双侧肾上腺原发性NK/T细胞淋巴瘤1例并文献复习

目的探讨肾上腺原发性NK/T细胞淋巴瘤(NK/T cell lymphoma)的临床病理学特征、免疫表型、分子表型、诊断及鉴别诊断、治疗及预后。方法回顾性分析1例NK/T细胞淋巴瘤的临床病理学特征、影像学资料、免疫表型、治疗及预后,并复习相关文献。结果患者女性,68岁,肾上腺双侧巨大实性占位。镜下正常肾上腺固有结构消失,瘤细胞呈弥漫性片状分布,以小圆蓝细胞为主,核分裂象多见。免疫表型:瘤细胞表达TIA-1、Granzyme B、CD56、CD2、CD3,Ki-67增殖指数为90%,EBER原位杂交结果阳性,符合肾上腺原发性NK/T细胞淋巴瘤。结论肾上腺淋巴瘤少见,其中以继发性多见,原发性罕见。病理类型为NK/T细胞淋巴瘤则更为罕见,其治疗以手术联合放、化疗为主,预后差。熟悉NK/T细胞淋巴瘤的临床病理特征及免疫表型,EBV的存在与否,结合临床病史,有助于正确诊断。     

富于T细胞/组织细胞的B细胞淋巴瘤病理形态、免疫表型及鉴别诊断

目的 探讨富于T细胞／组织细胞的B细胞淋巴瘤（TCRBCL）的组织学特点、免疫表型及鉴别诊断。方法 根据WHO淋巴瘤新分类（2001）回顾性研究245例霍奇金淋巴瘤,发现8例TCRBCL;另有5例会诊病例及3例外检诊断病例,共16例;应用免疫组织化学SP方法检测瘤细胞及背景细胞的免疫表型,所用抗体包括CD20、CD79a、CD3、CD8、CD45RO、CDl0、bcl-6、CD21、CD35、CD57、T细胞限制性细胞内抗原（TIA）-1、CD15、CD30、上皮膜抗原（EMA）、细胞周期蛋白（cyclin）D1、CD68、潜伏膜抗原（LMP）-1;4例行原位杂交检测EBER;4例应用聚合酶链反应技术检测瘤细胞IgH基因重排。结果 16例TCRBCL,男8例,女8例,男女比为1：1。年龄10～68岁,平均年龄40．3岁,中位年龄46．5岁。主要表现为淋巴结肿大,伴发热及肝脾肿大。临床分期Ⅱ期3例,Ⅲ期10例,Ⅳ期3例。组织学上见少数非典型性大细胞散在分布于小淋巴细胞和组织细胞背景中。免疫组织化学显示大细胞呈CD20、CD79a、EMA阳性,CD15、CD30阴性;背景小淋巴细胞呈CD3、CD45RO阳性,其中CD8、TIA-1阳性细胞多于CD57阳性细胞;组织细胞呈CD68阳性。CD21、CD35均为阴性反应。所检测的4例均为EBER1／2阴性,4例行IgH基因重排检测均可见单克隆条带。结论 TCRBCL有着独特的组织学和免疫表型特征,诊断应结合形态学和免疫表型特征。鉴别诊断包括霍奇金淋巴瘤、反应性淋巴组织增生、淋巴瘤样肉芽肿病等。     

原发皮肤NK/T细胞淋巴瘤2例临床病理分析

目的探讨原发皮肤NK/T细胞淋巴瘤的临床病理特征、诊断与鉴别诊断。方法对2例下肢皮肤NK/T细胞淋巴瘤行HE及免疫组化EnVision法染色,并复习相关文献。结果 2例肿瘤侵犯至皮下组织,肿瘤细胞为小至中等大小的淋巴细胞,胞质丰富、透明,异型性明显,核不规则,围绕血管生长,核分裂象活跃。免疫表型:瘤细胞表达CD2、CD3、CD56、TIA-1、perforin等,原位杂交检测EBER阳性,Ki-67增殖指数为60%～70%,初诊无其他脏器查见肿瘤,提示本组病例为原发皮肤的NK/T细胞淋巴瘤。结论原发皮肤NK/T细胞淋巴瘤临床罕见,侵袭性高,预后差,其组织形态复杂多样,需与其他T、B细胞淋巴瘤、鳞状细胞癌等鉴别。     

