Effects of aminoguanidine on nitric oxide production induced by inflammatory cytokines and endotoxin in cultured rat hepatocytes

AIM To study the effects of aminoguanidine(AG) and two L-arginine analogues Nω-nitro-L-arginine methyl ester (L-NAME) and Nω-nitro-L-arginine (L-NNA) on nitric oxide (NO) productioninduced by cytokines (TNF-α, IL-11β, and IFN-γ)and bacterial lipopolysaccharide (LPS) mixture(CM) in the cultured rat hepatocytes, andexamine their mechanisms action.METHODS Rat hepatocytes were incubatedwith AG, L-NAME, L-NNA, Actinomycin D (ActD)and dexamethasene in a medium containing CM(LPS plus TNF-α, IL-1β, and IFN-γ) for 24 h. NOproduction in the cultured supernatant wasmeasured with the Griese reaction. IntracellularcGMP level was detected with radioimmunoasey.RESULTS NO production was markedlyblocked by AG and L-NAME in a dose-dependentmanner under inflammatory stimuli conditiontriggered by CM in vitro. The rate of themaximum inhibitory effects of L-NAME (38.9%)was less potent than that obtained with AG(53.7%, P<0.05). There was no significantdifference between the inhibitory effects of AGand two L-arginine analogues on intracellularcGMP accumulation in rat cultured hepatocytes.Non-specific NOS expression inhibitordexamethasone ( DEX ) and iNOS mRNAtranscriptional inhibitor ActD also significantlyinhibited CM-induced NO production. AG(0.1mmol.L-1) and ActD (0.2ng@Lt) wereequipotent in decreasing NO production inducedby inflammatory stimuli in vitro, and botheffects were more potent than that induced bynon-selectivity NOS activity inhibitor L-NAME(0. 1 mmol@ L- 1) under similar stimuli conditions(P＜O.O1).CONCLUSION AG is a potent selectiveinhibitor of inducible isoform of NOS, and themechanism of action may be not onlycompetitive inhibition in the substrate level, butalso the gene expression level in rathepatocytes .

Effects of Taxotere on invasive potential and multidrug resistance phenotype in pancreatic carcinoma cell line SUIT-2

INTRODUCTIONDevelopment of drug-resistance to chemotherapyand subsequent metastasis of tumor are primarilyresponsible for treatment failure and the death fromcancer. There have been many previous studies onthe relationship between expression of multidrugresistance (MDR) phenotype P-glycoprotein (P-gp)and the malignant properties of tumors, but theresults are often conflicting[1-8]. The difference intumor types or MDR phenotype induced by specificagents might account for this discrepancy. Taxotere(TXT), a member of the family of taxanes, hasantitumor activity through its effect of promotingthe polymerization of tubulin[9,10].

Experimental study on antitumor effect of arsenic trioxide in combination with cisplatin or doxorubicin on hepatocellular carcinoma

INTRODUCTIONThe main component of a traditional Chinese drug 'Pishuang'. arsenic trioxide (As2O3), has obviously selective anti-tumor effect on human hepatocellular carcinoma (HCC)in both in vitro and in vivo studies[1-5]. Due to limited effectiveness when any anti-carcinogen is used alone and obviously increased toxicity when the dose is raised, there is no exception for As2O3. Furthermore, combined chemotherapy contributes to improve therapeutic effectiveness, disperse toxicity and surmount drug-resistance,in which the combination of traditional Chinese and modern medicine has more advantages and characteristics. As a result,we made an experimental study on anti-tumor effect of As2O3in combination with cisplantin (PDD) or doxorubicin (ADM)on HCC. to investigate the possibility of AS2O3 in combination with PDD or ADM and nature of interaction between them,and to provide experimental basis for clinical application.

