back to cited text no. 15
    
16.
Shui R, Yang W. Invasive breast carcinoma arising in microglandular adenosis: A case report and review of the literature. Breast J 2009;15:653-6.  Back to cited text no. 16
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

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