CD20阳性结外NK/T细胞淋巴瘤1例并文献复习

目的探讨CD20阳性结外NK/T细胞淋巴瘤(extranodal natural killer/T-cell lymphoma,ENKTCL)的临床病理学特征、分子遗传学改变及预后,以提高对此罕见病的诊断及鉴别诊断。方法回顾性分析1例原发小脑CD20阳性ENKTCL的临床病理学特征、免疫表型、分子遗传学改变及预后,并复习相关文献。结果患者男性,27岁,以神经系统症状为主要表现,MRI提示小脑绒球占位。免疫表型:瘤细胞CD2、CD3ε、粒酶B、TIA-1及CD20阳性,CD5、CD7、CD56及其它B细胞标记阴性,EBER原位杂交阳性和T细胞受体(TCR)基因重排阴性,Ig H单克隆性重排。结论 CD20阳性ENKTCL罕见,较易见于年轻患者及播散病灶中,多呈高侵袭性,个别呈惰性临床过程,少数病例可同时伴有Ig基因重排,其诊断应结合组织学形态特征、多种抗体联合使用、EBER及基因重排等多种检测。     

皮下脂膜炎样T细胞淋巴瘤的免疫表型、基因重排检测及其在诊断中的意义

目的 探讨免疫表型和基因重排检测在皮下脂膜炎样T细胞淋巴瘤(SPTL)的诊断和鉴别诊断中的意义.方法 参照2005年世界卫生组织-欧洲癌症研究与治疗组织(WHO-EORTC)皮肤淋巴瘤分类标准收集20例SPTL.采用10种抗原标记进行免疫表型检测,运用PCR技术检测TCRγ、IgH基因重排,并用EB病毒编码的小RNA1/2(EBER1/2)原位杂交检测EB病毒感染.结果 (1)本组病例中男9例、女11例,平均年龄29.5岁;(2)所有病例的瘤细胞均表达1个或多个T细胞分化抗原(CD2、CD3或CD45RO),18/19病例表达BF1,18/20病例表达CD8,20/20、16/20病例分别表达细胞毒颗粒相关蛋白TIA-1、颗粒酶B,瘤细胞不表达CD4、CD20和CD56;(3)16/20病例检出TcRγ基因重排,未检出IgH基因重排;(4)5/20病例EBERl/2原位杂交阳性.结论 SPTL的瘤细胞具有克隆性TCR基因重排,综合临床病理、免疫表型及基因重排检测有助于本病确诊.     

EB病毒相关与不相关的肠道T细胞淋巴瘤临床病理研究

目的：探讨EB病毒相关与不相关的肠道T细胞淋巴瘤的临床病理特征、免疫分型和肿瘤细胞属性。方法：运用EBER1／2原位杂交检测EB病毒感染,采用免疫组化检测32例肠肠道原发T细胞淋巴瘤的免疫表型以及LMP－1、TIA－1、bcl-2和CD21的表达。结果：（1）27例（84．4％）为EB病毒相关淋巴瘤,其中11例（40．75）表达LMP－1。（2）32例瘤细胞均表达CD45RO,CD8＋。4例（12．5％）,CD4＋8例（25．0％）,CD56＋9例（28．1％）,17例（53．7％）为CD4－、CD8－、CD56－。TIA－1＋31例（96．9％）。无1例表达bcl2-,CD21。形态上28例为多形性中一大细胞性,单形性中等大细胞性和多形性各2例。临床上多见于青壮年男性,以腹痛、便血、发热、体重下降为主要症状,预后较差（中位生存期1．7月）。（3）EB病毒相关与相关者出现便血和发热以及CD3,CD8、CD56的表达方面差异有显著性。结论：在我国,绝大多数肠道T细胞淋巴瘤为EB病毒相关,具有特殊临床病理表现和免疫表型。其肿瘤细胞源自不同T细胞亚群（包括细胞毒性T细胞）或者NK细胞。     

肺部NK/T细胞淋巴瘤3例临床病理分析

目的探讨肺部NK/T细胞淋巴瘤(NK/T-cell lymphoma,ENKTL)的临床病理学特征、诊断及鉴别诊断。方法回顾性分析3例肺部ENKTL的临床病理学和免疫表型特征、原位杂交结果及鉴别诊断。结果 3例中2例女性,1例男性,发病年龄52~68岁,临床表现及影像学无特异性。镜下见肿瘤侵犯肺实质及支气管,以血管为中心浸润和血管破坏性生长为特征,伴不同程度的炎症反应及凝固性坏死。免疫表型:肿瘤细胞均表达CD3、CD56、细胞毒性标志物(TIA-1、Perforin、Gran-B),2例表达CD5、CD30。3例EBER原位杂交检测均阳性。2例行TCR基因重排,结果均阴性。结论肺部ENKTL临床罕见,诊断难度大,预后差,明确诊断需综合病理组织学、免疫表型及分子病理学检测。     

