CD168在胃癌组织中的表达及预后意义

目的 探讨胃癌组织中透明质酸介导的细胞游走受体(CD168)的表达情况与各临床病理因素及其预后的关系,评估其在胃癌侵袭转移过程中的作用及预测胃癌患者预后的价值.方法 采用免疫组织化学法检测72例胃癌组织和26例正常胃黏膜组织中CD168的表达情况.同时评估CD168的表达与临床病理因素(年龄、性别、组织学、肿瘤浸润深度、淋巴结转移和临床分期)之间的关系.用Kaplan-Meier法评估胃癌患者术后5年生存率.结果 胃癌组织中CD168阳性表达率为58.3％,与正常胃黏膜中的阳性表达率(19.2％)比较,差异有统计学意义(P=0.001);CD168阳性表达率与肿瘤分化程度(P=0.001)、淋巴结转移(P=0.003)、临床分期等(P=0.020)有显著相关性.CD168阳性表达率与年龄、性别、肿瘤大小和肿瘤浸润深度无显著相关性.胃癌患者的生存期分析显示,CD168阴性组5年生存率(67.2％)显著高于CD168阳性组5年生存率(29.8％),两组间差异有统计学意义(P=0.01).结论 CD168高表达与胃癌的浸润和转移密切相关,可以作为预测胃癌预后的一个生物学指标.     

非小细胞肺癌组织CD137L表达及其临床意义

目的:观察人非小细胞肺癌( NSC LC)组织中CD137L的表达,探讨CD137L与NSCLC临床病理参数和预后的关系.方法:采用免疫组织化学技术分析61例NSCLC组织中CD137L的表达.将免疫组化检测结果与患者的临床病理特征以及生存时间进行统计学分析.结果:CD137L阳性表达定位于细胞质,部分位于细胞核.在NSCLC组织中的阳性表达率为45.90％(28/61),统计学分析显示,NSCLC组织CD137L表达与年龄、性别和病理类型等无明显相关性(P＞0.05),而与临床分期相关(P=0.027),且CD137L表达阳性患者生存期较表达阴性患者延长,P=0.023.结论:CD137L在NSCLC组织中有表达,其阳性表达率可能与临床分期相关;CD137L阳性表达与患者预后呈正相关,对判断NSCLC的预后有一定的参考价值.     

三阴性乳腺癌CD133和HER-1表达及其与预后相关性的探讨

目的:检测三阴性乳腺癌CD133和HER-1表达状况并分析其与临床病理特征及预后相关关系。方法:用免疫组化方法检测67例三阴性乳腺癌的CD133、HER-1表达,并对其进行临床病理学分析。结果:三阴性乳腺癌中CD133、HER-1表达分别为43.3%(29/67)和53.7%(36/67)。CD133表达与肿瘤大小(P=0.025)、临床分期(P=0.003)、淋巴结转移有关(P=0.001);与年龄、组织学分级无关;CD133表达与患者总体生存率(Log-rank=9.346,P=0.002)和无瘤生存率(Log-rank=38.840,P=0.000 1)有关。HER-1表达与肿瘤大小(P=0.030)、临床分期(P=0.021)、淋巴结转移有关(P=0.002);与年龄、组织学分级无关;HER-1表达与患者总体生存率(Log-rank=7.998,P=0.005)和无瘤生存率(Log-rank=4.227,P=0.040)有关。结论:CD133、HER-1表达可能与三阴性乳腺癌的预后相关。     

CD133和CD44在骨肉瘤中的表达及其临床意义

 目的
探讨CD133和CD44在骨肉瘤中的表达情况及其与骨肉瘤患者预后的关系。方法应用免疫组织化学方法检测CD133和CD44在79例骨肉瘤
患者石蜡切片标本中的表达情况,应用卡方检验比较CD133、CD44表达与患者临床病理资料的相互关系,Kaplan-Meier法计算患者生存
率,Log rank检验比较CD133、CD44阴性低表达组与高表达组患者之间的生存差异,并以性别、年龄、肿瘤部位、肿瘤大小、
Ennecking 分期、CD133和CD44表达水平、局部复发及肺转移为变量指标,应用Cox回归模型进行多因素分析,研究这些因素与骨肉瘤
患者生存率之间的关系。结果CD133和CD44的表达水平与患者性别、年龄、肿瘤部位、肿瘤大小、Ennecking分期及局部复发无关,发
生肺转移的骨肉瘤患者其CD133和CD44的表达明显高于未发生转移的骨肉瘤患者,差异有统计学意义(P值分别为0.00014和0.0008)。
经单因素生存分析表明,影响骨肉瘤患者预后的因素有：肿瘤大小,局部复发,肺转移,CD44和CD133表达水平。多因素分析显示CD133
和CD44表达水平及肿瘤大小是影响患者预后的独立影响因素。结论CD133和CD44表达水平与骨肉瘤肺转移密切相关,检测CD133和CD44
的表达可以作为骨肉瘤患者肺转移及预后预测的指标。     