Effects of“Moxibustion Serum”on Proliferation and Phenotypes of Tumor Infiltrating Lymphocytes

Tumor infiltrating lymphocytes (TIL) were cultured with “moxibustion serum”(MS), and the results were examined by flow cytometry. The results indicated that MS could enhance the proliferation of TIL,accelerate it to reach the exponential growth phase, and assist recombinant interleukin 2 (rIL-2) to enhance successively the percentage of CD3^+ positive cells, maintain the number of CD4^+ positive T cells, promote greatly the percentage of CD8^+ positive T cells among TILs, and reverse the CD4^+/CD8^+ ratio. Such cooperative effects rely on relative specificity of acupoints. It is suggested that MS is beneficial to the growth of TIL both in the aspects of proliferation and phenotypes.

Neutron-induced apoptosis of HR8348 cells in vitro

INTRODUCTIONTo date ,the major therapy for rectal carcinoma is extensive abdomino-perineal resection[1]. Unfortunately ,after resection of rectal carcinoma ,many patients still die of blood-borne metastases ,usually in the liver or lungs ,or local prlvic recurrence[2,3],which is the major cause of morbidity and mortality in patients with rectal carcinoma .Pre-or postoperative radiotherapy can reduce the incidence of local rdcurrence[4-7].

Blockage of IGF-1R signaling sensitizes urinary bladder cancer cells to mitomycin-mediated cytotoxicity

A major problem which is poorly understood in the management of bladder cancer is low sensitivity to chemotherapy and high recurrence after transurethral resection. Insulin-like growth factor 1 receptor (IGF-1R) signaling plays a very important role in progression, invasion and metastasis of bladder cancer cells. In this study, we investigated whether IGF-1R was involved in the growth stimulating activity and drug resistance of bladder cancer cells. The results showed: The mRNAs of IGF-1, IGF-2 and IGF-1R were strongly expressed in serum-free cultured T24 cell line, whereas normal urothelial cells did not express these factors/receptors or only in trace leve1s; T24 cell responded far better to growth stimulation by IGF-1 than did normal urothelial cells; blockage of IGF1R by antisense oligodeoxynucleotide (ODN) significantly inhibited the growth of T24 cell and enhanced sensitivity and apoptosis of T24 cells to mitomycin (MMC). These results suggested that blockage of IGF-IR signaling might potentially contribute to the treatment of bladder cancer cells which are insensitive to chemotherapy.

Recombinant scorpion insectotoxin AaIT kills specifically insect cells but not human cellss

The nucleotide sequence deduced from the amino acid sequence of the scorpion insectotoxin AaIT was chemically synthesized and was expressed in Escherichia coli. The authenticity of this in vitro expressed peptide was confirmed by N-terminal peptide sequencing. Two groups of bioassays, artificial diet incorporation assay and contact insecticidal effect assay, were carried out separately to verify the toxicity of this recombinant toxin. At the end of a 24 h experimental period, more than 60% of the testing diamondback moth (Plutella xylostella) larvae were killed in both groups with LCs0 value of 18.4 uM and 0.70 μM respectively. Cytotoxicity assay using cultured Sf9 insect cells and MCF-7 human cells demonstrated that the toxin AaIT had specific toxicity against insect cells but not human cells. Only 0.13 μM recombinant toxin was needed to kill 50% of cultured insect cells while as much as 1.3μM toxin had absolutely no effect on human cells. Insect cells produced obvious intrusions from their plasma membrane before broken up. We infer that toxin AaIT bind to a putative sodium channel in these insect cells and open the channel persistently, which would result in Na+ influx and finally cause destruction of insect cells.

Synergistic effects of focus ultrasound with different frequency and hematoporphyrin on human tumor cells

Human hematopoietic cell K 562 , human melenoma cell LiBr and human stomach cancer cells were exposed to ultrasound (US, 1.75 W/cm\+2, 1.4, 2.16 and 2.4 MHz) in vitro in the presence or absence of hematoporphyrin (Hp, 100 μg/mL). The cell damaging effects of treatments were determined by means of the Trypan Blue dye exclusion test, MTT test and FDA test. The experimental results showed that the same cell line had different sensibilities to the US of different frequencies, and different cell line had different damage at the same acoustical radiation. The combined treatment with US and Hp enhanced greatly the cell damage, and no sensibility of insonation cells to US with Hp was observed. The cell damage tests showed that the results of MTT test corresponded well with that of Trypan Blue dye test.