鼻NK/T细胞淋巴瘤--15年研究报道

目的 :探讨鼻NK/T细胞淋巴瘤 (原诊断为“中线恶性网织细胞增生症”)的临床病理及免疫表型特征、病变性质及其与EB病毒感染的关系。方法 :过去 15年中对近 2 0 0例“中线恶网”病例做了一系列研究 ,包括临床病理分析、LSAB法免疫组化染色作免疫表型分析、用PCR技术作T细胞受体β和γ链基因重排及EBV DNA检测、EBER原位杂交和原位末端标记DNA片段技术检测细胞凋亡。结果 :①鼻NK/T细胞淋巴瘤有特征性临床及病理形态学表现 ;②瘤细胞表达CD3ε:89 8% ;CD45RO :81 2 % ;CD5 6 :81 2 % ;TIA 1:10 0 %。不表达B淋巴细胞和组织细胞分化抗原 ;③TCR β链基因重排检出率为85 7% ,TCR γ链基因重排检出率为 94 45 % ;④EBV DNA检出率为 6 7 86 % ;EBER原位杂交阳性率为 90 6 3% ;⑤肿瘤组织中的凋亡细胞与Ki 6 7 呈明显正相关 (P <0 0 0 6 3) ,Ki 6 7 细胞数量变化与患者的平均生存期有明显关系 (P <0 0 2 )。结论 :“中线恶网”实为EB病毒相关、细胞毒性NK/T细胞淋巴瘤。     

142例结外NK/T细胞淋巴瘤免疫组织化学分析

目的:探讨结外NK/T细胞淋巴瘤(extranodal NK/T-cell lymphoma,ENKTL)的免疫组织化学特征.方法:回顾性分析142例ENKTL的免疫组织化学结果及EBER原位杂交结果,并用PCR方法检测1例ENKTL的TCR基因重排.结果:ENKTL免疫组织化学阳性率CD2为87.9％(116/132),CD3为99.3％(141/142),CD5为33.3％(44/132),CD7为74.7％(74/99),CD4为30.2％(13/43),CD8为35.9％(14/39),CD56为92.9％(132/142),TIA-1为100％(132/132),颗粒酶B为99％(111/112),穿孔素为100％(6/6),CD30为40.9％(36/88),PDGFRA为51.9％(28/54),CMYC为53.7％(29/54),Ki-67指数50％～90％,中位数为80％.EBER原位杂交阳性率为100％(142/142).TCR基因重排结果阴性.结论:结外NK/T细胞淋巴瘤存在较为特征性的免疫组织化学表型,并且EBER原位杂交呈阳性.     

应用2008版WHO造血和淋巴组织肿瘤分类对4例母细胞性NK细胞淋巴瘤重新评估

目的 探讨2008版WHO淋巴造血系统分类对母细胞性NK细胞淋巴瘤的重新分类和命名,观察此类淋巴瘤的组织形态、免疫表型分型及临床特点,并探讨其起源.方法 对符合2001版WHO造血和淋巴系统肿瘤分类(WHO分类)中母细胞性NK细胞淋巴瘤标准的4例,结合临床特点,观察其组织学形态、行免疫组织化学EliVision法染色,按2008版WHO分类进行重新分类.结果 4例的组织形态均呈母细胞性NK细胞淋巴瘤改变,CD56阳性,不表达T、B细胞和髓系标记,EBER原位杂交4例均阴性,均符合2001版WHO分类中NK母细胞性淋巴瘤的诊断标准.按2008版WHO分类,3例原发于皮肤,表达CD56、CD4和CD123,应诊断为母细胞性浆细胞样树突细胞肿瘤;1例发生于淋巴结,CD56和CD4阳性,CD123阴性,也无皮肤病变,只能暂时纳入来源不确定的白血病-NK细胞淋巴母细胞白血病/淋巴瘤.结论 2001版WHO分类中所谓的母细胞性NK细胞淋巴瘤实际上是一组异源性肿瘤,具有不同的免疫表型和临床特点,对此类肿瘤的细化分类和准确命名是2008版WHO淋巴瘤分类的一大进步.     

