波纹蛋白在NHL及RH中的表达及其在鉴别诊断中的意义

采用Ｓ－Ｐ法对３８例非何杰金氏病淋巴瘤，４０例淋巴组织反应性增生及３例何杰金氏病进行了波纹蛋白标记，结果１１例Ｔ－ＮＨＬ中６例和２７例－中２２例表达Ｖｉｍｅｎｔｉｎ．Ｖｉｍｅｎｔｉｎ对ＮＨＬ的分型作用是有限的。其中滤泡型淋巴瘤表达率低于弥漫型淋巴瘤；分化差的Ｔ淋巴母细胞性淋巴瘤及Ｂ小无裂细胞性淋巴瘤表达率低于中大细胞型淋巴瘤。Ｖｉｍｅｎｔｉｎ标记可显示ＲＨ组成细胞的多样性，显示血管分面优越性以及某     

淋巴细胞免疫表型分析在NHL与RH鉴别诊断中的意义

使用10种单克隆抗体(McAbs),以一种比ABC法更为敏感的免疫组化染色方法-链菌素生物素蛋白-过氧化物酶连结法(Streptavidin-peroxidase conjugate method,S-p法),对59例非何杰金氏病(NHL)及57例淋巴组织反应性增生症(RH)石蜡切片进行了淋巴细胞免疫表型标记。结果表明:(1)90％左右(54/59)淋巴瘤经过免疫表型标记可以明确细胞来源;(2) 80％以上(47/     

淋巴组织反应性增生与非何杰金病中网状纤维分布的比较观察

对80例淋巴组织反应性增生(RH)与104例非何杰金淋巴瘤(NHL)的组织切片,进行了网状纤维的比较观察,初步提出二者的不同网状纤维分布类型:RH组,窦隙疏网型,滤泡窦隙疏网型。NHL组,滤泡型中分空环密集型、空环均匀疏网型。弥漫型中分疏网型、密网型、网格型、交错网格型、混合型。网状纤维分布型在这两类病变中主要区别在于RH为正常分布型的扰乱;而NHL则为新生的分布型,且可能与肿瘤细胞类型,恶性程度等相关。上述分型有助于RH与NHL病变的诊断和鉴别诊断。     

免疫组织化学法诊断恶性淋巴瘤的研究——(Ⅱ,石蜡切片)

应用ABC免疫组化方法标记10多种单克隆抗体,用常规石蜡切片对100例临床诊断为恶性淋巴瘤的病例进行了研究。结果证明,在石蜡切片中能对恶性淋巴瘤发生阳性反应。否认了以往认为抗淋巴细胞各种单克隆抗体仅能用于冰冻切片新鲜淋巴组织的论点,检出淋巴瘤81例(B细胞性71例、T细胞性10例),何杰金氏病9例。单克隆抗体MT-1、CUHL-1、对T细胞性淋巴瘤呈阳性反应,MB-1、MB-2、LN-2、LN-3、L-26对B细胞性淋巴瘤呈阳性反应。Leu-M_1对何杰金氏病的诊断可起相当大的作用。     

肠道原发性非霍奇金淋巴瘤32例的临床与病理学分析

目的研究肠道原发性非霍奇金淋巴瘤(NHL)的临床表现、病理特点及预后因素。方法复习32例肠道原发性NHL的临床资料、大体标本、HE切片及免疫组织化学染色结果,按2001年WHO淋巴造血系统肿瘤的标准重新进行分类。结果B细胞性NHL 21例,其中弥漫大B型15例,套细胞型2例,滤泡型1例,Burkitt淋巴瘤1例,黏膜相关淋巴组织淋巴瘤2例。T细胞NHL 10例(其中肠病相关型NHL2例和非肠病相关型NHL8例),组织细胞NHL1例。诊断时,9例为Ⅰ～Ⅱ期,23例为Ⅲ～Ⅳ期。随访4—168个月,死亡15例。B细胞NHL死亡率为7／21例(33％),T细胞NHL的死亡率为8／10。Ⅱ期死亡2例,均为T细胞NHL。Ⅲ-Ⅳ期死亡13例,占死亡数的86．6％。Cox多因素分析显示,最重要的预后因素是肿瘤的分期及肿瘤类型(分期P=0．002、肿瘤类型P=0．032)。结论肠道原发性NHL以弥漫大B型最多见。以结肠最多见,其次为小肠和回盲部,直肠最少。就诊时65．6％为Ⅲ-Ⅳ期患者。比较同期T、B细胞NHL,T细胞NHL预后差,死亡率高。分期越高预后越差,黏膜相关淋巴组织淋巴瘤等恶性度较低的淋巴瘤预后较好。     