In vitro cultures of circulating tumor cells:a potential tool to unravel drug sensitivity

Since taking part as leading actors in driving the metastatic process,circulating tumor cells(CTCs)have displayed a wide range of potential applications in the cancer-related research field.Besides their well-proved prognostic value,the role of CTCs in both predictive and diagnostics terms might be extremely informative about cancer properties and therefore highly helpful in the clinical decision-making process.Unfortunately,CTCs are scarcely released in the blood circulation and their counts vary a lot among different types of cancer,therefore CTC detection and consequent characterization are still highly challenging.In this context,in vitro CTC cultures could potentially offer a great opportunity to expand the number of tumor cells isolated at different stages of the disease and thus simplify the analysis of their biological and molecular features,allowing a deeper comprehension of the nature of neoplastic diseases.The aim of this review is to highlight the main attempts to establish in vitro CTC cultures from patients harboring different tumor types in order to highlight how powerful this practice could be,especially in optimizing the therapeutic strategies available in clinical practice and potentially preventing or contrasting the development of treatment resistance.

奥希替尼在老年非小细胞肺癌患者靶向治疗中的应用效果及对T细胞水平的影响

目的 探讨奥西替尼在老年非小细胞肺癌患者靶向治疗中的效果及对免疫水平的影响。方法 回顾性选择2018年1月至2020年12月老年非小细胞肺癌患者116例研究,根据治疗方法不同分为2组,各58例。对照组采用常规放化疗治疗,观察组在对照组基础上联合奥西替尼治疗,3个月治疗后评估患者效果,比较2组总有效率、T细胞水平(CD3^(+)、CD4^(+)、CD8^(+)、CD4^(+)/CD8^(+))、肿瘤标志物水平、不良反应发生率。结果 观察组治疗3个月总有效率为44.8%高于对照组25.9%(P<0.05);2组治疗后3个月CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+)水平均低于治疗前(P<0.05);CD8^(+)水平高于治疗前(P<0.05);观察组治疗后3个月CD3^(+)(58.95±4.21)%、CD4^(+)(32.59±3.11)%、CD4^(+)/CD8^(+)(1.21±0.22)高于对照组(P<0.05);CD8^(+)(26.81±3.32)%低于对照组(P<0.05);观察组干预3个月后CA125(91±8)U/ml、CYFRA21-1(1.26±0.24)μg/L及癌胚抗原(CEA)水平(34±5)μg/L均低于对照组(P<0.05);2组不良反应发生率差异无统计学意义(P>0.05)。结论 奥西替尼用于老年非小细胞肺癌患者靶向治疗中,能获得较好的总有效率,对患者T细胞水平影响较小,可降低肿瘤标志物水平,未增加不良反应发生率,值得临床推广应用。

养肺益气汤联合载药微球支气管动脉化疗在非小细胞肺癌治疗中的临床效果分析

目的:分析养肺益气汤联合载药微球支气管动脉化疗治疗非小细胞肺癌的临床效果。方法:选择2020年1月—2023年1月启东市中医院肿瘤科收治的82例非小细胞肺癌患者,根据随机数表法分为化疗组、联用组,各41例。其中化疗组采用载药微球支气管动脉化疗治疗,而联用组采用养肺益气汤联合载药微球支气管动脉化疗治疗。比较两组肿瘤标志物、中医症候积分、毒副作用发生率。结果:治疗前,两组肿瘤标志物比较,差异无统计学意义(P>0.05);治疗后,两组肿瘤标志物均低于治疗前,且联用组低于化疗组,差异有统计学意义(P<0.05)。治疗前,两组中医症候积分比较,差异无统计学意义(P>0.05);治疗后,两组中医症候积分均低于治疗前,且联用组低于化疗组,差异有统计学意义(P<0.05)。联用组毒副作用总发生率低于化疗组,差异有统计学意义(P<0.05)。结论:在针对非小细胞肺癌进行治疗时,在载药微球支气管动脉化疗基础上予以养肺益气汤治疗能够进一步控制癌症病变,缓解各项临床症状,并降低毒副作用发生的可能性。

