Cd56 clone 1b6

Selected sections from both Fallopian tube lesions were analyzed immunohistochemically using the avidin-biotin complex method with antibodies directed against the following antigens: inhibin (clone R1, ready-to-use, Dako, Glostrup, Denmark), WT-1 (clone 6F-H2, 1:100, Dako), calretinin (clone DAK-Calret1, 1:200, Dako), estrogen receptor (clone SP1, 1:100, Thermo Fischer Scientific, Waltham, MA, USA), progesterone receptor (clone 15, 1:100, Novocastra, Leica Biosystems, IL, USA), S100-A1 protein (1:600, Dako), CD56 (clone 1B6, 1:50, Novocastra), smooth muscle actin (clone 1A4, 1:400, Sigma-Aldrich, MS, USA), and PAX8 (1:50, Cell Marque, CA, USA).

The subjects were 107 patients (64 males and 43 females) of median age 69 years (range, 39-92 years). All cases were newly diagnosed with PCM at Showa University Hospital between January 2004 and September 2013. Medical records were reviewed to obtain clinical information, including therapy regimens, laboratory data, and overall survival (OS). Morphologic and immunophenotypic data were reviewed to confirm the diagnosis according to 2008 WHO criteria.
Morphological findings were obtained using H&E stains of 3-µm sections. Formalin-fixed, paraffin-embedded specimens were used for immunohistochemistry with the following antibodies: CD200 (polyclonal, goat; R&D Systems, Minneapolis, MN, USA), CD138 (clone MI15; Dako Cytomation A/S, Glostrup, Denmark), CD56 (clone 1B6; Novocastra, Newcastle, UK). CD200 and CD56 immunostained slides were defined as positive if > 30% of plasma cells had moderate to strong membranous staining. Statistical analysis was performed using JMP 11 (SAS Institute Inc., Cary, NC, USA). A c 2 test was used to compare clinical and pathological features between the CD200-positive and CD200-negative groups. A Wilcoxon signed-rank test was used to compare laboratory data between these groups. OS was analyzed using the Kaplan-Meier method and compared by generalized Wilcoxon test. A p value < 0.05 was considered significant in all analyses.