Epstein-Barr病毒与外周T细胞淋巴瘤关系的研究

ＥｐｓｔｅｉｎＢａｒｒ(ＥＢ)病毒感染与许多淋巴组织肿瘤发生有关,如非洲Ｂｕｒｋｉｔｔ淋巴瘤、大细胞非何杰金淋巴瘤、何杰金氏病等。我们用原位杂交法检测了40例外周Ｔ细胞淋巴瘤(ＰＴＣＬ)ＥＢ病毒基因的表达,探计ＥＢ病毒和ＰＴＣＬ的关系。103例淋巴瘤石蜡切片,用...     

淋巴组织良性病变和淋巴瘤中SHP-1蛋白的表达及意义

目的探讨淋巴组织良性病变和淋巴瘤的SHP-1蛋白表达及其意义。方法应用免疫组化SP方法检测111例不同类型淋巴瘤和27例淋巴组织良性病变。结果(1)SHP-1的正常表达部位在淋巴结和扁桃体生发中心的套区和边缘区及部分的滤泡间区,脾脏主要在边缘区及部分动脉周围淋巴鞘;在淋巴瘤中残留的淋巴组织和反应性成分也可表达;淋巴瘤的SHP-1蛋白表达比良性病变弱。(2)SHP-1在淋巴瘤中的阳性表达率(36·04%,40/111)远低于良性病变的阳性表达率(100%,27/27),包括霍奇金淋巴瘤(62·5%,5/8)、B细胞非霍奇金淋巴瘤(37·68%,26/69)、T细胞非霍奇金淋巴瘤(26·47%,9/34);不同亚型淋巴瘤表达上有差异,其阳性表达率分别是:黏膜相关淋巴瘤(12·5%,2/16),弥漫性大B细胞淋巴瘤50%(11/22),滤泡性淋巴瘤42·11%(8/19),大细胞间变性淋巴瘤中有80%(4/5),NK/T细胞淋巴瘤16·67%(1/6),前驱T淋巴母细胞淋巴瘤14·29%(1/7),外周T细胞淋巴瘤0(0/7)。(3)滤泡性淋巴瘤的表达方式有:肿瘤性滤泡有阳性表达;肿瘤性滤泡无表达,滤泡周围也是阴性。结论(1)SHP-1在淋巴瘤鉴别诊断中有参考意义,尤其适合滤泡反应性增生的良性病变和滤泡性淋巴瘤的鉴别。(2)SHP-1蛋白的缺失与淋巴瘤的发生、发展密切相关,是重要的抑癌基因。     

