摘要目的:探讨肌细胞增强因子2B（myocyte enhancer factor 2B，MEF2B）在套细胞淋巴瘤（mantle cell lymphoma, MCL）中的表达，分析其与病理亚型、结构亚型、SOX11表达的相关性及临床意义。方法:收集中山大学附属佛山医院及中山大学肿瘤防治中心2002年1月至2019年5月60例MCL患者的临床及病理资料、石蜡组织，采用HE、免疫组织化学法（EnVision法）、荧光原位杂交（FISH）法进行染色，并结合临床资料进行统计分析。结果:60例MCL，男性占优势（男女比为3∶1）。组织学分组，经典型MCL居多（经典型48例，变异型12例）。结构学分组，非全网型比例高（非全网型50例，全网型10例）。经典型MCL的患者多见于>60岁老年人（29例）。无论病理亚型还是结构亚型MCL，病变多为结内、结外共存病变。SOX11（+）MCL常见于经典型（ P=0.040），倾向于全网型（ P=0.086）。MEF2B在MCL的表达率为60.0%（36/60），MEF2B在经典型、全网型、SOX11（+）MCL中表达率高，分别显著高于变异型、非全网型、SOX11（-）MCL（ P<0.05）。MEF2B阳性及阴性组MCL临床特点差异无统计学意义（ P>0.05）。与SOX11（-）MCL相比，SOX11（+）MCL的瘤细胞表达MEF2B百分比显著增高（ P=0.027）。MEF2B表达与瘤细胞增殖无关（ P=0.341）。MEF2B及SOX11不同表达组之间的生存率差异无统计学意义（分别为 P=0.304， P=0.819）。变异型（母细胞/多形性）MCL的2年内病死率明显高于经典型MCL（ P<0.05）。 结论:MEF2B在MCL的表达与病理亚型、结构亚型、SOX11的表达有关，但与增殖及预后无关。2年内病死率高仅见于变异型MCL。然而有关MEF2B在MCL中的作用需要进一步研究。

abstractsObjective:To investigate the expression of myocyte enhancer factor 2B (MEF2B) in mantle cell lymphomas (MCL), and to analyze the correlation between the expression of MEF2B and pathological subtypes, structural subtypes, SOX11 expression and its clinical significance.Methods:Paraffin-embedded tissues were stained with HE, immunohistochemistry (EnVision method) and fluorescence in situ hybridization (FISH) , in addition, the clinical and pathological data of 60 cases of MCL were collected at Sun Yat-sen University Foshan Hospital and Sun Yat-sen University Cancer Center from January,2002 to May, 2019 for analysis.Results:Of the 60 MCLs, males is predominant (M∶F =3∶1). Histologically, the typical MCL is the majority (classical MCL: variant type MCL=48 cases:12 cases) . Fifty cases were classified into non-complete FDC meshwork type MCL, and the remaining 10 cases were classified into the complete-FDC meshwork type MCL group. Patients with classical MCL were more than 60 years old. The coexistent lesion sites both node and extranode in pathological subtype or structural subtype was the most common lesion sites. SOX11(+) MCL was common in classical MCL ( P=0.040) and tended to be complete-FDC meshwork type MCL ( P=0.086). The expression rate of MEF2B in MCL was 60.0%(36/60). This rate of MEF2B in classical type, complete-FDC meshwork type and SOX11(+) MCL was significantly higher than that variant type, no complete-FDC meshwork type, SOX11(-)MCL ( P<0.05), respectively. There was no difference in clinical characteristics of MCL between MEF2B positive and negative groups. Compared with SOX11(-)MCL, the percentage of MEF2B expressed in tumor cells of SOX11(+)MCL was significantly higher ( P=0.027). The expression of MEF2B was not related to the proliferation of tumor cells ( P=0.341). There was no significant difference in the survival rate between different expression groups of MEF2B and SOX11 ( P=0.304 and P=0.819, respectively). Only the mortality of variant type (blastoid/pleomorphic) MCL within 2 years was significantly higher than that of classical type MCL ( P<0.05). Conclusions:The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. The high mortality rate within 2 years is only found in variant MCL. However, the role of MEF2B in MCL needs to be further studied.