33例小肠非霍奇金淋巴瘤治疗分析

目的探讨小肠非霍奇金淋巴瘤的临床特点、诊断、治疗和预后。方法回顾性分析33例小肠非霍奇金淋巴瘤，其中滤泡型裂细胞性2例，弥漫型裂细胞性7例，弥漫型裂-无裂细胞性5例，弥漫型无裂细胞性6例，免疫母细胞性1例，黏膜相关淋巴组织淋巴瘤2例，弥漫性大B细胞淋巴瘤9例，另有1例为T细胞淋巴瘤。Ann Anbor分期ⅠE期12例，ⅡE期15例，ⅣE期6例。手术治疗33例，29例行根治术，另4例行姑息性切除术。26例行术后放疗，移动条照射12例，全腹盆腔大野照射14例；中位总剂量2543．5cGy。术后化疗33例，其中CHOP方案17例，COMP方案6例，COP方案3例，MINE方案2例，COPP方案3例，BACOP方案2例。结果5年总生存率和无病生存率分别为48％和39％，中位值分别为47、23个月。各期的生存率分别为ⅠE期42％，ⅡE期67％，ⅣE期17％。结论小肠淋巴瘤多为ⅠE、ⅡE期，病理以中、高度恶性为主，治疗多采用以手术为主的综合治疗，术后放疗及化疗可提高生存率。     

软组织淋巴瘤的临床病理特征

本文对我科800余例淋巴瘤中8例软组织淋巴瘤从临床及病理组织学方面进行了分析。部位上臂3例、前臂2例、胸壁2例、下肢1例。临床均以无痛性包块而就诊,病程从1周至3个月。8例中有6例位于骨骼肌内,2例位于皮下结缔组织中。手术切除时大小从2.5×2cm至12×6cm之间。病理组织学上均为非何杰金氏淋巴瘤,均呈弥漫型。细胞形态上为淋巴母细胞性1例、淋巴浆细胞样1例、裂细胞性3例、无裂细胞性1例、裂无裂混合性2例。     

睾丸原发性非何杰金氏淋巴瘤11例病理分析

睾丸淋巴瘤约占睾丸肿瘤的5％;原发性者更为少见。现报告11例,年龄3～69岁,其中3例为儿童。病程20天～2年。均为单侧性(右6,左5)。 病理材料:肿瘤大小从4×3×3cm～10×5×5cm。多数境界清楚,部分有包膜,质实,切面灰红或谈黄白色,鱼肉状。一例见分叶状结构,并有囊性变及出血。二例副睾肿大呈结节状。 显微镜检查:全部病例均见肿瘤细胞呈弥漫性分布于曲细精管间,癌细胞大小较一致,胞浆较少。按非何杰金氏淋巴瘤工作分类(修订洛阳方案,1982年上海),小核裂细胞性4例(2例为儿童)、大核裂细胞性2例、淋巴母细胞性2例(1例为儿童)、淋巴浆细胞样2例、小无裂细胞性1例。瘤细胞核分裂较小。5例可见“星空现象”,1例有较明显的纤维化。9例曲细精管不同程度萎缩或数目减少,2例曲细精管消失,2例癌细胞浸润副睾管,9例浸润白膜。     

8例卵巢非霍奇金淋巴瘤临床分析

[目的]探讨卵巢非霍奇金淋巴瘤 (NHL)的临床表现、诊断、治疗及预后。 [方法]8例临床资料的回顾性分析。 [结果]本组病例占同期卵巢恶性肿瘤 0.51％ (8/1552)，继发 5例，原发 3例。按 FIGO分期Ⅰ期 1例，Ⅱ期 1例，Ⅲ期 3例，Ⅳ期 2例， 1例未行手术分期不明。病理类型均属非霍奇金淋巴瘤， B细胞性，裂 无裂细胞、混合细胞、小细胞各 2例，大无裂及中心细胞各 1例。本组单纯化疗 1例，余 7例均采用综合治疗。随访结果 5例死亡，生存期 1～ 21个月， 3例存活。 [结论]对于青壮年卵巢肿瘤患者，如肿瘤呈实性、双侧性且伴有 CA125增高者，应警惕卵巢淋巴瘤的可能；治疗多采用手术和化疗为主的综合治疗；原发较继发预后好，但原发甚罕见。     