根据WHO淋巴造血系统肿瘤新分类对山西省淋巴瘤分布特点的分析

目的根据WHO淋巴造血系统肿瘤新分类标准、分析山西省恶性淋巴瘤的分布特点。方法重新阅读HE切片,选用免疫组织化学ABC法标记间变性淋巴瘤激酶（ALK）1、bcl-6、CD（1α、3、4、5、7、8、10,15、20、23、30、43、56、68、79α和99）、细胞周期蛋白（cyclin）D1、上皮膜抗原（EMA）、IgD,k,λ、潜伏膜抗原（LMP）1、PAX5、末端脱氧核苷酸转移酶（TdT）和Vs38C;原位杂交方法标记EBER RNA。按照WHO淋巴造血系统肿瘤新分类标准,对山西省肿瘤医院存档的447例淋巴瘤组织标本重新分类。结果447例淋巴瘤中,385例（86．1％）为非霍奇金淋巴瘤（NHL）,62例（13．9％）为霍奇金淋巴瘤（HL）。68．3％NHL为B细胞来源,30．6％为T和NK细胞来源,组织细胞来源的肿瘤仅占3例（0．8％）。弥漫大B细胞淋巴瘤（DLBCL）为最常见的类型（35．1％）,其他依次为外周T细胞淋巴瘤、非特殊型（PTun,12．0％）、黏膜相关淋巴组织结外边缘区B细胞淋巴瘤（MALT淋巴瘤,11．7％）,滤泡性淋巴瘤（FL,8．6％）,前体淋巴母细胞性淋巴瘤（T-LBL,7．0％）,间变性大细胞淋巴瘤（ALCL,4．2％）,小淋巴细胞性淋巴瘤（B-SLL,3．6％）和套细胞淋巴瘤（MCL,2．6％）。263例B细胞淋巴瘤105例（39．9％）表达免疫球蛋白轻链,包括52例K和53例λ。263例B细胞淋巴瘤14例表达LMP-1,14例表达EBER;119例T和NK细胞淋巴瘤6例表达LMP-1,19例表达EBER,NHL中LMP-1和EBER表达具有不一致性。62例HL37例（59．7％）一致表达LMP-1和EBER RNA,包括7例富于淋巴细胞型HL、11例混合细胞型HL和19例结节硬化型HL。结论所搜集到的山西省DLBCL的比率类似于美国、澳大利亚、日本和韩国,FL的比率明显低于美国和澳大利亚。     

鼻咽喉部淋巴瘤免疫表型与发病部位的关系

鼻咽喉部淋巴组织丰富，是淋巴瘤的好发部位，非何杰金氏淋巴瘤（NHL）在此部位的淋巴瘤中占绝对优势。根据WHO关于淋巴瘤新的分类方案，NHL可分为B细胞淋巴瘤和T/NK细胞淋巴瘤两大类，每一大类进一步又分为不同的型，不同的免疫表型具有不同的临床病理和预后特征。鉴于我国淋巴瘤的类型及部位分布与西方国家存在一定差异，     

B细胞特异性激活蛋白Pax-5在淋巴瘤组织中的表达

目的探讨B细胞特异性激活蛋白(BSAP)／Pax-5在淋巴瘤的表达情况及应用价值。方法按2001年WHO关于淋巴造血组织肿瘤分类标准收集102例弥漫性大B细胞淋巴瘤(DLBCL)、3例滤泡型淋巴瘤(FL)、3例黏膜相关淋巴组织结外边缘区B细胞淋巴瘤(MALT淋巴瘤)、1例结节性淋巴细胞为主型的霍奇金淋巴瘤(NLPHL)、10例间变性大细胞淋巴瘤(ALCL)和10例浆细胞瘤,用免疫组织化学LSAB法同步检测比较BSAP与CD20的表达情况。结果102例DLBCL全部表达CD20,100例表达BSAP,3例FL、3例MALT淋巴瘤和1例NLPHL BSAP和CD20全部阳性表达,10例ALCL、10例浆细胞瘤BSAP和CD20全部阴性表达。BSAP与CD20的表达差异无统计学意义。结论。BSAP/Pax-5是一种新的B细胞标记,阳性信号定位于细胞核,抗BSAP抗体在常规外科病理诊断工作中的应用价值有限。     

Expression of Vimentin and Epithelial Membrane Antigen in Human Malignant Lymphomas