Antihepatoma effect of alpha-fetoprotein antisense phosphorothioate oligodeoxyribonucleotides in vitro and in mice

AIM To evaluate antihepatoma effect ofantisense phosphorothioate oligodeo-xyribonucleotides (S-ODNs) targeted to alpha-fetoprotein (AFP) genes in vitro and in nudemice.METHODS AFP gene expression was examinedby immunocytochemical method or enzyme-linked immunosorbent assay. Effect of S-ODNson SMMC-7721 human hepatoma cell growth invitro was determined using microculturetetrazolium assay. In vivo antitumor activitiesof S-ODNs were monitored by measuring tumorweight differences in treated and control micebearing SMMC-7721 xenografts. Induction of cellapoptosis was evaluated by fluorescence-activated cell sorter (FACS) analysis.RESULTS Antisense S-ODN treatment led toreduced AFP gene expression. Specificantisense S-ODNs, but not control S-ODNs,inhibited the growth of heaptoma cells in vitro.In vivo. only antisense S-ODNs exhibitedobvious antitumor activities. FACS analysisrevealed that the growth inhibition by antisenseS. ODNs was associated with their cell apoptosisinduction.CONCLUSION Antisense S-ODNs targeted toAFP genes inhibit the growth of human hepatomacells and solid hepatoma, which is related totheir cell apoptosis induction.

Personalized targeted therapy for esophageal squamous cell carcinoma

Esophageal squamous cell carcinoma continues to heavily burden clinicians worldwide. Researchers have discovered the genomic landscape of esophageal squamous cell carcinoma, which holds promise for an era of personalized oncology care. One of the most pressing problems facing this issue is to improve the understanding of the newly available genomic data, and identify the driver-gene mutations, pathways, and networks. The emergence of a legion of novel targeted agents has generated much hope and hype regarding more potent treatment regimens, but the accuracy of drug selection is still arguable. Other problems, such as cancer heterogeneity, drug resistance, exceptional responders, and side effects, have to be surmounted. Evolving topics in personalized oncology, such as interpretation of genomics data, issues in targeted therapy, research approaches for targeted therapy, and future perspectives, will be discussed in this editorial.

Taxotere resistance in SUIT Taxotere resistance in pancreatic carcinoma cell line SUIT 2 and its sublines

AIM: To investigate the specific mechanisms of intrinsic and acquired resistance to taxotere (TXT) in pancreatic adenocarcinoma (PAC).METHODS: MTT assay was used to detect the sensitivity of PAC cell line SUIT-2 and its sublines (S-007, S-013, S-020,S-028 and TXT selected SUIT-2 cell line, S2/TXT) to TXT.Mdr1 (P-gp), multidrug resistance associated protein (MRP), lung resistance protein (LRP) and β-tubulin isotype gene expressions were detected by RT-PCR. The functionality of P-gp and MRP was tested using their specific blocker verapamil ( Ver ) and indomethacin ( IMC ),respectively. The transporter activity of P-gp was also confirmed by Rhodamine 123 accumulation assay.RESULTS: S-020 and S2/TXT were found to be significantly resistant to TXT(19 and 9.5-fold to their parental cell line SUIT-2, respectively ). RT-PCR demonstrated strong expression of Mdr1 in these two cell lines, but weaker expression or no expression in other cells lines. MRP and LRP expressions were found in most of these cell lines. The TXT-resistance in S2-020 and S2/TXT could be reversed almost completely by Ver, but not by IMC. Flow cytometry showed that Ver increased the accumulation of Rhodamine-123 in these two cell lines. Compared with S-020 and SUIT-2,the levels of β-tubulin isotype II, III expreesions in S-2/TXTwere increased remarkably.CONCLUSION: The both intrinsic and acquired TXT-related drugresistance in these PAC cell lines is mainly mediated by P-gp, but had no relationship to MRP and LRP expressions.The increases of β-tubulin isotype II, III might be collateral changes that occur when the SUIT-2 cells are treated with TXT.

