乳腺癌区域淋巴结中CD4+T、CD3+/HLA-DR+T细胞的对比分析

目的:探讨乳腺癌区域淋巴结在转移和无转移状态下免疫细胞数量的变化,认识区域淋巴结在机体抗肿瘤中的免疫状态.方法:选择女性非特异性导管癌26例,术中共取腋窝淋巴结42枚,按HE染色结果将淋巴结分为转移和无转移两组,采用流式细胞技术,检测CD4+T、CD3+/HLA-DR+T细胞占总淋巴细胞数的比例,并在两组之间进行比较.结果:42枚淋巴结18枚有转移,24枚无转移；CD4+T细胞在淋巴细胞中占的比例在两组间有显著性差异(P ＜0.001),在发生癌转移的淋巴结中所占的比例明显少于无转移淋巴结；CD3 +/HLA-DR+T细胞在两组间也有显著性差异(P＜0.05),即转移组少于无转移组.结论:乳腺癌腋窝淋巴结发生癌转移后,细胞免疫功能发生改变,在机体抗肿瘤免疫中具有免疫辅助和直接杀伤作用的CD4+T细胞的比例下降,同时CD3 +/HLA-DR+T细胞即能有效抗肿瘤的活化,T细胞的比例也发生下降.     

CD95、CD44V6与乳腺癌淋巴结微小转移的关系

目的探讨乳腺癌组织中CD95、CD44V6的表达与腋窝淋巴结转移的关系及其临床病理意义。方法筛选101例乳腺癌根治标本,癌组织免疫组织化学标记CD95与CD44V6其中40例腋窝淋巴结阴性者淋巴结全部标记MCKo并进行统计学分析。结果在常规病理诊断淋巴结未转移的病例中,免疫组化标记检出9例（22．5％,9／40）有微小转移。CD95与CD44V6的表达在转移组与微转移组相似。淋巴结转移组CD95的阳性率与未转移组之间差异具有统计学意义。当肿瘤〉2cm时,CD95的阳性率及CD44V6的高表达率具有统计学意义（P〈0．05）。结论通过检测乳腺癌组织中CD95与CD44V6的表达,有助于预测淋巴结微小转移情况,为临床判断预后和选择治疗方案提供更加可靠的依据。     

乳腺癌前哨淋巴结淋巴细胞亚群的初步研究

目的　研究乳腺癌发生转移和未发生转移时前哨淋巴结 (sentinellymphnode,SLN)的免疫功能。方法　采用流式细胞技术 ,检测乳腺癌患者SLN中免疫细胞CD3 T、CD4 T、CD8 T、CD16 NK和CD19 B的改变 ,并与非SLN的检测结果进行比较。结果　肿瘤未发生转移时 ,SLN的CD3 T、CD4 T、CD8 T、CD16 NK、CD19 B数量与非SLN差异无显著性。当肿瘤发生转移时 ,SLN的CD4 T、CD8 T发生显著性改变 ,由正常的以CD4 T(6 9.0 7± 5 .0 2 )细胞为主 ,转变为以CD8 T细胞 (6 6 .15±5 .97)为主 ;而CD3 T、CD16 NK、CD19 B与肿瘤未发生转移的SLN相比 ,差异无显著性。结论　SLN免疫细胞数量与非SLN相比 ,差异无显著性。但肿瘤细胞转移后 ,改变了淋巴结的微环境 ,使淋巴结内CD4 T、CD8 T免疫细胞比例发生改变。     