Immunoreactivity with monoclonal antibodies against the intermediate filament protein, vimentin, and epithelial membrane antigen (EMA) was examined in 330 cases of lymphoma (317 non-Hodgkin's and 13 Hodgkin's lymphomas), 12 reactive lymph nodes and mononuclear cells of the peripheral blood using either indirect immunoperox-idase staining or the avidin-biotin immunoperoxidase complex technique. The cell origin of each tumor was established using a panel of monoclonal antibodies against lymphocyte differentiation antigens. There were 41 T cell, 247 B cell and 29 undetermined lymphomas, and 13 cases of Hodgkin's disease in the series. Vimentin was expressed in 24 T-cell lymphomas (58.5%) and 60 B cell lymphomas (24.2%). This difference in frequency was statistically significant. Vimentin expression in follicular lymphomas was less frequent than in diffuse B-cell lymphomas. In diffuse lymphomas, small and medium cell types were more reactive with anti-vimentin than large cell types. Reed-Sternberg cells (R-S cells) in Hodgkin's disease were positive for vimentin in 11 cases (84.6%). The frequency of EMA reactivity in lymphomas was low, particularly in T cell lymphomas. No positive cases were found among follicular lymphomas. In diffuse non Hodgkin's lymphomas, EMA was expressed only in mixed and large cell types, but never in smaller ones. In conclusion, monoclonal antibodies against vimentin and EMA appear to be of limited usefulness for the diagnosis of non Hodgkin's lymphomas, but anti vimentin antibody may be used as an adjunct to the diagnosis of R-S cells in Hodgkin's disease.     

Expression of vimentin and epithelial membrane antigen in human malignant lymphomas

Immunoreactivity with monoclonal antibodies against the intermediate filament protein, vimentin, and epithelial membrane antigen (EMA) was examined in 330 cases of lymphoma (317 non-Hodgkin's and 13 Hodgkin's lymphomas), 12 reactive lymph nodes and mononuclear cells of the peripheral blood using either indirect immunoperoxidase staining or the avidin-biotin immunoperoxidase complex technique. The cell origin of each tumor was established using a panel of monoclonal antibodies against lymphocyte differentiation antigens. There were 41 T-cell, 247 B-cell and 29 undetermined lymphomas, and 13 cases of Hodgkin's disease in the series. Vimentin was expressed in 24 T-cell lymphomas (58.5%) and 60 B-cell lymphomas (24.2%). This difference in frequency was statistically significant. Vimentin expression in follicular lymphomas was less frequent than in diffuse B-cell lymphomas. In diffuse lymphomas, small and medium cell types were more reactive with anti-vimentin than large cell types. Reed-Sternberg cells (R-S cells) in Hodgkin's disease were positive for vimentin in 11 cases (84.6%). The frequency of EMA reactivity in lymphomas was low, particularly in T-cell lymphomas. No positive cases were found among follicular lymphomas. In diffuse non-Hodgkin's lymphomas, EMA was expressed only in mixed and large cell types, but never in smaller ones. In conclusion, monoclonal antibodies against vimentin and EMA appear to be of limited usefulness for the diagnosis of non-Hodgkin's lymphomas, but anti-vimentin antibody may be used as an adjunct to the diagnosis of R-S cells in Hodgkin's disease.     

Study of Vimentin Expression in Non-Hodgkin's Lymphoma Using Paraffin Sections

Human non-Hodgkin's lymphomas were studied by means of an avidin biotin complex immunoperoxidase method using several monoclonal antibodies against the intermediate filament protein, vimentin. The study cases were 61 B cell lymphomas (including 2 plasmacytomas) and 30 T cell lymphomas (including 8 cases of mycosis fungoides). Twelve of the 61 B cell lymphomas were positive for vimentin, and were composed of extrafollicular center cells such as immunoblastic and plasmacytoid cells. On the other hand, lymphomas of follicular center cell origin were negative for vimentin. All cases of T cell lymphoma except for 14 (all of 9 AlLD- type lymphomas, all of 4 lymphoblastic lymphomas and one diffuse mixed small/ large lymphoma) were positive for vimentin. Although vimentin expression appeared to be influenced by various conditions such as the proportion of T- and B cell subsets, or B cell proliferation rate, follicular center cells were constantly negative for vimentin.     

