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A 73-year-old woman diagnosed with symptomatic multiple myeloma (MM; IgG-κ type, D&S: IIIA, ISS: 2) was administered bortezomib plus dexamethasone (BD) therapy. Post BD therapy, although autologous hematopoietic stem cell transplantation and thalidomide, lenalidomide, and melphalan/prednisolone/thalidomide (MPT) therapies were also performed, the patient remained unresponsive. However, the disease relapsed, and she eventually developed pantalgia.

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Overexpression of salivary-type amylase reduces the sensitivity to bortezomib in multiple myeloma cells.

Int J Hematol

November 2015

Division of Hematology, Department of Internal Medicine, Aichi Medical University, 1, 1 Karimata, Yazako, Nagakute, Aichi, 480-1195, Japan.

Amylase-producing myeloma exhibits refractoriness to chemotherapy and a dismal prognosis. In this study, we established a human myeloma cell line, 8226/AMY1, in which a lentivirally transfected AMY1 gene was stably expressed and explored its biological characteristics. 8226/AMY1 showed a survival advantage over mock control when treated with dexamethasone, bortezomib, and lenalidomide in vitro partly through inhibition of apoptosis induced by these reagents.

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Successful therapy for radiation-induced salivary gland (SG) hypofunction is currently unavailable; however, tissue-specific stem cells are expected to be promising candidates for SG regeneration. Here, we present our method for the establishment of single cell-derived clonal stem cells from mouse SGs and describe their characteristics. Salivary gland-derived clonal stem cells (SGSCs) were isolated and expanded in vitro by a modified subfractionation culture method.

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A 60-year-old woman was diagnosed with metastatic pulmonary adenocarcinoma (c-stage IV) with an L858R point mutation in the gene encoding epidermal growth factor receptor (EGFR). Serum amylase levels were elevated (1,531 IU/L) with the salivary-type enzyme dominating. First-line chemotherapy using carboplatin plus paclitaxel reduced serum amylase levels, although second-line gefitinib eventually failed to control tumor growth and hyperamylasemia after 4.

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