细胞毒颗粒相关蛋白TIA-1在鼻NK/T细胞淋巴瘤及淋巴增生组织中的表达

目的 观察２７例鼻ＮＫ／Ｔ细胞淋巴瘤之瘤细胞表达细胞毒颗粒相关蛋白ＴＩＡ－１的情况及其与该肿瘤的免疫表型,基因型及ＥＢ病毒感染的关系。方法 采用ＳＰ法免疫组织化学染色,选用的抗体有：ＴＬＡ－１,ＣＤ５６,ＣＤ３ε,ＣＤ４５ＲＯ,ＣＤ８和ＣＤ２０等;聚合酶链反应,作ＴＣＲγ链及免疫球蛋白ＪＨ链基因重排,ＥＢＥＲ１／２原位杂交及与ＴＬＡ－１和ＣＤ８等的双标记染色,还与１０例鼻咽淋巴增生病例进行了比较。     

肠道T细胞淋巴瘤中的EB病毒感染和T细胞内抗原1的表达

目的 探讨ＥＢ病毒感染在肠道Ｔ细胞淋巴瘤发病中的意义。方法 用ＥＢＥＲ１／２原位杂交及三步ＡＢＣ法免疫组织化学染色技术,观察２４例肠道Ｔ淋巴瘤患者中ＥＢ病毒感染及Ｑ细胞内抗原（ＴＩＡ－１）抗原表达情况,选用的抗体有ＴＬＡ－１,ＬＭＰ－１,ＣＤ３,ＣＤ２０,ＣＤ３０和ＣＤ４５ＲＯ等。     

Histological and immunophenotypic profile of nasal NK/T cell lymphomas from Peru: high prevalence of p53 overexpression.

Nasal NK/T-cell lymphoma is a unique form of lymphoma highly associated with Epstein-Barr virus (EBV). These lymphomas are rare in Western populations and much more prevalent in some Asian and Latin American countries. Although there are several sizable studies from Asian countries, the same is not true from South America. The aim of this study was to analyze a series of 32 cases of nasal T-cell lymphoma from Peru and to further extend the characterization of this disease. Immunohistochemistry was performed on paraffin sections using the following antibodies: CD20 (L26), CD45RO, CD3, Ki67, CD57, CD56, TIA-1, bcl-2, and p53. The presence of EBV was investigated with immunohistochemical analysis for latent membrane protein (LMP)-1 and in situ hybridization using an antisense riboprobe to EBER 1. The 32 patients included 18 men and 14 women (M:F ratio, 1.2:1), with a median age of 43 years (11 to 72). Three categories were identified: (1) Nasal NK/T cell lymphomas (28 cases): The morphology ranged from small or medium-sized cells to large transformed cells. Necrosis was present in 86% of the cases, and angioinvasion was seen in 36% of the cases. All cases were positive for CD45RO, CD3, and for TIA-1. CD56 was positive in 21 of 27 cases (78%), and CD57 was negative in all cases. EBER 1 positivity was identified in most of the tumor cells in 27 of 28 cases (96%), including the six cases in which CD56 was negative. Overexpression of p53 was detected in 24 cases (86%). (2) Blastic NK cell lymphoma (1 case): The neoplastic cells resembled those of lymphoblastic lymphoma. CD56 and CD45RO were positive; TIA-1, TdT, and EBER-1 were negative. (3) Peripheral T-cell lymphoma (PTCL) unspecified (3 cases): CD56, TIA-1, and EBER-1 were negative. Nasal lymphomas from Peru with a T cell phenotype are predominantly EBV-associated NK/T cell lymphomas, similar to those described in Asian countries. The expression of CD56, TIA-1, and EBER-1, in combination, are very useful markers for the diagnosis of nasal NK/T cell lymphoma in paraffin-embedded tissue. The differential diagnosis of T-cell lymphomas in the nasal region should include rare cases of PTCL unspecified and the blastic variant of NK cell lymphoma. P53 is overexpressed in 86% of the cases. The significance of this finding with regard to clinical behavior and prognosis remains to be determined.     