茶多酚的尿生物标志物与结肠直肠癌：上海队列研究

目标：评估上尿路移行细胞癌（UUT—TCC）患者接受经皮处理后的肿瘤学转归。方法：作者回顾性审阅了1989年至2005年期间因UUT—TCC而行经皮保守手术患者的相关资料：性别。确诊年龄；诊断模式；吸烟史；膀胱癌史；手术类型；并发症；肿瘤部位、体积、分期、分级、复发和进展状况。对复发率和存活率进行了评估。结果：共有24例患者的资料纳入研究。中位年龄70岁。肿瘤位于肾盂者11例．位于肾盏系统者13例。肿瘤平均体积为1．8cm（范围：O．8—2．9）；4例患者既往有膀胱癌史。3例患者曾因围手术期失血而接受输血，1例患者发生过结肠损伤。中位随访期为62个月。8例（33．3％）出现局部复发（3例在经治后泌尿道。1例在对侧泌尿道。4例在膀胱）。5例在随访期间行肾输尿管切除（NUT）。5例（20．8％）死亡，4例病情进展。1例出现心血管疾病。5年疾病特异性存活率和无病存活率分别为79．5％和68％。结论：对于病变局限于肾腔的低级或浅表UUT—TCC．经皮处理可作为NUT或输尿管镜的替代治疗方案。患者经治后应接受长期术后随访。对于高级或侵袭性肿瘤。开放式NUT仍是金标准。     

小细胞肺癌的临床病理与预后

本文报告随诊5年以上的小细胞肺癌164例,着重分析病理类型(WHO分型以及IASLC分型)治疗方式与预后的关系。其中15例采用免疫组化学方法,研究它的内分泌表达以及上皮性抗原的表达,3例作透射电镜观察。结果显示,小细胞癌的组织学类型与患者生存时间无肯定关系,在38例单纯手术或伴有放(化)等辅助治疗的5年存活率为21％(8/38),非手术治疗的123例5年存活率为7.3％(9/123),显示小细胞肺癌手术+放(化)疗能够提高患者5年存活率;在15例进行内分泌和上皮性抗原标记中,7例内分泌表达(S-100、NSE)阳性,12例上皮性抗原(CAM5.2)表达阳性,显示小细胞肺癌来自内胚层和内分泌细胞。     

乳腺原发性恶性淋巴瘤四例

乳腺原发性恶性淋巴瘤属于结外型恶性淋巴瘤，临床相当少见。现将我们所遇4例报道如下。临床资料见表。病理变化本组4例，肿瘤均位于乳腺组织内，呈结节状或分叶状，边界清楚者3例，不清楚1例。切面均为灰白色均质、鱼肉状，其中例2肿瘤切面伴灶性出血。镜下见瘤细胞弥漫性浸润乳腺小叶及周围脂肪组织和结缔组织，未累及皮肤。送检腋窝淋巴结2例，1例见瘤细胞侵犯，另1例淋巴结显示反应性增生。本组4例按成都会议分类，弥漫性无裂细胞性3例，淋巴母细胞性1例。免疫组化染色，3例L26阳性、1例L26阴性。讨论乳腺原发性恶性淋巴瘤占乳腺恶性肿…     

新辅助化疗结合手术治疗局限期小细胞肺癌的临床观察

目的探讨手术结合新辅助化疗治疗局限期小细胞肺癌的临床疗效及化疗和手术的相互影响。方法回顾性总结367例局限期小细胞肺癌临床资料,比较不同方法的疗效,评价化疗的毒性反应及对术后并发症发生的影响。结果根治性手术术前开始化疗组和术后开始化疗组1、3、5年存活率分别为87.5%、57.8%、49.6%和86.8%、47.4%、34.2%,二组间1年存活率无显著差异(P>0.05),3、5年的存活率差异显著(P<0.05);姑息性手术组1、3存活率低,无5年存活者;围手术期死亡2例(0.5%),术后并发症69例(18.6%);术前化疗期间无死亡病例,术后化疗死亡2例。结论根治性手术结合术前、术后化疗治疗局限期小细胞肺癌可获得满意的临床效果,化疗不增加手术危险性,术后1月开始化疗是安全的。     