CD34阳性及阴性成年人急性T淋巴细胞白血病临床分析

目的 分析CD34阳性及阴性成年急性T淋巴细胞白血病(T-ALL)患者的临床特点及预后,探讨CD34表达对T-ALL预后的价值.方法 回顾性分析郑州大学第一附属医院血液科2012年1月至2015年7月收治的75例初治成年T-ALL患者.根据CD34的表达情况,分为CD34阳性组与阴性组,对两组患者的临床特点及预后进行比较.结果 75例初治成年T-ALL患者中,CD34阳性组24例(32.0％),CD34阴性组51例(68.0％).CD34阳性组与阴性组在性别、年龄、肝脾大、淋巴结肿大、血小板减少、白细胞增高、染色体异常、4周完全缓解(CR)率、中枢神经系统白血病(CNSL)方面,差异均无统计学意义(均P＞ 0.05);初诊时CD34阳性组血红蛋白(Hb) ＜90g/L、伴髓系抗原表达者的比例高于阴性组,差异均有统计学意义(x 2=5.888,P=0.015;x 2=10.758,P=0.001).18例选择造血干细胞移植(HSCT),57例未选择HSCT.在未选择HSCT的患者中,CD34阳性组中位生存期为5个月,阴性组为32个月,两者差异有统计学意义(x2=9.172,P=0.002).结论 成年T-ALL患者CD34表达与Hb＜ 90 g/L及髓系抗原表达有关;未选择HSCT患者的CD34表达可能与预后呈负相关.     

鼻咽癌组织中MMP-9 CD44v6蛋白表达的检测及其临床意义

目的:探讨鼻咽癌组织中MMP-9、CD44v6蛋白表达与鼻咽癌侵袭转移和患者预后的关系.方法:采用免疫组化ISAB法检测100例存档、石蜡包埋鼻咽癌组织中MMP-9、CD44v6蛋白表达,并分析其与各临床指标和患者总生存率之间的关系.结果:鼻咽癌组织中MMP-9蛋白表达阳性率为85.0%(85/100),其中( )23.0%,( )53.0%,( )9.0%.CD44v6蛋白表达阳性率63.5%(60/96),其中( )37.5%,( )8.3%,( )16.7%.MMP-9表达( )的鼻咽癌患者总生存率显著低于MMP-9表达(-)、( )、( )的患者.CD44v6表达为(-)、( )、( )、( )的各组鼻咽癌患者之间的总生存率无差异.鼻咽癌组织中MMP-9和CD44v6表达与患者年龄、性别、T分期、N分期及92'分期无关.结论:鼻咽癌组织中MMP-9、CD44v6蛋白表达与患者年龄、性别、颈淋巴结转移无关.MMP-9蛋白表达强阳性提示患者预后差.     

肺神经内分泌癌CD133蛋白表达临床病理意义的探讨

目的:探讨CD133蛋白在肺神经内分泌癌中的表达及其临床病理意义.方法:采用免疫组化法检测90例肺神经内分泌癌患者癌组织中CD133蛋白表达并分析其与各临床病理指标及预后的关系.结果:CD133蛋白表达定位于癌细胞胞膜及胞质;CD133表达阳性率分别为类癌14.3%(2/14),不典型类癌45.0%(9/20)、大细胞神经内分泌癌55.6%(10/18)和小细胞癌60.5%(23/38),差异有统计学意义,P=0.005.CD133 表达癌在Ⅰ期为21.1%(4/19),Ⅱ期56.0%(14/25),Ⅲ期54.8%(23/42),Ⅳ期75.0%(3/4),差异有统计学意义,P=0.015.CD133表达癌在肿瘤直径大小的分布为<5 cm者39.2 %(20/51),≥5 cm者61.5%(24/39),差异有统计学意义,P=0.035.CD133表达在淋巴结转移癌为56.3%(40/71),未转移癌为21.1%(4/19),差异有统计学意义,P=0.009.CD133阴性表达癌患者的中位生存时间为55个月,CD133阳性癌的患者中位生存时间为13个月,两者比较差异有统计学意义(Log-rank=35.91,P=0.0001).CD133蛋白表达与患者年龄(P=0.191)和性别(P=0.242)无关.结论:CD133蛋白在肺神经内分泌癌的发生、演进过程中起着重要作用,并可作为分子指标监测患者预后.     