原发性皮肤间变性大细胞淋巴瘤临床病理分析

目的 探讨原发性皮肤间变性大细胞淋巴瘤(C-ALCL)的临床病理特征、免疫表型及预后.方法 分析8例C-ALCL的临床病理资料,复习HE切片,进行T淋巴细胞、B淋巴细胞、活化淋巴细胞和细胞毒性等16种标记的免疫组织化学染色,原位杂交检测EB病毒.结果 8例中男3例,女5例,中位年龄49.5岁.临床上以皮肤无症状的单个红色结节、肿块为主要表现,组织学上肿瘤细胞在真皮与皮下脂肪内大片状、弥漫性浸润.瘤细胞以大细胞为主,异形性明显.8例C-ALCL的瘤细胞CD30阳性细胞数均大于75%.瘤细胞均表达1～3个T细胞标记(CD3、CD5或CD45RO)及1～3个细胞毒性标记[T细胞内抗原(TIA)-1、颗粒酶B或穿孔素].表达白细胞共同抗原(LCA)为8例、CIM为5例、CD8为1例、间变性淋巴瘤激酶(ALK)-1为1例、上皮细胞膜抗原(EMA)为3例,均不表达CD15、CD20、CK和HMB45.EBER 1/2原位杂交均为阴性.获随访的6例中5例存活,1例死亡(死因不详).结论 C-ALCL有独特的临床病理表现和免疫表型,预后较好.EB病毒与C-ALCL可能无明确的相关性.     

Lymphomatous features of aggressive NK cell leukaemia/lymphoma with massive necrosis, haemophagocytosis and EB virus infection

AIMS : Aggressive natural killer (NK) cell leukaemia will be categorized as a distinct entity in the new WHO classification of malignant lymphomas. However, its non-leukaemic features remain unclear. We therefore investigated the morphological and immunophenotypic features of this lymphoma. METHODS AND RESULTS : Four cases with aggressive NK cell lymphoma were morphologically and immunohistochemically studied. All cases followed an aggressive course with death occurring within about 3 months of initial presentation. In these cases, the neoplastic cells disseminated throughout systemic lymph nodes and invaded various tissues and organs. The lymphoma cells were large cells showing nuclear irregularity and a pattern of sinusoidal invasion in lymph nodes. Apoptosis and coagulation necrosis were both frequently observed. Haemophagocytosis was observed in all cases. Neoplastic cells in paraffin-embedded tissue specimens from these patients had CD3(CD3epsilon)+ CD56(123C3)+ granzyme+ TIA-1+ EBERT+ CD43(MT1)- CD45RO(UCHL-1)- CD57(Leu7)- CD20(L26)- phenotypes. In the two cases where tissue was available for immunohistochemical study in frozen sections, neoplastic cells showed CD56(Leu19)+ perforin+ Fas ligand(FasL)+ CD2(Leu5b)- CD3(Leu4)- CD4(Leu3)- CD5(Leu1)- CD7(Leu9)- CD8(Leu2)- betaF1- TCRdelta1- phenotypes. CD16(Leu11b) was positive in one case. CONCLUSIONS: : Natural killer cell lymphomas appear to represent a non-leukaemic counterpart of aggressive natural killer cell leukaemia, a relationship similar to that in adult T-cell leukaemia/lymphoma. Awareness and diagnosis of this aggressive lymphoma is important because of its fulminant course.     

Clinicopathologic differences between 22 cases of CD56-negative and CD56-positive subcutaneous panniculitis-like lymphoma in Japan

CD56 is an important marker for prospecting clinicopathologic features of cytotoxic T-cell and natural killer (NK)/T-cell lymphomas. We examined 22 cases of subcutaneous panniculitis-like lymphoma and classified these into CD56-positive and CD56-negative groups. The 11 CD56-negative cases were mainly in the younger age group and had systemic subcutaneous nodules without ulceration. They exhibited subcutaneous invasion by medium-sized lymphoma cells, scattered erythrophagocytosis, patchy necrosis, and little tumor invasion in the superficial dermis. Their lymphoma cells had characteristics of CD3 epsilon-, CD8-, TcR beta F1-, T-cell intracellular antigen (TIA)1-, and granenzyme B-positive cytotoxic T cells and were negative for apoptosis-promoting proteins CD95 (Fas), Bax, CPP32 (caspase 3), and p53 (DO7). Ten patients were alive despite clinical signs of hemophagocytic syndrome and relapses in 7 cases. The 11 CD56-positive cases had systemic ulcerative skin tumors composed of pleomorphic lymphoma cells with massive necrosis and little erythrophagocytosis involving the subcutis and also often the whole dermis. Their tumor cells were positive for CD3 epsilon, TIA1, granenzyme B, CD95, CD95L (Fas ligand), Bax, and CPP32. Three cases were of the TcR beta F1-positive phenotype, 1 was of the TcR gamma/delta-positive T-cell phenotype, and 6 were of the TcR beta F1- and TcR gamma/delta-negative NK/T-cell phenotype. Six cases were p53 (DO7) positive. Seven cases had complications of liver dysfunction and cytopenia, and 8 died of disease. One CD56-negative case and 3 CD56-positive cases had nuclear signals of Epstein-Barr virus-encoded RNA in their lymphoma cells. The 2 groups had significantly (P <0.01) different prognoses by Kaplan-Meier and log-rank methods. Patients with CD56-negative and CD56-positive groups had statistically different clinicopathologic, immunohistologic, and functional findings and prognoses.     