20例胃小细胞癌的临床分析

摘 要：［目的］ 探讨胃小细胞癌的临床特点、临床诊断、治疗方法及预后。［方法］回顾性分析20例胃小细胞癌患者的临床资料。［结果］ 20例患者中, 17例行手术治疗,其中13例行根治性肿瘤切除术,4例行姑息性手术;3例行单纯化疗。全组患者中位生存时间为11个月,1、2、3年生存率分别为60.1％、26.2％和12.7％。患者的预后与肿瘤分期、有无淋巴结转移和手术根治程度有关（P<0.05）,而与年龄、性别无关(P>0.05)。［结论］ 胃小细胞癌是胃恶性肿瘤中的罕见病理类型,恶性程度高,病情进展迅速,治疗方法以手术、化疗、放疗为主,总体疗效不佳。     

肝动脉栓塞加门静脉置泵治疗晚期原发性肝癌(附160例病例分析)

延长晚期原发性肝癌患者的生存时间，提高生活质量，为二期手术切除创造条件。方法：采用肝动脉栓塞化疗加门静脉置泵，术中栓塞药物为：ADM、泛影葡胺、碘化油及MMC；术后门静脉药泵常用ADM、干扰素注射。结果：术后二个月复查B超，肿瘤缩小明显者（缩小至原肿瘤1／3）者74例，占46％，其中18例施行二期肝癌切除术，160例1年后存活率78．6％，2、3、5年存活率分别为65．6％、43．5％及16．3％。结论：采取肝动脉栓塞加门静脉置泵治疗晚期原发性肝癌160例，效果良好，延长了晚期原发性肝癌的生存时间，为二期手术切除创造了条件。     

Production of fibronectin by human tumor cells and interaction with exogenous fibronectin: comparison of cell lines obtained from colon adenocarcinomas and squamous carcinomas of the upper aerodigestive tract

Cell lines derived from 13 different human colon adenocarcinomas were examined for production of fibronectin by ELISA and for cell-surface expression of fibronectin by indirect immunofluorescence. Two squamous epithelial cell lines obtained from tumors of the upper aerodigestive tract were used as controls. None of the 13 colon carcinoma lines produced detectable amounts of fibronectin or showed detectable cell-surface staining with anti-fibronectin. The 2 squamous epithelial cell lines, in contrast, produced large amounts of fibronectin which could be detected in the culture medium and bound to the substratum. The squamous carcinoma cells also stained brightly when examined in the viable state by immunofluorescence with anti-fibronectin. In addition to being studied for fibronectin production, each cell line was also examined for the ability to interact with exogenous fibronectin in an adhesion assay. None of the colon carcinoma cells were adherent to fibronectin-coated culture dishes while the 2 squamous carcinoma cells rapidly attached and spread on this substratum. These data suggest that cell lines derived from adenocarcinomas of the colon are deficient in production of fibronectin and in their ability to interact with exogenous fibronectin. In their degree of deficiency, the colon carcinoma cells are significantly different from several different types of human tumor cell. The failure of the colon carcinoma cells to synthesize detectable amounts of fibronectin endogenously or to interact with exogenous fibronectin may explain, in part, the low degree of adhesive interaction which these cells have for their substratum. This, in turn, may influence the in vitro and in vivo properties of colon carcinoma cells.     