肝细胞癌组织CD133与VEGF及CD34表达预后意义分析

目的:研究肝癌干细胞标志CD133、血管内皮生长因子(VEGF)及CD34在肝癌组织中的表达及其预后价值。方法:应用免疫组织化学染色方法检测CD133、VEGF和CD34在190例肝癌组织中的表达水平,分析其与各项临床病理指标以及预后之间的相关性。结果:CD133、VEGF和CD34在肝癌组织中的阳性表达率分别为22.1%(42/190)、52.1%(99/190)和50.0%(95/190)。CD133表达与VEGF表达水平、CD34表达水平、肝癌分化程度和镜下血管侵犯相关,42例CD133阳性肝癌组织中,VEGF阳性34例,阴性8例,r=0.785 3,P<0.01;CD34阳性30例,阴性12例,r=0.837 2,P<0.01;低分化肝癌(Ⅲ+Ⅳ)30例,高分化肝癌(Ⅰ+Ⅱ)12例,r=0.842 3,P<0.01;存在镜下血管侵犯33例,无镜下血管侵犯9例,r=0.884 5,P<0.05。生存分析结果表明,CD133阳性组、VEGF阳性组及CD34阳性组肝癌根治术后无瘤生存率均低于阴性组,差异有统计学意义,Log-rank检验统计量值分别为9.31、8.73和8.68,P值分别为0.036、0.012和0.013。结论:肝癌干细胞标志CD133表达影响肝癌新生血管形成以及肝癌分化程度;CD133蛋白表达程度与肝癌术后无瘤生存呈负相关,原因可能与肿瘤细胞低分化以及肿瘤血管微环境有关。     

骨肉瘤CD133 CD117 Ki-67的表达及与临床病理因素和危险度的相关性研究

  目的  研究骨肉瘤组织CD133、CD117及Ki-67在蛋白水平的表达情况及其与临床病理因素和危险度的关系。  方法  应用免疫组织化学PV-9000二步法检测55例骨肉瘤组织标本中CD133、CD117和Ki-67的表达,并与临床病理学指标和术后无瘤生存期进行比较分析,对照组为20例骨软骨瘤。应用SPSS 17.0软件统计分析,检验标准为P＜0.05具有统计学意义。  结果  骨肉瘤组织CD133、CD117、Ki-67蛋白表达阳性率显著高于良性的骨软骨瘤组织,差异有统计学意义（分别为P=0.016、P=0.008、P＜0.001）;CD133或Ki-67蛋白阳性表达骨肉瘤患者平均生存时间及平均转移时间短于CD133或Ki-67蛋白阴性骨肉瘤患者,差异有统计学意义（P＜0.05）;CD133、Ki-67在外科分期和远处转移对骨肉瘤患者预后有影响,其中CD133是外科分期及远处转移而影响骨肉瘤患者预后的独立因素。  结论  CD133和Ki-67表达可能在骨肉瘤发生、发展过程中起重要作用,有望成为判断其预后的指标。      