应用组织芯片技术探讨"恶性组织细胞增生症"肿瘤细胞属性及其与EB病毒感染的关系

目的：初步探讨所谓“恶性组织细胞增生症”（简称恶组）肿瘤细胞的属性及其与EB病毒感染之间的关系。方法：用组织芯片技术将5例“恶组”尸检病例的每例不同组织各集成在一张组织芯片上,用免疫组织化学标记链霉素卵白素生物素（LSAB）法检测瘤细胞的免疫表型,用EBER1／2原位杂交检测Epstein-Barr(EB)病毒感染的情况。结果：（1）5例瘤细胞均表达CD45RO、CD3ε、T细胞限制性细胞内抗原－1（TIA－1）、Granzyme B,无瘤细胞表达CD56、CD30、CD20、CD68。（2）5例EBER1／2原位杂交均为阳性（簇型3例、弥漫型2例）。结论：至少部分“恶组”为EB病毒相关的侵袭性T细胞淋巴瘤。     

脾脏非霍奇金淋巴瘤的临床病理特征及其与免疫表型的关系

目的 探讨脾脏非霍奇金淋巴瘤（NHL）的临床病理特征及其与瘤细胞属性的关系。方法 复习19例NHL的临床病理资料、进行随访、并用SP法行CD45RO、CD20及髓过氧化物酶等免疫组织化学染色,对CD45RO阳性的病例加作CD8、CD56、TLA-1、CD68免疫表型检测和EBER原位杂交。结果 （1）19例均有脾脏肿大,其中52.6%(10/19)有脾脏占位病变,（2）73.7%(14/19)为B细胞性,滤泡型5例,经济危弥漫型9例;中心母细胞性8例,中心母细胞/中心细胞性3例,小细胞性4例,10例原发脾脏NHL均为B细胞性;（3）26.3%(5/19)为外周T细胞性,大细胞性4例,小细胞性1例;TLA-1阳性3例,其中CD8阳性和CD56阳性各1例,且均为EBNER1/2阳性,余1例为CD8、CD56、EBER均阴性;均为继发脾脏NHL;（4）73.7%(14/19)有随访,9例生存者中有8例为原发脾脏NHL,生存时间为8个月-10年不等;5例死亡病例均为继发脾脏NHL,生存时间为2-6个月不等。结论 脾脏NHL的临床病理表现与瘤细胞的属性有一定关系。原发脾脏NHL的预后明显优于继发脾脏NHL,对原发脾脏NHL的诊断应从严把握。     

原发淋巴结套细胞淋巴瘤临床病理分析

目的：探讨原发淋巴结套细胞淋巴瘤（MCL）的临床病理与免疫组化特点。方法：收集6例淋巴结MCL,免疫组化ABC法确定肿瘤细胞特征,使用的抗体有CD45、CD20、CD79、CD45RO、CD30、CD68、TdT、CD43、CD5、cyclinD1、c-myc,IgD,IgM等。结果：光镜可将MCL分为4种亚型：套区型1例,结节型1例,弥漫型2例,母细胞化型2例。肿瘤细胞表达全B细胞标记,IgD CD43 ,cyclinD1(5/6),CD5(4/6) 。结论：MCL是一种具有特殊免疫表型的B细胞淋巴瘤,不同的组织学构型其预后可能不同,临床应与其它类型B细胞淋巴瘤鉴别,如淋巴结边缘区B细胞淋巴瘤（MZL）,滤泡性淋巴瘤（FL）及CLL／SLL等鉴别。