AEBP1通过激活Wnt/β-catenin信号通路调控EMT促进结肠癌细胞增殖迁移

目的:探讨脂肪细胞增强结合蛋白1（AEBP1）对结肠癌细胞增殖迁移的影响及其机制。方法:Oncomine数据库对结肠癌中AEBP1表达情况进行分析;GEPIA、ualcan数据库对AEBP1表达与结肠癌患者预后进行分析。分析AEBP1在正常结肠上皮细胞和结肠癌细胞中的表达情况。在HCT116细胞过表达AEBP1建立过表达细胞系,在过表达细胞系中对AEBP1进行敲降。利用CCK-8实验、克隆形成实验检测AEBP1对细胞增殖的影响;Transwell实验检测AEBP1对细胞迁移能力的影响。实时荧光定量PCR与免疫组化实验检测结肠癌组织及配对正常组织AEBP1表达水平,Western blot法检测过表达AEBP1的结肠癌细胞AEBP1、β-catenin、cyclinD1、c-myc、E-cadherin、Vimentin蛋白的水平。结果:结肠癌组织中AEBP1表达增加。高表达AEBP1与结肠癌患者总生存期、无病生存期负相关,高表达AEBP1与结肠癌患者肿瘤分期、淋巴转移相关。过表达AEBP1后,HCT116结肠癌细胞增殖加快,克隆形成数增加、Transwell迁移细胞数增加,在过表达细胞中敲降AEBP1后得到相反结果。过表达AEBP1后β-catenin,cyclinD1,c-myc,Vimentin蛋白表达增加,E-cadherin蛋白表达下降。结论:AEBP1在结肠癌中高表达并通过激活Wnt/β-catenin信号通路诱导EMT进程促进结肠癌细胞增殖迁移。     

结肠癌 COLO 耐药株的构建及其与肿瘤干细胞的关系

目的：构建结肠癌 COLO 耐药株,探索其功能特性及其与肿瘤干细胞的关系。方法通过逐渐递增化疗药5-氟尿嘧啶（5-FU）浓度的方法,构建了耐0．10μmol／ml 和0．20μmol／ml 5-FU 的结肠癌 COLO 耐药株各1株,分别命名为 COLO／5-FU-1、COLO／5-FU-2。从增殖能力、克隆形成能力、迁移和侵袭能力、微球体形成能力、干性基因的表达、交叉耐药等方面与亲本结肠癌细胞株 COLO 进行对比。结果在存活检测中,常规培养后第4天,结肠癌耐药株 COLO／5-FU-2、COLO／5-FU-1、亲本 COLO 细胞的 A 值分别为0．61±0．13、0．54±0．07、0．41±0．09,差异有统计学意义（F ＝63．43,P ＝0．033）。随着耐5-FU 药物浓度的增加,COLO 耐药株的克隆形成率逐渐增强,COLO／5-FU-2、COLO／5-FU-1、亲本 COLO的克隆形成率依次为（87．6±12．7）％、（65．3±9．7）％、（38．5±7．6）％,差异有统计学意义（F ＝33．64, P ＝0．017）。COLO／5-FU-2、COLO／5-FU-1、亲本 COLO 每高倍视野中迁移穿过基底膜的细胞数分别为（482±39）个、（434±45）个、（373±38）个,侵袭穿过基底膜的细胞数分别为（174±42）个、（112±31）个、（87±29）个,差异均有统计学意义（F ＝109．61,P ＝0．009;F ＝67．31,P ＝0．032）。与亲本结肠癌细胞株COLO 比较,耐药株表达更高的干性基因,差异有统计学意义（F ＝47．31,P ＝0．042）;且耐药株对其他化疗药如米托蒽醌存在交叉耐药[如给药96 h,米拖蒽醌对亲本 COLO 的抑制率高于 COLO／5-FU-1、COLO／5-FU-2（0．749±0．042、0．423±0．024、0．342±0．018）,差异有统计学意义（F ＝12．61,P ＝0．028）]。COLO／5-FU-2、COLO／5-FU-1、亲本 COLO 细胞的微球体形成率依次为（8．90±0．97）％、（6．20±0．75）％、（3．90±0．32）％,差异有统计学意义（F ＝164．32,P ＝0．006）。结论结肠癌 COLO耐药株有肿瘤干细胞样细胞的特点,是富集了的肿瘤干细胞。     

Expression profiling of colon cancer cell lines and colon biopsies: towards a screening system for potential cancer-preventive compounds.