E-cadherin、N-cadherin与CD44+/CD24-/low表型在乳腺癌中表达的相关性及其意义

背景与目的:上皮细胞-间质转化(epithelial-mesenchymal transition,EMT)可以诱导上皮细胞来源的肿瘤表达CD44+/CD24-/low表型细胞,上皮性钙黏蛋白(E-cadherin)和神经性钙黏蛋白(N-Cadherin)是分别表达于上皮细胞和间质细胞的两个重要钙黏蛋白,癌细胞从E-cadherin表达向N-cadherin表达转移是EMT的一个重要机制,此钙黏蛋白转移增加了癌细胞的侵袭转移性.本研究旨在探讨CD44+/CD24-/low表型、E-cadherin及N-cadherin在乳腺癌中的表达及其意义.方法:采用免疫组织化学检测15例正常乳腺组织、20例乳腺癌癌旁组织(癌边缘2～5 cm)、58例乳腺癌组织及18例腋窝转移淋巴结组织中CD44+/CD24-low表型、E-cadherin及N-cadherin的表达,分析其与乳腺癌发生及浸润转移的关系.结果:正常乳腺组织、乳腺癌癌旁组织、乳腺癌组织和腋窝转移淋巴结组织中CD44+/CD24-/low表型表达率分别为6.7%、10.0%、41.4%和44.4%,E-cadherin阳性表达率分别为100%、90.0%、51.7%和33.3%,N-cadherin阳性表达率分别为0、15.0%、44.8%和55.6%,3种蛋白在正常乳腺组织、乳腺癌癌旁组织、乳腺癌组织和腋窝转移淋巴结组织中的表达差异均有统计学意义(P＜0.05).CD44+/CD24-/low表型表达与E-cadherin及N-cadherin表达有显著差异,且与E-cadherin表达关联程度较强,与N-cadherin表达关联程度相对较弱.E-cadherin 表达与N-cadherin表达有显著差异,且具有高度相关性(P＜0.05).结论:CD44+/CD24--1/low表型表达增加、E-cadherin蛋白表达降低及N-cadherin蛋白反常表达与乳腺癌的发生及浸润转移有密切的关系;在乳腺癌发展过程中,E-cadherin向N-cadherin转化及CD44+/CD24-/low表型表达增加可能发挥重要作用.     

1个前哨淋巴结阳性乳腺癌患者的腋窝非前哨#br# 淋巴结转移情况及危险因素分析#br#

目的研究1个前哨淋巴结阳性的乳腺癌患者腋窝非前哨淋巴结（NSLN）转移情况及危险因素,为该类患者豁免腋窝淋巴结清扫（ALND）提供指导。方法选取2013年1月至2020年12月在哈尔滨医科大学附属肿瘤医院行前哨淋巴结活检（SLNB）证实仅有1个前哨淋巴结阳性且行ALND的乳腺癌患者465例,根据其腋窝NSLN转移情况,分为NSLN转移组104例,NSLN未转移组361例。比较两组的一般资料,采用二元Logistic回归分析腋窝NSLN转移的独立影响因素。结果465例仅1个前哨淋巴结转移的乳腺癌患者中,104例（224%）发生腋窝NSLN转移。其中,多个亚组患者的腋窝NSLN转移率<10%,如肿瘤T1a+b期的NSLN转移率仅91%、肿瘤T1期且前哨淋巴结数量＞5个的腋窝NSLN转移率仅70%等。单因素分析结果显示,NSLN转移组与NSLN未转移组前哨淋巴结数、肿瘤T分期差异有统计学意义（P<005）。前哨淋巴结2～5个、肿瘤分期为T2～T3期的患者更容易发生腋窝NSLN转移。多因素Logistic回归分析显示,肿瘤分期为T2～T3期、前哨淋巴结数≤5个是患者腋窝NSLN转移的独立危险因素。结论仅有1个前哨淋巴结转移的乳腺癌患者总体腋窝NSLN转移率为224%,肿瘤T分期和前哨淋巴结数为腋窝NSLN转移的影响因素,在对仅1个前哨淋巴结阳性的乳腺癌患者豁免ALND时应重点考虑。     

前哨淋巴结微转移与腋窝淋巴结复发关系的研究进展

乳腺癌是女性最常见的恶性肿瘤，而腋窝淋巴结的转移状态与乳腺癌患者的预后相关。自从开展乳腺癌前哨淋巴结活组织检查以来，一部分乳腺癌患者因前哨淋巴结阴性而免除了腋窝淋巴结清扫，而另一部分患者因前哨淋巴结微转移选择术后放射治疗或是化疗以替代腋窝淋巴结清扫，从而减少了患侧上肢淋巴水肿、运动障碍以及感觉障碍等并发症的发生。近年来，少部分前哨淋巴结微转移患者发生了不同程度的腋窝淋巴结复发。对此，部分学者认为前哨淋巴结微转移患者即使不做腋窝淋巴结清扫，腋窝淋巴结复发率也未见明显增加；但部分学者则认为前哨淋巴结微转移应被视为腋窝淋巴结转移，残留的肿瘤病灶能增加腋窝淋巴结复发率，因此应行腋窝淋巴结清扫术。对于前哨淋巴结微转移的处理方式，国内外专家尚未得出一致的结论。目前众多研究者仍在不懈地进行相关临床试验及大数据分析，旨在为前哨淋巴结微转移患者寻求更佳的治疗方案。     

