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Objective@#To investigate the clinicopathologic features and grading of adenoid cystic carcinoma (ACC) of the breast.@*Methods@#Sixteen cases of ACC of the breast were analyzed and graded according to the previous report. Immunohistochemical (IHC) staining was used to detect the immunophenotype, Ki-67 proliferative index and expression of EZH2, and the association with tumor grade and outcome was analyzed.@*Results@#Of the 16 cases, 11 were grade Ⅰ, with the epithelial and myoepithelial cells being arranged into tubular and cribriform structure with no solid component; three were grade Ⅱ, which were composed of mixed tubular, cribriform and solid component (<30%); and two were grade Ⅲ, which showed mainly solid component (>90%) and the tumor cells showed basaloid features with scanty cytoplasm and hyperchromatic nuclei, and mitotic count was>5/10 HPF. Immunophenotypically, the epithelial cells expressed CK7, CK8/18 and CD117; the myoepithelial cells expressed p63 and CK5/6; while the basaloid cells were positive for CK5/6 and CD117.Tubular and cibriform ACC showed low Ki-67 and EZH2 expression, while the two cases of solid variant with basaloid features showed high level of Ki-67 and EZH2 expression. Follow-up data were available in 13 cases with a median follow-up period of 42 months. Lung metastasis occurred after 12 months in one grade Ⅱ case and the patient died of disease after 34 months. Vertebral metastasis occurred after 12 months in one grade Ⅲ case and axillary lymph node metastasis occurred in another grade Ⅲ case. All other patients were free of disease at the end of the follow-up periods.@*Conclusions@#ACC shows morphologic spectrum varying from low to high grade, the latter can may give rise to local and distant metastasis. ACC should not be regarded simply as low malignant potential, and should be graded for optimal treatment.
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Objective To investigate the role and the mechanism of Apr-1 gene on cholangiocarcinoma QBC939 cell lines proliferation and cell cycle regulation. Methods Apr-1 gene was transfected into QBC939 cells by using liposomes to establish a QBC939 cell model ( QBC939-Apr-1 ) stably expressing Apr-1 gene. Apr-1 mRNA expression and the changes in cell cycle and cell growth of QBC939 cells were analyzed by RT-PCR, flow cytometry ( FCM ) and growth curve before and after transfection. The regulatory effect of Apr-1 gene on the expression of cell cycle-related genes was investigated in QBC939 cells before and after Apr-1 transfection using cell cycle gene microarrays. Results Significant suppression of cell growth was observed with the cell model stably expressing Apr-1 gene. Apr-1 over-expression caused cell arrest from 9% to 13% (P ＜0. 01 ) increase in G2 population. Cell cycle gene microarrays demonstrated that the expression of Skp2 、UBE1 was up-regulated, while the expression of MRE11A 、CKS2 、CDK8 、CDC45 was down-regulated by more than 3 folds. Conclusions Apr-1 gene suppresses QBC939 cell proliferation in vitro, QBC939 cells presented with differences in the expression of cell cycle-related genes after Apr-1 gene transfection.
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Objective: To explore the effects of exogenous APMCF1 gene on the growth and cell cycle of HHCC cells. Methods: A full human APMCF1 gene was cloned into expression vector pcDNA3.0 and transfected into human hepatocellular carcinoma cell HHCC by lipofectamine,and the positive clone was screened by G418.The expression of APMCF1 protein in HHCC cells were examined by semi-quantitative RT-PCR,and its effects on cell growth and cell cycle were observed by MTT and flow cytometer(FCM). Results: Semi-quantitative RT-PCR indicated that APMCF1 had been successfully transfected into HHCC cells.The growth speed of APMCF1 infected cells decreased markedly.Analysis of cell cycle by FCM showed that 85.3% of the infected cells were in G_1 phase and 12.5% in S phase,while 66.4% of the control HHCC cells were in G_1 phase and 24.7% in S phase. Conclusion:Exogenous APMCF1 gene can inhibit the growth and cell cycle of human hepatocellular carcinoma cell HHCC.It may be a cell cycle regulative gene.