Ji-Young Choe1,2, Ji Yun Yun1,2, Hee Young Na2,3, Jooryung Huh4, Su-Jin Shin4, Hyun-Jung Kim5, Jin Ho Paik1, Young A Kim6, Soo Jeong Nam3, Yoon Kyung Jeon3, Gyeongsin Park7, Ji Eun Kim2,6. 1. Department of Pathology, Seoul National University Bundang Hospital, Seongnam, Korea. 2. Department of Pathology, College of Medicine, Seoul National University, Seoul, Korea. 3. Department of Pathology, Seoul National University Hospital, Seoul, Korea. 4. Department of Pathology, Asan Medical Centre, Seoul, Korea. 5. Department of Pathology, Inha University Hospital, Incheon, Korea. 6. Department of Pathology, Seoul National University Boramae Hospital, Seoul, Korea. 7. Department of Pathology, Seoul St Mary's Hospital, The Catholic University of Korea, Seoul, Korea.
Abstract
AIMS: We aimed to investigate MYC expression and chromosomal aberration in mantle cell lymphoma (MCL), and the clinical significance of these factors. METHODS AND RESULTS: Sixty-five patients with MCL, including 54 classic, nine blastoid and two pleomorphic variants, were enrolled. Expression of MYC, Ki67 and p53 was assessed by immunohistochemistry. MYC amplification or translocation was examined by fluorescence in-situ hybridization. MYC expression was higher in blastoid/pleomorphic MCL variants (mean, 19.0%) than in classic MCL (mean, 1.9%; P < 0.001). Expression of p53 and Ki67 was also significantly higher in these variants. MYC amplification was found in two of 53 cases tested, both of which were blastoid variants with high MYC expression (29.7% and 20.4%). MYC translocation was found in two of 52 cases tested, both of which were pleomorphic variants with remarkably high MYC expression (68.5% and 71.0%). High MYC or p53 expression was significantly associated with shortened overall survival and progression-free survival in univariable and multivariable analyses (all P < 0.05). CONCLUSIONS: MYC overexpression is a negative predictor of MCL patient outcomes. MYC gene amplification or translocation might be related to the pathogenesis of MCL, particularly in blastoid/pleomorphic variants.
AIMS: We aimed to investigate MYC expression and chromosomal aberration in mantle cell lymphoma (MCL), and the clinical significance of these factors. METHODS AND RESULTS: Sixty-five patients with MCL, including 54 classic, nine blastoid and two pleomorphic variants, were enrolled. Expression of MYC, Ki67 and p53 was assessed by immunohistochemistry. MYC amplification or translocation was examined by fluorescence in-situ hybridization. MYC expression was higher in blastoid/pleomorphic MCL variants (mean, 19.0%) than in classic MCL (mean, 1.9%; P < 0.001). Expression of p53 and Ki67 was also significantly higher in these variants. MYC amplification was found in two of 53 cases tested, both of which were blastoid variants with high MYC expression (29.7% and 20.4%). MYC translocation was found in two of 52 cases tested, both of which were pleomorphic variants with remarkably high MYC expression (68.5% and 71.0%). High MYC or p53 expression was significantly associated with shortened overall survival and progression-free survival in univariable and multivariable analyses (all P < 0.05). CONCLUSIONS:MYC overexpression is a negative predictor of MCLpatient outcomes. MYC gene amplification or translocation might be related to the pathogenesis of MCL, particularly in blastoid/pleomorphic variants.
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