Acinic cell carcinoma of the breast is an uncommon neoplasm. Since the first case of this rare variant of breast carcinoma was reported in 1996, only 10 cases have been reported in the English-language literature. Reported herein is the first case of primary acinic cell carcinoma of the breast in a Japanese woman. To the naked eye, the tumor appeared well circumscribed and the cut surface was grayish-pink and hemorrhaging. Microscopically, the tumor was predominantly made up of a monotonous proliferation of cells with a finely granular cytoplasm, resembling acinic cells of the parotid gland. Some neoplastic cells had a clear cytoplasm. In spite of extensive sampling, no common histological patterns of breast carcinoma such as in situ and invasive ductal carcinoma were recognized in the present case, indicating that the present case was pure acinic cell carcinoma. In addition, the immunohistochemical profile of this tumor was identical to that of the acinic cell carcinoma of the salivary gland: estrogen receptor, progesterone receptor, HER2 and cytokeratin (CK)20 were negative and amylase and CK7 were positive. The patient has been well for 22 months since the wide local excision of the tumor and no signs of salivary neoplasm are evident to date.

Activation-induced cell death (AICD) in T lymphocytes is important for the maintenance of peripheral tolerance. We studied AICD of peripheral blood T cells from patients with primary Sj6gren's syndrome (SS). AICD was induced in mitogen-activated T cells in vitro using mAb to CD3 or Fas (CD95). Cell death and proliferation, Fas and Fas ligand (FasL) expression, and soluble Fas and soluble FasL production were measured. Surface phenotypes and cytokine production of AICDsurviving cells and effects of cytokines on AICD were examined. Anti-CD3 mAb induced cell death in SS and normal T cells in the presence of exogenous interleukin (IL)-2. In the absence of IL-2 anti-CD3 mAb induced cell proliferation in SS and normal T cells. There was no significant difference in Fas/FasL expression and sFas/sFasL production between SS patients and normals. AICD-surviving cells consisted of more CD4 + T cells and less CD8 + T cells in SS compared to normals. AICDsurviving cells produced abundant interferon-y and little IL-4. There was no significant difference in the effects of cytokines on AICD between SS patients and normals. These findings suggest that IL-2 is a critical factor for AICD. AICD works almost normally in SS T cells when sufficient IL-2 is present prior to T cell receptor re-stimulation.

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