Specific CEA-producing colorectal carcinoma cell killing with recombinant adenoviral vector containing cytosine deaminase gene

瞄准：到杀死 CEA 积极颜色明确地使用 E 关口 i cytosine 脱氨基酶(CD ) 的表面的癌房间自杀基因，新复制缺乏的 recombinant adenoviral 向量在在哪个 CD，基因在 CEA 倡导者下面被控制被构造并且它的在里面 vitro 细胞毒素的效果被评估。方法：梭原生质标志包含 CD 基因和 CEA 基因的规章的顺序在 293 房间紧张与侵入人体气管粘膜的病菌染色体 DNA 的右手臂被构造并且重新结合。点弄污， PCR 被用来识别积极的匾。侵入人体气管粘膜的病菌的纯化被执行与在 CsCl 步坡度和滴定极端集中与匾形成试金被测量。细胞毒素的效果是有 MTT 方法的 assayed， 5-FC 的百分之五十抑制集中(IC (50 )) 用一个曲线试穿参数被计算。表面的癌房间线，是生产 CEA，和 CEA-nonproducing Hela 房间衬里的人的颜色在 cytological 测试被使用。确定的 recombinant 侵入人体气管粘膜的病菌向量 AdCMVCD， CD 基因在 CMV 倡导者下面在被控制，被用作病毒控制。量的结果被表示为平均数的吝啬的 +/- SD。统计分析用 ANOVA 测试被执行。结果：需要的 recombinant 侵入人体气管粘膜的病菌向量被称为 AdCEACD。点弄污和 PCR 的结果证明 recombinant 侵入人体气管粘膜的病菌包含了 CEA 倡导者和 CD 基因。病毒 titer 是大约 5.0 X 10 (14 ) pfu/L (在纯化以后的 -1) 。 生产CEA Lovo 房间对 5-FC 敏感并且与 AdCEACD 和 AdCMVCD 在感染以后有一样的细胞毒素的效果(在父母 Lovo 房间，感染 100 M.O.I AdCEACD 的 Lovo 房间和感染 10 M.O.I AdCMVCD 的 Lovo 房间的 5-FC 的 IC ( 50 )价值是 】15000 ， 216.5+/-38.1 和 128.8+/-25.4 micromol.L (-1), P【0.001 ，分别地)，并且当侵入人体气管粘膜的病菌的 m.o.i 被提高时， 5-FC 的 cytotoxicity 因此增加了( 5-FC 的 IC ( 50 )的价值被归结为 27.9+/-4.2 micromol.L (在 1000 M.O.I AdCEACD 的-1)感染了 Lovo 房间和 24.8+/-7.1 micromol.L (在 100 M.O.I AdCMVCD 的-1)感染了 Lovo 房间， P【0.05 ， P【0.01 ，分别地)。CEA-nonproducing Hela 房间没与 AdCEACD 在感染以后有效果，但是 Hela 房间与 AdCMVCD 在感染以后有细胞毒素的敏感到 5-FC (在在 10 M.O.I 感染 AdCMVCD 的父母 Hele 房间和 Hela 房间的 5-FC 的 IC (50 ) 是 】15000 和 214.5+/-31.3 micromol.L (-1), P【0.001 ) 。AdCEACD/5-FC 系统也有旁观者效果，并且当 transfected 房间的比例仅仅是 10% 时，生存能力是大约 30% 。结论：recombinant 侵入人体气管粘膜的病菌向量 AdCEACD 有房间的特性类型特定的基因交货。AdCEACD/5-FC 系统可以变得一新，为 CEA 积极的瘤的基因治疗的有势力和特定的途径，特别结肠癌。

