title: Increased expression of the spindle checkpoint protein BubR1 is associated with high cell proliferation in primary gastrointestinal diffuse large B cell lymphoma.
abstract: Primary gastrointestinal diffuse large B cell lymphoma (PGI-DLBCL) is a relatively rare malignancy with limited results on clinical characteristics and carcinogenesis. Chromosome instability (CIN) is a hallmark of cancer cells, including lymphoma. As a key component of spindle assembly checkpoint (SAC), BubR1 plays a crucial role in maintaining genome stability. To elucidate the roles of BubR1 in the pathogenesis of PGI-DLBCL, and its relationship to cell proliferation, Helicobacter pylori infection, and BCL-6 gene translocation, we examined the possible alterations of BubR1 protein expression in PGI-DLBCL patients. Paraffin-embedded cancer tissues from 20 PGI-DLBCL patients were evaluated for BubR1 and H. pylori expression by immunohistochemistry, as well as cell proliferative activity measured by Ki-67 proliferation index (PI). BCL-6 gene rearrangement was assessed by fluorescence in situ hybridization (FISH) and BubR1 expression status was compared with clinicopathological parameters in PGI-DLBCL patients. Overexpression of BubR1 was observed in the majority of PGI-DLBCL patients. The mean expression level of BubR1 was 57.33 ± 23.27% in PGI-DLBCL, which was higher than normal gastrointestinal tissue (10.18 ± 5.65%) and reactive lymph node (26.74 ± 8.60%) (P < 0.01), while it was comparable to nodal lymphoma (54.32 ± 21.28%) (P > 0.05). BubR1 overexpression had a positive correlation with Ki-67 proliferation index (PI) (r = 0.51, P < 0.01) in PGI-DLBCL, but had no relationship to H. pylori infection and BCL-6 gene translocation. In addition, no correlation was found between BubR1 expression levels and overall survivals (P > 0.05). BubR1 overexpression was associated with cell proliferation and may play a role in the carcinogenesis of PGI-DLBCL. Aberrant BubR1 expression may potentially be a biomarker for estimating biologic characteristics of PGI-DLBCL.
authors: Department of Gastroenterology, Zhongnan Hospital of Wuhan University School of Medicine, Wuhan, People's Republic of China.
authors: Fei
authors: F
authors: Chen
authors: Guifang
authors: G
authors: Yang
authors: Bing
authors: B
authors: Xia
mesh_terms: D000328:Adult; D000368:Aged; D049109:Cell Proliferation; D004268:DNA-Binding Proteins / Q000235:genetics; D005260:Female; D005770:Gastrointestinal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D015972:Gene Expression Regulation, Neoplastic; D015321:Gene Rearrangement; D006801:Humans; D019394:Ki-67 Antigen / Q000378:metabolism; D016403:Lymphoma, Large B-Cell, Diffuse / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D059566:M Phase Cell Cycle Checkpoints; D008297:Male; D008875:Middle Aged; D017346:Protein Serine-Threonine Kinases / Q000378:metabolism*; D051560:Proto-Oncogene Proteins c-bcl-6
chemical_list: C084103:BCL6 protein, human; D004268:DNA-Binding Proteins; D019394:Ki-67 Antigen; D051560:Proto-Oncogene Proteins c-bcl-6; C584277:BUB1 protein, human; D017346:Protein Serine-Threonine Kinases