Some recent works on diagnosis and treatment of gastric cancer

ＰＲＥＰＡＲＡＴＩＯＮＡＮＤＵＳＥＳＯＦＭＯＮＯＣＬＯＮＡＬＡＮＴＩＢＯＤＩＥＳＢｙｍｅａｎｓｏｆｃｅｌｆｕｓｉｏｎｔｅｃｈｎｉｃｗｅｅｓｔａｂｌｉｓｈｅｄｓｅｖｅｒａｌｈｙｂｒｉｄｏｍａｃｅｌｌｉｎｅｓｃａｐａｂｌｅｏｆｐｒｏｄｕｃｉｎｇａｎｔ...     

Telomerase activity in gastric cancer and its clinical implications

ＩＮＴＲＯＤＵＣＴＩＯＮＴｈｅｄｅｖｅｌｏｐｍｅｎｔｏｆｃａｒｃｉｎｏｍａｒｅｓｕｌｔｓｆｒｏｍｍｕｌｔｉｐｌｅｉｎｄｅｐｅｎｄｅｎｔｇｅｎｅｔｉｃｃｈａｎｇｅｓｔｈａｔａｃｔｉｖａｔｅｐｒｏｔｏｏｎｃｏｇｅｎｅｓｏｒｉｎａｃｔｉｖａｔｅｔｈｅａｃ...     

MUC2反义脱氧寡核苷酸对胃癌细胞体外黏附侵袭活性的影响

目的 探讨黏蛋白MUC2反义脱氧寡核苷酸（ASODN）对人胃癌细胞株SGC7901黏附侵袭活性的影响。方法 采用人工合成的MUC2 ASODN经阳离子脂质体包裹后转染入SGC7901细胞中,采用黏附试验、Boyden小室体外侵袭试验观察比较转染前后癌细胞黏附率,穿膜细胞相对百分率及组织蛋白酶D、钙黏蛋白表达的变化。结果 转染SGC7901细胞48h后,癌细胞黏附率在30、60、90、120min各时间段逐渐升高,但低于空白对照组（P均〈0．01）;转染后癌细胞穿膜细胞相对百分率明显下降;转染后SGC7901细胞的E-钙黏蛋白表达明显增高,组织蛋白酶D水平明显降低。结论 人工合成的MUC2 ASODN能有效抑制胃癌细胞株SGC7901黏附侵袭能力。     

促胃液素及其受体拮抗剂丙谷胺对人胃癌细胞系生长的影响

目的观察和分析五肽促胃液素ＰＧ及其受体拮抗剂丙谷胺ＰＧＭ对人胃癌细胞系ＭＧＣ生长的影响,为临床应用促胃液素受体拮抗剂协助治疗胃癌提供依据．方法选用５ｍｇ／Ｌ,１０ｍｇ／Ｌ,１５ｍｇ／Ｌ,２０ｍｇ／Ｌ４种浓度的ＰＧ和３０ｍｇ／Ｌ的ＰＧＭ分别作用于体外培养的浓度为２５×１０８／Ｌ的ＭＧＣ,分别培养２４,４８,７２ｈ,于酶标仪上选用波长５４０ｎｍ测定吸光值Ａ,并对数据进行比较分析．结果４种浓度的ＰＧ作用于ＭＧＣ,ＭＧＣ连续３ｄ的生长状态与对照组无明显差异,而ＭＧＣ在ＰＧＭ作用下,其连续３ｄ的平均Ａ值分别为００２９,００４６和００８４,而未被ＰＧＭ作用的ＭＧＣ的平均Ａ值分别是０１０１,０１１５和０１８２,ＭＧＣ在ＰＧＭ作用下生长明显低于对照组（Ｐ＜００５）．结论外源性的ＰＧ对ＭＧＣ无营养促进作用,而ＰＧＭ能抑制ＭＧＣ的生长     

Quantitation of CD 44 in tumor cells and peripheral blood of patients with gastric cancer

ＱｕａｎｔｉｔａｔｉｏｎｏｆＣＤ４４ｉｎｔｕｍｏｒｃｅｌｓａｎｄｐｅｒｉｐｈｅｒａｌｂｌｏｏｄｏｆｐａｔｉｅｎｔｓｗｉｔｈｇａｓｔｒｉｃｃａｎｃｅｒＺＨＡＯＪｕｎ，ＰＡＮＸｕｅａｎｄＹＩＮＧｅＰｉｎｇＳｕｂｊｅｃｔｈｅａｄｉｎｇｓｒｅｃｅｐｔｏｒ...     