Interest in mechanisms of colon cancer prevention by food compounds is strong and research in this area is often performed with cultured colon cancer cells. In order to assess utility for screening of potential cancer-preventive (food) compounds, expression profiles of 14 human cell lines derived from colonic tissue were measured using cDNA microarrays with 4000 genes and compared with expression profiles in biopsies of human colon tumours and normal tissue. Differences and similarities in the gene expression profiles of the cell lines were analysed by clustering and principal component analysis (PCA). Cytoskeleton genes and immune response genes are two functional classes of genes that contributed to the differences between the cell lines. A subset of 72 colon cancer-specific genes was identified by comparing expression profiles in human colon biopsies of tumour tissue and normal tissue. A separation of the cell lines based on the tumour stage of the original adenocarcinoma was observed after PCA of expression data of the subset of colon cancer-specific genes in the cell lines. The results of this study may be useful in the ongoing research into mechanisms of cancer prevention by dietary components.     

Associations between tissue-specific DNA alkylation,DNA repair and cell proliferation in the colon and colon tumour yield in mice treated with 1,2-dimethylhydrazine

Putative risk factors (DNA damage) and risk modifying factors (DNA repair and cell proliferation) were examined in an experimental mouse model in which treatment with dimethylhydrazine (6.8 mg/kg DMH i.p. once weekly) for up to 20 weeks induces colon tumours in a site specific manner with 0, 43 and 87% of animals having proximal, mid and distal colon tumours respectively at the highest cumulative dose. Levels of the pro-carcinogenic DNA adduct, O(6)-methylguanine (O(6)-MeG), in colonic DNA were found to vary with time after final treatment and with location within the colon but not with total DMH dose. O(6)-MeG levels were generally lowest in proximal colon DNA and highest in distal colon DNA. Steady state O(6)-MeG levels were obtained at the highest cumulative DMH dose with O(6)-MeG levels in mid and distal colon DNA being 5 and 10 times higher those in proximal colon DNA. O(6)-alkylguanine-DNA alkyltransferase (MGMT) activity, and cell proliferation indices in the colon were also found to vary with time after final treatment but not with either location within the colon or total DMH dose. O(6)-MeG levels, MGMT activity and cell proliferation indices at specific time points as well as basal MGMT activity were not associated with differences in tumour yield within the colon. However tumour yield was associated with the cumulative amount of O(6)-MeG present in DNA over the treatment period and with the treatment induced cumulative increase in cell proliferation, particularly within regions of the colon crypt where stem cells reside but not with cumulative changes in MGMT activity. Results are consistent with an increased cancer risk arising from an increased mutation load in the target stem cell population due to increased adduct formation/persistence and cell proliferation but also suggest that other cell specific factors may help to determine tumourigenic response.     

Cell culture of human colon adenomas and carcinomas

Cell lines were established from colon adenomas, including tubular and villous polyps, primary adenocarcinomas, and metastases arising in patients with colon adenocarcinomas. The protocol for cultivating these diverse tissues includes primary cultivation of tissue explants on a type I collagen gel followed by nonenzymatic subculture of the epithelial outgrowth. All early passages were accomplished using low subculture ratios. Cultured cells elaborate morphological structures which are similar to features present in the tissues from which they were cultivated. Specifically, all structural features of colon epithelial cells were identified, including junction formation, prominent microvilli, and mucin secretion, in several cell lines. Five cell lines cultured from colonic neoplasms at different stages of cancer progression were selected for detailed characterization. Cells grown from two tubular polyps had normal human karyotypes. Cells from a villous polyp and all adenocarcinomas were aneuploid with stable marker chromosomes. The established cell lines exhibit distinct phenotypes based on growth characteristics in vitro and in athymic mice; and it is suggested that these cell lines represent useful models for studying the evolution of colon cancer from a benign to an aggressive cell type.     