Composite lymphoma. A clinicopathologic analysis of nine patients with Hodgkin's disease and B-cell non-Hodgkin's lymphoma

Nine patients had composite lymphoma in which Hodgkin's disease (HD) and non-Hodgkin's lymphoma (NHL) involved the same anatomic site. Two of these patients had relapses of their tumors. In one, the initial biopsy specimen contained follicular and diffuse large cell NHL with unclassifiable HD, but the relapse showed diffuse large cell NHL with nodular sclerosis HD. In the other patient, both biopsy specimens showed follicular mixed NHL; the HD component in the initial biopsy specimen was nodular sclerosis, whereas, at relapse, it had the appearance of interfollicular HD. In the remaining seven patients, the HD component was subclassified as nodular sclerosis (three specimens) or mixed cellularity (three specimens), or it was unclassifiable (one specimen). The NHL component was categorized as diffuse large cell (two specimens), diffuse large cell immunoblastic (two specimens), follicular and diffuse large cell (one specimen), diffuse mixed small and large cell (one specimen), and lymphocytic lymphoma of intermediate differentiation (modified Rappaport classification) (one specimen). Paraffin section immunoperoxidase studies were done on the NHL component in eight patients (nine specimens) and on the HD component in six patients (seven specimens). In each of these, the NHL component was leukocyte common antigen (LCA) positive and Leu-M1 negative. In addition, the neoplastic cells were L26 positive and UCHL-1 negative, indicating a B-cell phenotype. In five of seven immunophenotyped cases, Reed-Sternberg (RS) and Hodgkin's (H) cells from the HD areas were Leu-M1 positive and LCA negative, reflecting an immunophenotype that is typical of non-lymphocyte-predominant HD. In two specimens, the malignant cells were negative for Leu-M1 and LCA (with positive internal controls). Composite lymphomas composed of HD and NHL are unusual, and cases of coexistent HD of the non-lymphocyte-predominant subtype and NHL are even less common. The results of the current study and a review of the literature indicate that this phenomenon usually involves a B-cell NHL that coexists with HD, perhaps further suggesting a close relationship between the malignant cells of HD (RS and H cells) and B lymphocytes.     

Value of monoclonal antibodies in the diagnosis of Hodgkin's disease in paraffin sections]

A comprehensive panel of monoclonal antibodies that mark R-S/H cell, T- and B-cell, monocyte/histocyte was tested in paraffin sections of 107 cases of Hodgkin's disease (HD) including 21 cases of lymphocyte predominance (LP) and 86 cases of Non-LP HD. Thirty cases each of peripheral T-cell lymphoma and B-cell lymphoma were also tested for comparison. R-S/H cells were not stained with T-cell marker (UCHL-1) or monocyte/histocyte marker (Mac387) in all of these cases of HD. The results showed presence of certain difference in the phenotype of LP from non-LP. The H+L type of R-S/H cells of LP often reacted with B-cell markers including L26, LN2, LN1 and MB2 (93.3%-100%), LCA (83.3%) and EMA (92.3%), but rarely with LeuM1,T mü 9, or BerH2. On the contrary, most of the R-S/H cells of non-LP reacted with LeuM1 (80%), T mu 9(84%), BerH2(65%) but not with B-cell markers, LCA or EMA. Our study suggests a B-cell (probably the follicular center cell) derivation for L+H type of R-S/H cells in LP. The fact that 1 case of LP in this group transformed to a large cell B-cell lymphoma also supports this consideration. PNA is a sensitive marker of R-S/H cells but is not a specific one, since PNA stains 43.3% of the peripheral T-cell lymphoma and 20% of the B-cell lymphomas. Our findings indicate that using a panel of antibodies which mark R-S/H cells, T- and B-cells in paraffin sections will be helpful in the diagnosis and subtyping of Hodgkin's disease.     

Value and limitations of fine-needle aspiration cytology in diagnosis and classification of lymphomas: A review.

