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Presented by Pedram Argani, M.D. and prepared by Justin Poling, M.D.
Case 2: This is a 65 year old female with a breast mass.
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Question 1 of 1
1. Question
Week 516: Case 2
This is a 65 year old female with a breast mass.images/jsp6182012/6182012case24x.jpg
images/jsp6182012/6182012case24x2.jpg
images/jsp6182012/6182012case210x.jpg
images/jsp6182012/6182012case220x.jpgCorrect
Answer: Ductal carcinoma in situ colonizing adenosis
Histology: The background breast in this case demonstrates prominent sclerosing adenosis, with centrally-placed, spindled myoepithelial cells and peripheral open ducts. The adenosis is colonized by atypical apocrine proliferation, featuring enlarged nuclei, pale cytoplasm, and luminal necrosis. The apocrine cells have sheet like and cribriform architecture. These features support the diagnosis of ductal carcinoma in situ. While there is stromal reaction associated with small ducts within the lesion, these ducts have a rounded contours and retain peripheral myoepithelial cells as demonstrated by myoepithelial stains p63 and actin. These findings support the diagnosis of ductal carcinoma in situ colonizing sclerosing adenosis.
Discussion: Invasive ductal carcinoma is excluded by the intact myoepithelial cells surrounding the lesion. The clues that this is not invasive carcinoma are the pre-existing adenosis and rounded nature of atypical glands on the H&E. The apocrine proliferation in this case demonstrated solid architecture, marked cytologic atypia and necrosis, excluding simple apocrine change and indicating that the apocrine change is neoplastic. Histiocytoid lobular carcinoma in situ characteristically shows apocrine differentiation; however, lobular carcinoma in situ should not form duct spaces as seen the current lesion.
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Answer: Ductal carcinoma in situ colonizing adenosis
Histology: The background breast in this case demonstrates prominent sclerosing adenosis, with centrally-placed, spindled myoepithelial cells and peripheral open ducts. The adenosis is colonized by atypical apocrine proliferation, featuring enlarged nuclei, pale cytoplasm, and luminal necrosis. The apocrine cells have sheet like and cribriform architecture. These features support the diagnosis of ductal carcinoma in situ. While there is stromal reaction associated with small ducts within the lesion, these ducts have a rounded contours and retain peripheral myoepithelial cells as demonstrated by myoepithelial stains p63 and actin. These findings support the diagnosis of ductal carcinoma in situ colonizing sclerosing adenosis.
Discussion: Invasive ductal carcinoma is excluded by the intact myoepithelial cells surrounding the lesion. The clues that this is not invasive carcinoma are the pre-existing adenosis and rounded nature of atypical glands on the H&E. The apocrine proliferation in this case demonstrated solid architecture, marked cytologic atypia and necrosis, excluding simple apocrine change and indicating that the apocrine change is neoplastic. Histiocytoid lobular carcinoma in situ characteristically shows apocrine differentiation; however, lobular carcinoma in situ should not form duct spaces as seen the current lesion.