老年患者恶性胸水中肿瘤浸润免疫细胞体外活化

目的 观察老年患者恶性胸水中肿瘤浸润免疫细胞的活性.方法 分离恶性胸水单个核细胞(PEMCs),采用两步贴壁法,获得非贴壁细胞,树突细胞及淋巴细胞是其主要功能细胞成分.IL-2活化肿瘤浸润免疫细胞,SP法检测T淋巴细胞亚群的数量及免疫功能,SP法S-100蛋白染色检测树突细胞.结果 IL-2活化培养7 d后肿瘤浸润树突细胞(TIDC)和肿瘤浸润T淋巴细胞(TIL)数量明显增加(P<0.01).恶性胸水TIDC经过IL-2活化后具有抗原提呈功能.结论 IL-2活化肿瘤微环境中TIDC,使其恢复免疫监视功能,有效地负载肿瘤抗原,协同TIL等其他免疫细胞有效杀伤肿瘤细胞.     

Study on the expression of matrix metallo proteinase-2 mRNA in human gastric cancer

lNTRODUCTlONDuringtumorinvasionandmetastasis,malignantcellsinprimarysiteacquiretheabilityt0degradeextracellularmatrix(ECM)andpenetratetissuebarriers.Ainongthepr0teolyticenzymeswhichdegradeECM,matrixmetalloprotenase(MMP)isoneoftheimportantones.MMP-2(72kDatypelVcollagenase)isamember0ftheMMPsgenefamilywhichdegradesthemacromoleculesofconnectivetissueandECM,suchascollagen,proteoglycans,lamininandfibr0nectin.ThusMMP-2isbelievedtoplayanimp0rtantroleintumorinvasionandmetastasis.Severalimm…     

中量醛氢叶酸和5－FU联合治疗胃肠道肿瘤

目的探讨生化调制剂醛氢叶酸（ＣＦ）和氟脲嘧啶联合应用治疗胃肠道肿瘤的效果。方法采用ＣＦ＋５＿ＦＵ＋ＤＤＰ或／和ＭＭＣ联合方案。ＣＦ用中剂量２００－３００ｍｇ／（ｍ２·ｄ）静脉滴注，２ｈ后接着用５－ＦＵ３７５ｍｇ／（ｍ２·ｄ）静脉滴注ＤＤＰ２０ｍｇ／（ｍ２·ｄ）静脉推注，以上药物连用５ｄ，ＭＭＣ６－８ｍｇ于化疗第１天静脉推注。结果３２例可评价的胃癌有效率（ＣＲ＋ＰＲ）为６２５％，治疗有效病例，治疗后生存３－１４个月，仍在继续观察中。３６例可评价的结直肠癌有效率为４１７％，有效病例中位生存期１３个月，无效病例８个月。毒副反应以骨髓抑制和消化道反应为主。结论本方案对晚期胃肠道肿瘤是一种疗效比较好的化疗方案，毒副反应可以忍受，值得推广。     

康莱特对老年癌症恶病质患者生存质量影响及恶病质因子的调控

目的 探讨康莱特对老年癌症恶病质( cancer cachexia,CC)患者的生存质量影响及时恶病质因子的调控作用. 方法 62例2009年1月至2011年4月住院的老年癌症患者,根据CC的诊断标准,各项评分＞5分者42例入组,分别用康莱特进行干预,比较干预前后患者KPS评分、三酰甘油(TG)、血红蛋白(HB)、血清白蛋白(ALB)、肿瘤坏死因子(TNF-2α)及新的恶病质因子锌-α2-糖蛋白(zinc-alpha 2-glycoprotein,ZAG)的变化. 结果 治疗后与治疗前相比,患者KPS评分升高,血HB和TNF-2α升高、ZAG降低(P＜0.05);TG明显升高(P＜0.01).ALB治疗前后比较没有统计学差异(P＞0.05). 结论 康莱特可以降低老年癌症患者的恶病质因子TNF-2α、ZAG水平,有改善患者恶病质症状,提高患者生存质量的作用.     