The fine needle aspiration (FNA) cytologic diagnosis of non-Hodgkin's lymphoma (NHL) depends upon finding a relatively monotonous population of lymphoid cells in smears. Lymphomas have successfully been classified by FNA cytology following the prevalent histologic classifications. The success rate of FNA cytology ranges from 80%-90% in diagnosis of NHL and from 67.5%-86% in its subtyping. The cytodiagnosis of Hodgkin's disease (HD) depends upon demonstration of Reed-Sternberg cells or Hodgkin's cells amongst appropriate reactive cell components. The diagnostic accuracy of FNA cytology for HD has also been invariably high (>85%). Yet, the role of cytology in primary diagnosis, subclassification and management of patients with lymphoma remains controversial. The differential diagnostic problems for NHL include a group of small round cell tumors, nonlymphoid acute leukemias and HD. Reservations have been expressed regarding the efficacy of cytology in separating florid reactive hyperplasia from low-grade malignant lymphoma. The reported cytodiagnostic accuracy for follicular lymphomas and nodular sclerosis type of HD is less compared to other subtypes of NHL and HD respectively since nodular pattern and sclerosis are strict histologic criteria which can not be appreciated in cytologic preparations. Entities like atypical lymphoproliferative disorders, peripheral T-cell lymphomas and Ki-1 positive anaplastic large cell lymphomas pose diagnostic challenges to cytologists. Despite these limitations, FNA cytology remains the first line of investigations (screening test) used in cases of lymphadenopathy. Besides initial diagnosis of lymphoma, it helps in detection of residual disease, recurrences and progression of low-grade to high-grade lymphoma, and helps in staging the disease. Availability of prior FNA cytology report facilitates the histologic diagnosis and classification of NHL. Various special ancillary techniques are now being performed on lymph node aspirates to diagnose lymphoma versus other malignancies, and to decide the functional character of lymphomas and their clonal nature. Diagn. Cytopathol. 1999;21:240-249.     

Clinical implications of nodal reactive follicular hyperplasia in the elderly patient with enlarged lymph nodes

In older persons, the humoral immune response, as reflected morphologically by proliferation and expansion of germinal centers, is relatively subdued in comparison with the florid reactive follicular hyperplasia (RFH) which may be observed in younger age groups. The presence of RFH in lymph node biopsies in patients 60 yr or older, which we have regarded with concern since 1972, appears to represent an imbalance of the immune system, in some patients, on the background of which predominantly non-Hodgkin's malignant lymphoma (NHL) may be present or will develop. Fifty-eight patients 60 yr old or more who presented with enlarged lymph nodes exhibiting inappropriate RFH for age were identified during the interval from 1969 to 1989. An apparent etiology was initially identified for the reactive follicular hyperplasia in only 12 cases: five with documented rheumatoid arthritis; one each with a history of trauma, positive monospot test, and combination of thrombophlebitis and fungal skin infection, and two each with elevated Epstein-Barr virus (EBV) titers and human immunodeficiency virus type 1 (HIV-1) seropositivity. While most were alive or died of nonlymphomatous causes and one was lost to follow-up, 18 (31%) patients either had concurrent lymphoma or subsequently developed diffuse NHL. There were ten diffuse interfollicular (I-Foll) lymphomas (six concurrent), two diffuse mixed cell lymphomas (DMCL), one diffuse large cell lymphoma (DLCL), one diffuse immunoblastic sarcoma (DIBS), two diffuse small noncleaved cell lymphomas (DSNCL), one unclassified NHL, and only one Hodgkin's disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Analysis of human equilibrative nucleoside transporter 1 (hENT1) protein in non-Hodgkin's lymphoma by immunohistochemistry.