CD133和Ki-67在骨巨细胞瘤中的表达及其临床意义

目的 探讨CD133和Ki-67在骨巨细胞瘤（GCTB）中的表达及其与预后的关系,为临床判断其生物学行为及评估预后提供有力的证据。方法 采用用免疫组织化学染色检测CD133和Ki-67蛋白在80例GCTB组织中的表达,并分析2种蛋白的表达与GCTB临床病理特征及预后的关系。结果 GCTB组织中CD133阳性表达率为43.8％ （35／80）,Ki-67阳性表达率为57.5％（46／80）。CD133表达与肿瘤直径、肿瘤复发、Jaffe分级、Campanacci分期及手术方式有关（P＜0.05）;Ki-67表达与肿瘤直径、Jaffe分级和Campanacci分期有关（P＜0.05）。全组GCTB患者1、3、5年无复发生存率分别为93.0％、88.0％和80.0％。CD133阳性和阴性表达者的1、3、5年无复发生存率分别为89.0％、83.0％、75.0％和99.0％、91.0％、91.0％,差异有统计学意义（P＜0.05）。Ki-67阳性和阴性表达者的1、3、5年无复发生存率分别为89.0％、75.0％、68.0％和 97.0％、93.0％、90.0％,差异亦有统计学意义（P＜0.05）。结论 CD133和Ki-67表达与GCTB患者的预后密切相关,是评估其恶性程度以及预后的重要指标。     

Enhanced myeloid specificity of CD117 compared with CD13 and CD33

The c-kit proto-oncogene encodes a 145 kd tyrosine kinase transmembrane receptor, which plays a key role in haemopoiesis. The c-kit has been classified as CD117 and is especially useful in the differential diagnosis of acute myelogenous leukemia (AML) and acute lymphoblastic leukemia (ALL). We analysed 104 consecutive cases (55 AML, 23 B-cell lineage ALL, three T-cell ALL, 11 blast crisis of chronic myeloproliferative disorders and 12 cases of myelodysplastic syndromes with more than 10% of blasts) referred to our Hospital for immunophenotypic diagnosis and compared the expression pattern of CD13, CD33 and CD117 using the same fluorochrome (phycoerythrin-PE). The recommendations of the EGIL group were followed in order to establish lineage involvement of the blastic population. The threshold used to assign positivity for CD117 was 10%. Bcr/abl, TEL/AML-1 and MLL rearrangements were assessed by molecular methods. CD117 expression was detected in 91% of AML and MDS. All the negative cases corresponded to acute monocytic leukemias. The calculated specificity for myeloid involvement was 0.86 for CD117, 0.36 for CD13 and 0.44 for CD33 (P < 0.005). CD117 was also positive in four cases of ALL. None of these cases showed bcr/abl or MLL rearrangements. In the light of these findings, CD117 expression should yield a higher score, at least one point, in the system currently applied for the diagnosis of biphenotypic acute leukemias (BAL) as its myeloid specificity is greater than that of CD13 and CD33. Moreover, its absence in AML could identify two subgroups of M5b cases. The coexpression of CD117 with cytoplasmic CD79a is often associated with CD7 reactivity, suggesting a stem cell disorder. CD117 should be included on a routine basis for the immunophenotypic diagnosis of acute leukemias.     

CD5, CD10, and CD23 expression in Waldenstrom's macroglobulinemia

CD5, CD10, and CD23 are cell surface antigens used to distinguish B-cell disorders. The expression of these antigens and their clinical significance in Waldenstrom's macroglobulinemia (WM), an uncommon B-cell disorder, remains to be clarified. We therefore determined expression of CD5, CD10, and CD23 by flow cytometric analysis on bone marrow lymphoplasmacytic cells (CD19+ k/l light chain restricted) for 171 serially biopsied patients with findings of the consensus panel definition of WM. Importantly, we also correlated laboratory and clinical data, as well as existence of a familial history of a B-cell disorder in view of reports suggesting familial predisposition in WM. These studies demonstrated tumor cell expression of CD5, CD10, and CD23 in 15 of 171 patients (9%), 11 of 161 patients (7%), and 37 of 105 patients (35%), respectively. Coexpression of CD23 with CD5 or CD10 was common. Tumor Lymphoplasmacytic from 10 of 15 (66%) and 3 of 11 (27%) patients with WM that expressed CD5 and CD10, respectively, also showed expression of CD23 (P = 0.01 and P = 0.08, respectively). Among patients with CD23 expression, increased serum immunoglobulin (Ig) M levels were observed compared with patients without CD23 expression (P = 0.05). No differences in age at diagnosis; presence of adenopathy and/or splenomegaly; bone marrow involvement; serum IgA, IgB, and b2 macroglobulin levels; hematocrit; platelet count; or familial history of WM or a related B-cell disorder were observed among patients with and without CD5, CD10, and CD23 expression. These studies demonstrate that CD5, CD10, and CD23 are commonly found in WM and that their expression should not exclude the diagnosis of WM. Moreover, expression of CD23 may define a clinically distinct subset of patients with WM.     