紫杉醇增强TRAIL诱导的胃癌BGC823细胞凋亡的机制

目的 探讨紫杉醇增强TRAIL诱导的胃癌BGC823细胞凋亡的机制。方法胃癌BGC823细胞传代堵养后,取对数生长期细胞用于实验。采用MTT法测定细胞活力,流式细胞仪检测细胞凋亡,Westernblot检测Akt、p-Akt蛋白表达。结果在胃癌BGC823细胞中,100ng／ml的TRAIL可致少量的细胞凋亡,同时检测到Akt的磷酸化。紫杉醇作用胃癌BGC823细胞24h,IC50剂量为8．97μg／ml。与单药TRAIL和紫杉醇相比,TRAIL（100ng／m1）联合紫杉醇（8．97μg／ml,24h的IC50剂量）对细胞的诱导凋亡作用明显增强（P〈0．05）。免疫印迹结果显示,TRAIL（100ng／ml）作用BGC823细胞24h,活化了Akt蛋白,而8．97μg／ml的紫杉醇抑制了Akt的磷酸化。TRAII（100ng／ml）联合紫杉醇（8．97μg/ml）作用后,TRAIL引起的Akt磷酸化被抑制。结论紫杉醇通过抑制TRAIL引起的Akt磷酸化,从而增强了TRAIL诱导的胃癌BGC823细胞凋亡。     

Time course of changes in phenotypes of cultured tumor-infiltrating lymphocytes isolated from human colorectal cancer

A study was conducted to investigate the time course of changes in phenotypes of cultured tumor-infiltrating lymphocytes (TIL) isolated from 5 patients with colorectal cancer. Following initial incubation with protein phytohemagglutinin (PHA-P, final concentration 0.1w/v%), one of the inducers of interleukin-2 (IL-2) receptor, and recombinant interleukin-2 (rIL-2, 1000U/ml) for 3 days, TIL was further cultured with rIL-2 alone for another 46 to 79 days. Phenotypes of cultured TIL were analyzed by a two color flow-cytometry. The following results were obtained: 1) Yields of TIL isolated from cancerous tissues were 1.0 × 10⁶ to 1.6 × 10⁶ cells/g wet weight, and TIL grew 31 to 3700 folds in the entire period of culture. These growth rates were significantly higher than those obtained by the conventional method of culture with rIL-2 alone (1 to 720 folds). 2) The population of cytotoxic T cells (CD8 (+), CDU (−)) reached the maximum (92%, median value) at 5 weeks of culture, and thereafter gradually decreased to 61% at 9 and 10 weeks. In contrast, the population of activated natural killer cells (CD 16 (+) and Leu7 (+) or (−)) remained below 4% for the entire period of culture. 3) Maximum enhancement of specific cytotoxic activities of cultured TIL was observed during 3 to 4 weeks in culture, using K562 cells as well as Daudi cells as target cells. In conclusion, addition of PHA-P seems to beneficially affect the growth rate of TIL in culture. Moreover, time course of changes in phenotypes as well as cytotoxic activities suggest that TIL thus obtained is recommended to be used for adoptive immunotherapy during 3 to 5 weeks of culture when the highest killer activity is achieved. This work was supported in part by a Grant-in-Aid for Cancer Research from the Ministry of Health and Welfare of Japan (1–7).     

幽门螺杆菌感染对胃病细胞动力学的影响

目的　观察 Ｈｐ 感染在正常粘膜演变为胃癌过程中对细胞增殖动力学的影响,以探讨 Ｈｐ 的致癌机制．方法　研究对象为正常胃粘膜的消化不良患者（ ＮＳ,ｎ ＝ １４） 及慢性浅表性胃炎（ ＣＳＧ, ｎ ＝ ５６） 、慢性萎缩性胃炎（ ＣＡＧ,ｎ ＝ ２０） 、慢性萎缩性胃炎伴肠上皮化生（ＣＡＧＩＭ ,ｎ ＝ １６） 、不典型增生（Ｄｙｓ ,ｎ ＝ １８） 、胃癌（ ＧＣ,ｎ ＝ １７） Ｈｐ 阳性与阴性患者．应用Ｋｉ６７ 免疫组化技术评价胃幽门窦上皮细胞增生,并用标记指数百分率（ＬＩ％ ） 来表示．结果　Ｈｐ 阳性患者（ ｎ ＝ ７５） 的Ｋｉ６７ ＬＩ％ 为１７ ±５ , Ｈｐ 阴性患者（ ｎ ＝ ５２ ） 的 Ｋｉ６７ ＬＩ％ 为 １３ ±６ , 差异有 显著 性（ Ｐ＜ ０－０５） ;伴有 Ｈｐ 感染的ＣＳＧ 与ＮＳ 或 Ｈｐ 阴性的ＣＳＧ 患者相比ＬＩ％ 增加（ Ｐ＜ ０－０１） ;ＣＡＧ,ＣＡＧＩＭ ,Ｄｙｓ ,ＧＣ 的 Ｈｐ 阳性与阴性患者的ＬＩ％ 相比无显著差异;五种胃病无论 Ｈｐ 阳性或阴性患者与正常者相比,ＬＩ％ 明显增加（ Ｐ＜ ０－０１） ． ＬＩ％ 与胃粘膜炎症程度无关．结论　Ｈｐ 感染促进胃上皮细胞过度增殖主要发生在胃粘膜病变的早期,并不影响在癌前病变或胃癌患者中所     