乳腺癌患者淋巴结CD4＋CD25＋T细胞和相关细胞因子的检测及相关性分析

目的探讨CD4＋CD25＋T细胞在乳腺癌发生、发展中的作用。方法将取自35例乳腺癌患者的105个肿大淋巴结,制备成单细胞悬液,应用流式细胞仪检测CD4＋CD25＋T细胞比例及CD4＋CD25-、CD8＋T细胞、NK细胞的相对水平。采用定量RT-PCR法,检测IL-2、IL-10、TGF-β1和IFN-γ的细胞因子水平。结果乳腺癌患者淋巴结中的CD4＋CD25＋T细胞水平（在CD4＋T细胞中的百分含量）与淋巴结转移相关,转移淋巴结中其水平明显高于未转移淋巴结。乳腺癌患者淋巴结中CD4＋CD25＋T细胞与CD4＋CD25-、CD8＋T细胞和NK细胞的水平呈负相关关系。乳腺癌患者淋巴结中CD4＋CD25＋T细胞水平与TGF-β1呈正相关,与IL-2、IL-10、IFN-γ无相关性。乳腺癌患者淋巴结中TGF-β1、IL-10、IFN-γ水平与淋巴结转移相关,转移淋巴结中TGF-β1、IL-10含量高而IFN-γ含量较低。IL-2与淋巴结转移无相关性。结论乳腺癌患者转移淋巴结中的CD4＋CD25＋T细胞水平高于未转移淋巴结。     

T1期乳腺癌保留乳房手术不行前哨淋巴结活组织检查的可行性探讨

目的 通过对乳腺癌患者前哨淋巴结转移与原发肿瘤大小相关性分析,探讨T1期乳腺癌保留乳房手术中不行腋窝淋巴结干预的可行性.方法 回顾性分析2009-01-01-2014-01-31沧州市人民医院收治76例临床腋窝淋巴结阴性的T1期乳腺癌患者的临床资料,均实施保留乳房手术十亚甲蓝示踪法前哨淋巴结活组织检查术,分析肿瘤大小与前哨淋巴结转移及预后的关系.结果 76例患者中,1例未行腋窝淋巴结干预.75例行前哨淋巴结活组织检查,前哨淋巴结示踪成功率为97.3％(73/75),腋窝淋巴结转移率为8.0％(6/75).肿瘤直径≤1 cm组共39例,前哨淋巴结阳性率为0(0/39);肿瘤直径＞1 cm且≤2 cm组共36例,前哨淋巴结阳性率为16.7％(6/36),两组患者前哨淋巴结阳性率比较差异有统计学意义,P＜0.05.全部病例均获随访,随访时间6～69个月,中位随访时间32个月,均无复发及转移.结论 对临床与影像学检查提示腋窝淋巴结阴性的T1期乳腺癌患者,当原发肿瘤直径≤1 cm时,腋窝淋巴结转移的概率极低,在保留乳房手术治疗时,可以免行前哨淋巴结活组织检查术.由于样本量少,且没有远期随访结果,仍需要进一步深入研究.     

乳腺癌腋窝阳性淋巴结包膜外侵犯的研究现状

腋窝淋巴结是乳腺癌常见的转移部位，腋窝转移淋巴结包膜外侵犯并不少见。迄今为止，乳腺癌淋巴结包膜外侵犯对乳腺癌预后的影响缺乏共识，未纳入乳腺癌分期系统。文章对乳腺癌腋窝阳性淋巴结包膜外侵犯的病理定义、临床意义、影响因素、预后及与腋窝非前哨淋巴结转移的关系等进行了综述。     

活体染料注射法识别乳腺癌患者前哨淋巴结失败及假阴性原因分析

目的 探讨活体染料注射法识别乳腺癌患者前哨淋巴结失败及假阴性的原因。方法 84例早期乳腺癌患者采用活体染料亚甲蓝作为前哨淋巴结活检示踪剂。术中切除前哨淋巴结行常规冰冻切片检查,无肿瘤转移者进一步做免疫组化检测。术后分离出全部乳腺及腋窝淋巴结送病理检查。结果 11例患者术中未检出前哨淋巴结,失败率13.1%。73例检出前哨淋巴结的患者中,32例前哨淋巴结受肿瘤累及,病理证实这些患者均有腋窝淋巴结转移;2例患者前哨淋巴结未受肿瘤累及,但病理证实腋窝淋巴结转移,前哨淋巴结预测腋窝淋巴结状态的敏感性为90.4%,特异性1005,假阴性率2.7%。结论 活体染料注射法识别前哨淋巴结失败主要与外科医师的技术熟练程度及方法欠妥有关,而假阴性的出现多为原发肿瘤过大及前哨淋巴结位置变异所致。     

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.