人CD46、CD55和CD59与肿瘤免疫逃逸及免疫治疗

膜结合补体调节蛋白CD46、CD55和CD59在肿瘤细胞膜上表达或过表达,保护肿瘤细胞免受免疫系统的攻击,成为肿瘤细胞免疫逃逸的途径之一.如何下调肿瘤细胞表面三者表达或抑制其功能以增强其对补体依赖的细胞毒作用的敏感性备受关注.     

CD46 CD55 CD59在结肠癌组织中的表达及意义

目的:检测CD46、CD55、CD59在结肠癌组织中的表达情况,分析其与结肠癌临床病理参数间的相关性及意义。方法:选取有详细性别、年龄、组织分化、病理分期、肿瘤部位、组织类型资料的组织芯片标本,包括121 例结肠癌和121 例癌旁结肠组织,均为2004年10月至2006年6 月第四军医大学西京消化病医院胃肠外科手术切除标本。应用免疫组织化学改良二步法分别检测CD46、CD55、CD59的表达情况。结果:CD46、CD55及CD59在结肠癌组织中的阳性表达率均显著高于对应的癌旁组织（P < 0.001）。 CD46表达水平与性别、年龄、组织分化、TNM 病理分期、肿瘤位置、病理组织类型均无关（P > 0.05）。 CD55、CD59的表达水平与性别、年龄、肿瘤位置、病理类型无关（P > 0.05）,而与组织分化、TNM 病理分期有关（P < 0.05）。 其表达强度阳性率中低分化组明显高于高分化组（P < 0.05）。 TNM 分期中Ⅲ、Ⅳ期患者肿瘤病理组织强阳性表达率高于Ⅰ、Ⅱ期阳性表达率,两者比较有统计学意义（P < 0.05）。 结论:CD46、CD55及CD59在结肠癌组织中高表达,特别是CD55、CD59的表达与肿瘤分化、病理分期相关,提示三者表达水平与结肠癌生物学行为密切相关。      

Poor prognosis of mediastinal non-Hodgkin's lymphoma with an immature phenotype of CD2+, CD7 (or CD5)+, CD3-, CD4-, and CD8-

Nine children with mediastinal non-Hodgkin's lymphoma (NHL) were treated according to our new regimen which is characterized by intensified therapy with high-dose cytosine arabinoside (HDCA). After induction therapy with a combination of five drugs, such as vincristine, doxorubicin, cyclophosphamide, 1-asparaginase, and prednisolone, intermediate dosages of methotrexate (MTX) (1 g/m2) and HDCA (1.5 g/m2 x 12 doses) were administered. All but one patient (88.9%) achieved complete remission and then received this intensified therapy. With a median follow-up period of 25.5 months, five patients are still in complete remission, but three patients have relapsed. From the phenotypic point of view, these relapsed patients showed only very immature T-cell differentiation antigens such as CD2 and CD7 (or CD5). These results suggest that HDCA as intensified therapy for children with mediastinal NHL seems to be effective. However, for patients with an immature phenotype of T-lineage cells, more sophisticated regimens should be prepared.     

Agranular CD4+/CD56+ cutaneous neoplasm

CD4+ CD56+ cutaneous neoplasm with hematological relapse is a rare malignant disease and has been described recently in the literature as blastic or agranular NK-cell leukemia/lymphoma. The origin of this neoplasm is uncertain. We describe a 75-year-old patient with a primary cutaneous neoplasm CD4+ CD56+ who evolved to leukemic phase despite standard lymphoma chemotherapy. Morphologically, the cells were undifferentiated without granules in the cytoplasm. The immunophenotype showed the expression of CD4, CD56, CD68, CD33, CD7, CD2, CD45RA, and CD38. Histological analysis revealed a cell infiltration mainly located in the dermis. T-cell receptor and immunoglobulin heavy chain genes were in germline configuration. Cytogenetic study showed complex structural abnormalities with a deletion of the chromosome 5 del(5q). The clinical course was aggressive with an early hematological relapse.     

The CD11/CD18 leukocyte glycoprotein deficiency

CD11/CD18 leukocyte glycoprotein deficiency is a rare, inherited disorder of leukocyte function, manifested by recurrent severe bacterial infections. A deficiency in the expression of a family of leukocyte membrane glycoproteins (the CD11/CD18 glycoproteins) represents the molecular basis for this disease.