胃癌及癌前病变组织中MUC2基因的表达

目的揭示MUC2基因在正常胃肠道粘膜、癌前病变和胃癌组织中的表达规律及其临床病理意义.方法应用免疫组织化学SP法检测组织中MUC2核粘蛋白的表达,应用原位杂交方法检测组织中MUC2 mRNA的表达.结果 MUC2核粘蛋白及其mRNA主要在十二指肠内表达,正常胃粘膜内不表达;肠上皮化生(n=27)和胃癌组织(n=46)的表达率分别为85%,32%和67%,58%;肠化内MUC2基因表达与肠化分型之间无关(P＞0.05);胃癌组织中MUC2基因表达与肿瘤浸润、淋巴结转移、临床分期和胃癌的分型之间无关(P＞0.05),而MUC2核粘蛋白阳性组与阴性组之间的肿瘤分化存在明显的差别(P＜0.05).结论 MUC2基因在胃粘膜的癌变过程中是明显上调表达的,胃癌内MUC2核粘蛋白的表达与胃癌的分化有关.     

Treatment of postoperative gastric cancer with Fuzheng Huoxue anticancer prescription

ＴｒｅａｔｍｅｎｔｏｆｐｏｓｔｏｐｅｒａｔｉｖｅｇａｓｔｒｉｃｃａｎｃｅｒｗｉｔｈＦｕｚｈｅｎｇＨｕｏｘｕｅａｎｔｉｃａｎｃｅｒｐｒｅｓｃｒｉｐｔｉｏｎＺＨＯＵＡＧａｏ１，ＨＵＡＮＧＤａＷｅｉ２，ＤＩＮＧＹｕＸｉｏｎｇ１，ＪＩＡＮＧＨｕａ３ａｎ...     

Clinicopathological analysis of patients with gastric cancer in 1200 cases

INTRODUCTION Gastric cancer is one of the most common fatal malignancies in the world. The prognosis is generally poor in advanced gastric cancer .The low survival is related to delayed diagnosis, metastasis and recurrence after operation .The aim of this paper was to find correlation between clinical factors was to find correlation between clinical factors and biologic behavior of gastric cancer in a series of 1200 patients undergoing surgical resection.     

CD3-mediated activation of tumor-reactive lymphocytes from patients with advanced cancer

Lymphocytes from blood or tumors of patients with advanced cancer did not proliferate and produced very low levels of tumor necrosis factor and IFN-gamma when cultured with autologous tumor cells. Proliferation and lymphokine production dramatically increased in the presence of beads conjugated with mAbs to CD3 plus mAbs to CD28 and/or CD40, and the lymphocytes destroyed the tumor cells. Expression density of CD3 concomitantly increased from low to normal levels. Furthermore, beads providing a CD3 signal (in combination with CD28 or CD28 plus CD40) gave partial protection against the inhibitory effect of transforming growth factor type beta1 on lymphocyte proliferation and production of tumor necrosis factor and IFN-gamma. MHC class I-restricted cytolytic T cells lysing autologous tumor cells in a 4-h Cr(51) release assay were generated when peripheral blood leukocytes were activated in the presence of autologous tumor cells and anti-CD3/CD28 or anti-CD3/CD28/CD40 beads. Experiments performed in a model system using anti-V-beta1 or anti-V-beta2 mAbs to activate subsets of T cells expressing restricted T cell receptor showed that lymphocytes previously activated by anti-V-beta can respond to CD3 stimulation with vigorous proliferation and lymphokine production while retaining their specificity, also in the presence of transforming growth factor type beta1. Our results suggest that T lymphocytes from cancer patients can proliferate and form Th1 type lymphokines in the presence of autologous tumor cell when properly activated, and that antigen released from killed tumor cells and presented by antigen-presenting cells in the cultures facilitates the selective expansion of tumor-directed, CD8(+) cytolytic T cells.