Usual Ductal Hyperplasia (UDH)

Author(s):  
Anna Sapino ◽  
Davide Balmativola ◽  
Maria Giulia Disanto ◽  
Caterina Marchiò
2018 ◽  
Vol 6 ◽  
pp. 205031211881154 ◽  
Author(s):  
Ichiro Maeda ◽  
Shinya Tajima ◽  
Yoshihide Kanemaki ◽  
Koichiro Tsugawa ◽  
Masayuki Takagi

Objectives: The aim of this study was to use immunohistochemistry to differentiate solid papillary carcinoma in situ from intraductal papilloma with usual ductal hyperplasia (IPUDH). Three types of high-molecular-weight cytokeratins (CKs) – CK5/6, CK14, and CK34betaE12 – were targeted. Methods: We studied 17 patients with solid papillary carcinoma in situ and 18 patients with IPUDH diagnosed by at least two pathologists. Immunohistochemical analyses used antibodies to CK5/6, CK14, and CK34betaE12 to make the differential diagnosis of solid papillary carcinoma in situ versus IPUDH. Immunohistochemical staining was scored as 0–5 using Allred score. Results: Immunohistochemistry with CK5/6 and CK14 antibodies produced scores of 0–3 in all patients with solid papillary carcinoma in situ and 2–5 in all patients with IPUDH. Immunohistochemical staining with CK34betaE12 antibody produced scores of 1–3 in all patients with solid papillary carcinoma and 3–5 in all patients with IPUDH. In tissues from patients with IPUDH, significantly more cells were stained with CK34betaE12 than CK5/6 ( p < 0.05) or CK14 ( p < 0.05). Conclusion: The immunoreactivity of CK5/6, CK14, and CK34betaE12 antibodies was useful to differentiate solid papillary carcinoma in situ from IPUDH. CK34betaE12 is especially useful for distinguishing solid papillary carcinoma from IPUDH.


2019 ◽  
Vol 3 (2) ◽  
pp. 41
Author(s):  
Kelvin Setiawan ◽  
Bramastha Aires Rosadi ◽  
Terry Renata Lawanto ◽  
Primariadewi Rustamadji

Background: Benign breast disease have been broadly classified into non-proliferative lesions, proliferative lesions without atypia and hyperplasia with atypia. Proliferative disease, such as usual ductal hyperplasia, is associated with a 1.5 to 2 fold increased risk of developing invasive carcinoma. We reported a case of usual ductal hyperplasia in a young male. Case: A 22-year-old male complained of discomfort and enlargement of unilateral breast. Physical examination at that time revealed a palpable mass in the lateral upper quadrant of the patient’s left breast, three centimeters from nipple areola complex. The examination of axilla didn’t reveal any lymph node enlargement on both sides. His vital signs were normal without any abnormalities found on examination. Ultrasonography examination demonstrated fibroglandular tissue in the left breast with the volume of 11.13 cm3, consist of 4.8 cm length, 2.9 cm width and 0.8 cm depth. Excisional tumor biopsy was done on his left breast. Usual duct cell hyperplasia was present in microscopic examination with chronic inflammatory cells spreading around the fibrotic stromal cell. Physical examination, radiologic examination, and biopsy were all performed in this patient. Although the accuracy of the triple test is high, benign concordant results do not obviate further surveillance of a palpable mass. We advised our patient to routinely follow-up his condition every 6 months for 1 to 2 years, especially if there any changes found on his breasts. Conclusion: Any guidelines and further studies regarding patient’s follow-up examination after biopsy for male breasts tumor are needed in order of better understanding about this disease.


2017 ◽  
Author(s):  
Richard J Bleicher

Clinicians who treat breast disease deal with a variety of pathologic findings. Although there is often a focus on paradigms and data regarding malignant breast disease, benign breast disease ranges from that which requires no imaging, evaluation, or treatment to that which requires further testing to rule out concomitant cancer and ameliorate subsequent risk. This review discusses the most frequent types of high-risk lesions facing the breast practitioner, including atypical ductal hyperplasia, lobular neoplasia, radial scar, and papillary lesions. It is critical that the clinician understand the implications of each finding to advise about the risks associated with each of these entities, fully assess the need for further therapy, and mitigate the patient’s future risk.  This review contains 2 tables, and 69 references. Key words: atypical ductal hyperplasia, atypical lobular hyperplasia, lobular neoplasia, lobular carcinoma in situ, papillary lesions, pleomorphic, pseudoangiomatous stromal hyperplasia, radial scar, usual ductal hyperplasia


Author(s):  
Anna Sapino ◽  
Davide Balmativola ◽  
Maria Giulia Disanto ◽  
Caterina Marchiò

2019 ◽  
Vol 116 (23) ◽  
pp. 11444-11453 ◽  
Author(s):  
Stefan Florian ◽  
Yoshiko Iwamoto ◽  
Margaret Coughlin ◽  
Ralph Weissleder ◽  
Timothy J. Mitchison

As 3D culture has become central to investigation of tissue biology, mammary epithelial organoids have emerged as powerful tools for investigation of epithelial cell polarization and carcinogenesis. However, most current protocols start from single cells suspended in Matrigel, which can also restrict cell differentiation and behavior. Here, we show that the noncancerous mammary cell line HMT-3522 S1, when allowed to spontaneously form cell aggregates (“spheroids”) in medium without Matrigel, switches to a collective growth mode that recapitulates many attributes of “usual ductal hyperplasia” (UDH), a common benign mammary lesion. Interestingly, these spheroids undergo a complex maturation process reminiscent of embryonic development: solid-cell cords form their own basement membrane, grow on the surface of initially homogeneous cell aggregates, and form asymmetric lumina lined by two distinct cell types that express basal and luminal cytokeratins. This sequence of events provides a cellular mechanism that explains how the characteristic crescent-shaped, asymmetrical lumina form in UDH. Our results suggest that HMT-3522 S1 spheroids are useful as an in vitro model system to study UDH biology, glandular lumen formation, and stem cell biology of the mammary gland.


1998 ◽  
Vol 29 (12) ◽  
pp. 1539-1545 ◽  
Author(s):  
Ellen C.M Mommers ◽  
Paul J Van Diest ◽  
Angelique M Leonhart ◽  
Chris J.L.M Meijer ◽  
Jan P.A Baak

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