Antisense expression of protein kinase Cα improved sensitivity to anticancerdrugs in human lung cancer LTEPa-2 cells

目的：研究蛋白激酶Ｃα（ＰＫＣα）在人肺癌ＬＴＥＰａ２细胞对一些临床抗肿瘤药物敏感性中的作用．方法：通过基因转染，免疫印迹等方法建立表达反义ＰＫＣα的人肺癌细胞模型，Ｎｏｒｔｈｅｒｎ印迹检测多药抗性基因的表达，分析了几种抗癌药物对培养细胞的ＩＣ５０．结果：表达反义ＰＫＣαＲＮＡ降低胞内ＰＫＣα水平时可抑制肺癌细胞中多药抗性基因的表达，增强肺癌细胞对抗肿瘤药物（三尖杉酯碱、卡铂、博来霉素、长春新碱、阿霉素）的敏感性．

胶质母细胞瘤FGFR3-TACC3融合基因介导丙酮酸激酶M2入核促进DNA损伤修复基础研究

目的探讨胶质母细胞瘤FGFR3-TACC3(F3-T3)融合基因介导丙酮酸激酶M2(PKM2)入核激活DNA损伤修复致替莫唑胺(TMZ)耐药的作用机制。方法慢病毒转染构建稳定表达F3-T3融合基因和空载体的胶质母细胞瘤细胞系U87MG和U251MG,构建稳定表达F3-T3融合基因的胶质母细胞瘤裸鼠模型,小动物活体成像系统观察荷瘤鼠肿瘤荧光信号强度;采用生物信息学分析基因芯片转录组数据分析F3-T3融合基因的生物学功能,并分析肿瘤基因组学图谱计划(TCGA)数据库中胶质瘤患者生存期与PKM2基因表达的关系;瞬时转染小干扰RNA(siRNA)敲低PKM2基因表达;CCK-8细胞增殖实验观察经梯度浓度替莫唑胺处理后、转染siRNA后、替莫唑胺联合PKM2抑制剂Compound 3k处理后U87MG和U251MG细胞增殖活性;提取核质蛋白并观察经替莫唑胺处理后总蛋白提取物、胞质提取物和胞核提取物PKM2蛋白表达情况;Western blotting法检测稳定表达F3-T3融合基因的U87MG和U251MG细胞PKM2蛋白相对表达量、磷酸化组蛋白H2AX(p-H2AX)相对表达量、siRNA敲低PKM2基因p-H2AX相对表达量。结果(1)CCK-8细胞增殖实验显示,经替莫唑胺640、320、160、80、40μmol/L处理后F3-T3转染组的U87MG细胞存活率均高于空载体转染组(P=0.000,0.000,0.000,0.004,0.010),经替莫唑胺640、320、160、80、40、20、5μmol/L处理后F3-T3转染组的U251MG细胞存活率亦均高于空载体转染组(P=0.000,0.000,0.000,0.000,0.002,0.001,0.002);然而,经替莫唑胺640、320、160、80、40、20、10、5和2.50μmol/L处理后si-PKM2-1009转染组的U87MG细胞存活率均低于F3-T3转染组(P=0.000,0.000,0.000,0.012,0.006,0.030,0.000,0.007,0.025),经替莫唑胺640、320、160、80、40、20、5μmol/L处理后si-PKM2-1377转染组U251MG细胞存活率亦低于F3-T3转染组(P=0.000,0.000,0.002,0.000,0.002,0.048,0.042);经替莫唑胺640、320、160、80、40、20μmol/L处理后TMZ+Compound 3k组U87MG细胞存活率低于TMZ组(P=0.000,0.000,0.000,0.000,0.001,0.002),经高浓度(640、320、160、80、40μmol/L)替莫唑胺处理后TMZ+Compound 3k组U251MG细胞存活率亦低于TMZ组(P=0.000,0.000,0.000,0.000,0.003),而经低浓度(10、5、2.50μmol/L)替莫唑胺处理后TMZ+Compound 3k组U251MG细胞存活率高于TMZ组(P=0.000,0.000,0.006)。(2)胶质母细胞瘤动物模型显示,荷瘤鼠存在替莫唑胺耐药。(3)生物信息学分析,F3-T3融合蛋白的生物学功能显著富集于DNA修复通路(P=0.000)。TCGA数据库中胶质瘤患者PKM2基因高表达组生存率和总生存期均低于低表达组(P<0.05)。(4)Western blotting法显示,经替莫唑胺处理48 h再更换培养基后24、36和48 h,F3-T3转染组U87MG(P=0.000,0.000,0.004)和U251MG(P=0.000,0.007,0.005)细胞p-H2AX蛋白相对表达量均低于空载体转染组;经替莫唑胺处理后F3-T3转染组U87MG和U251MG细胞均可见明显的PKM2入核,而空载体转染组细胞均未见这一现象;si-PKM2-1009和si-PKM2-1377分别敲低U87MG(P=0.000,0.001,0.006)和U251MG(P=0.000,0.000,0.000)细胞PKM2基因表达的效果最显著。结论F3-T3融合基因可促进PKM2入核,激活DNA损伤修复相关通路,进而介导胶质母细胞瘤对替莫唑胺耐药,不同细胞株对替莫唑胺的耐药浓度不一致,PKM2抑制剂可逆转这种耐药。