The use of sesame oil and other vegetable oils in the inhibition of human colon cancer growth in vitro

Sesame contains large quantities of the essential polyunsaturated fatty acid (PUFA), linoleic acid, in the form triglycerides. The antineoplastic properties of many PUFAs such as linoleic acid and their metabolites are known. We tested the hypothesis that natural vegetable oils, such as sesame oil and its component linoleic acid, when added to human colon adenocarcinoma cells growing in tissue culture would inhibit their growth and that normal colon cells would not be similarly affected. Three human colon cancer cell lines and one normal human colon cell line were exposed to the following: (1) pure linoleic acid; (2) lipase-digested sesame oil; (3) undigested sesame oil; (4) five additional common vegetable oils; (5) mineral oil. Linoleic acid inhibited the in vitro growth of all three malignant human colon adenocarcinoma cell lines. The normal colon cell line showed dramatically less inhibition of growth. Lipase-digested sesame oil (LDSO) and undigested sesame oil (UDSO) produced greater inhibition of growth of all three malignant colon cell lines than of the normal colon cells. Five other common vegetable oils containing various amounts of PUFAs such as corn, soybean, safflower, olive and coconut oils, all in their lipase-digested form, were found to dramatically inhibit the growth of the HT-29 malignant human colon cell line. Undigested olive and safflower oils also inhibited the HT-29 cells although not as markedly as the lipase-digested oils. Mineral oil did not inhibit the growth of HT-29 cells. Both lauric and palmitic acid, which are saturated fatty acids found in abundance in coconut oil inhibits the HT-29 cells more strongly than linoleic acid, while oleic acid did not inhibit. We conclude that many vegetable oils including sesame contain in vitro antineoplastic properties and that this finding warrants further investigation both in vitro and in vivo to assess their possible chemotherapeutic potential.     

去泛素化酶USP9X在结肠癌组织中的表达及意义

目的:探讨去泛素化酶USP9X在结肠癌组织中的表达特点及对结肠癌细胞增殖的影响。方法:收集解放军中部战区总医院病理科存档的结肠癌组织标本和癌旁正常结肠组织标本76例，免疫组化法检测USP9X在不同性别、年龄患者的结肠癌组织、癌旁正常结肠组织中的表达情况。siRNA抑制人结肠癌HCT116细胞株USP9X的表达，MTT法检测HCT116细胞增殖能力。结果:76例结肠癌患者中，USP9X阳性表达53例，占69.7%。癌旁正常大肠组织中，USP9X阳性表达率19.7%。USP9X的表达与结肠癌淋巴结转移和浸润深度相关。siRNA抑制结肠癌HCT116细胞USP9X表达后，与空白对照组和阴性对照组比较，干扰组细胞增殖能力显著下降。结论:去泛素化酶USP9X在结肠癌组织中的表达高于癌旁正常结肠组织，并与肿瘤侵袭转移相关。特异性抑制USP9X基因的表达可抑制结肠癌细胞的增殖能力。     

结肠癌患者血清中E-钙粘蛋白和半乳糖凝集素-9的表达水平及临床意义

目的 分析与检测结肠癌患者血清中E-钙粘蛋白和半乳糖凝集素-9水平以及临床意义.方法 选择结肠癌患者88例,健康体检者50例作为对照观察.采用酶联免疫吸附法检测两组血清E-钙粘蛋白和半乳糖凝集素-9水平.结果 与对照组相比,结肠癌组血清E-钙粘蛋白和半乳糖凝集素-9水平显著降低(P＜0.05).血清E-钙粘蛋白和半乳糖凝集素-9水平与结肠癌患者年龄、性别、瘤灶直径、癌灶部位无明显相关性(P＞0.05),与临床分期和肿瘤分化程度显著相关(P＜0.05).死亡组患者E-钙粘蛋白和半乳糖凝集素-9水平显著低于存活组(P＜0.01).结论 结肠癌患者血清中E-钙粘蛋白和半乳糖凝集素-9水平明显降低,与结肠癌的恶性程度相关,对该病的临床预后评价具有重要价值.