The human equilibrative nucleoside transporter 1 (hENT1) is a member of the equilibrative nucleoside transporter family that mediates cellular entry of gemcitabine, cytarabine, and fludarabine. Deficiency in hENT1 confers resistance to toxicity of these drugs in a variety of model systems. Since some nucleoside analogs have a role in treating patients with non-Hodgkin's lymphoma (NHL), this study was undertaken to assess hENT1 abundance in NHL. A total of 115 cases of NHL of various subtypes and 15 reactive lymph nodes were evaluated for the presence of hENT1 protein using immunohistochemistry applied to frozen tissues. Samples were considered positive when >or=50% of neoplastic cells showed immunostaining. In reactive lymph nodes, hENT1 was confined to the germinal centers, whereas mantle zone B-cells and interfollicular T-cells were negative. In NHL, a relatively high frequency of hENT1 positivity was found in Burkitt lymphoma/leukemia (63%), diffuse large B-cell lymphoma (DLCL; 45%), and follicular lymphoma (40%). In DLCL, 26% of cases were positive for CD10, and CD10-positive DLCL cases were more likely to be hENT1 positive than CD10-negative cases (P=0.025). A lower frequency of hENT1 positivity was found in mantle cell lymphoma (13%) and peripheral T-cell lymphomas (37%). All marginal zone lymphomas (n=5), chronic lymphocytic leukemia small lymphocytic lymphomas (n=10), plasmacytoma (n=3), acute lymphoblastic lymphoma/leukemia, and anaplastic large-cell lymphomas (n=5) were negative. In conclusion, hENT1 was most frequently found in benign and malignant follicular center cells. Prospective studies to assess the value of hENT1 immunostaining in predicting resistance to nucleoside chemotherapy for NHL are warranted.     

Study of vimentin expression in non-Hodgkin's lymphoma using paraffin sections.

Human non-Hodgkin's lymphomas were studied by means of an avidin-biotin complex immunoperoxidase method using several monoclonal antibodies against the intermediate filament protein, vimentin. The study cases were 61 B-cell lymphomas (including 2 plasmacytomas) and 30 T-cell lymphomas (including 8 cases of mycosis fungoides). Twelve of the 61 B-cell lymphomas were positive for vimentin, and were composed of extrafollicular-center cells such as immunoblastic and plasmacytoid cells. On the other hand, lymphomas of follicular center cell origin were negative for vimentin. All cases of T-cell lymphoma except for 14 (all of 9 AILD-type lymphomas, all of 4 lymphoblastic lymphomas and one diffuse mixed small/large lymphoma) were positive for vimentin. Although vimentin expression appeared to be influenced by various conditions such as the proportion of T- and B-cell subsets, or B-cell proliferation rate, follicular center cells were constantly negative for vimentin.     

Kaposi sarcoma-associated herpesvirus in non-Hodgkin lymphoma and reactive lymphadenopathy in Uganda

Kaposi sarcoma-associated herpesvirus (KSHV) causes Kaposi sarcoma and is also associated with primary effusion lymphoma, a subset of diffuse large B-cell lymphomas, and multicentric Castleman disease. Because KSHV infection is endemic in sub-Saharan Africa, we sought to identify cases of KSHV-positive non-Hodgkin lymphomas (NHLs) and reactive lymphadenopathy in this region. One hundred forty-four cases (80 NHLs, 64 reactive lymph nodes) from the major pathology laboratory in Uganda were reviewed. One NHL was KSHV-positive, as indicated by staining for the viral latent nuclear antigen. This NHL was a diffuse large B-cell lymphoma in a 5-year-old boy. The tumor was also Epstein-Barr virus-positive. In addition, 2 reactive lymph nodes, both classified histologically as follicular involution, stained KSHV latent nuclear antigen-positive and thus most likely represent multicentric Castleman disease. In all 3 KSHV-positive cases, a minority of cells expressed KSHV viral interleukin 6, a biologically active cytokine homolog. In conclusion, we show that KSHV is rarely associated with lymphoproliferative disorders in sub-Saharan Africa. We describe the first case of a KSHV-positive NHL from this region; this case is also the first reported pediatric lymphoma associated with KSHV infection.