3D肿瘤支架的研究进展及其在药物筛选中的应用

3D肿瘤支架作为新兴的肿瘤细胞培养平台,能够重现肿瘤组织的3D结构,提供仿生微环境和降低肿瘤细胞的药物敏感性,在肿瘤生理学研究和肿瘤耐药机制研究中具有独特优势。综述了3D肿瘤支架的类型及其优缺点,从模拟肿瘤-间质细胞相互作用和肿瘤内部梯度缺氧环境两方面介绍了3D肿瘤支架模拟肿瘤微环境的研究进展,并对3D肿瘤支架在药物筛选中的应用进行分析。揭示了肿瘤支架在研究肿瘤耐药性机制、开发新型抗肿瘤药物,以及作为个性化肿瘤治疗临床前平台中的重要作用。最后对肿瘤支架的构建和应用提出设想和展望,旨在为构建高仿真肿瘤模型,研究肿瘤的异质性和肿瘤治疗方法提供参考。

免疫调节药物联合R-GemOx方案治疗复发/难治性弥漫大B细胞淋巴瘤的疗效及毒性影响评价

目的观察免疫调节药物联合R-GemOx方案治疗复发/难治性弥漫大B细胞淋巴瘤(relapsed/refractory diffuse large B-cell lymphoma,R/R-DLBCL)的疗效及毒性影响。方法选取2017年5月至2019年4月杭州市临平区第一人民医院收治的R/R-DLBCL患者144例,采用随机数字表法分为对照组(n=72)和观察组(n=72)。对照组采用R-GemOx方案治疗,观察组在对照组基础上加用沙利度胺治疗。比较两组肿瘤负荷指标、白细胞介素-10(interleukin-10,IL-10)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)的表达差异,观察两组疗效和不良反应,随访36个月,记录平均生存时间。结果治疗后,两组乳酸脱氢酶、β2-微球蛋白、IL-10、TNF-α均较治疗前下降,且观察组低于对照组,差异均有统计学意义(P<0.05)。观察组的客观缓解率和疾病控制率均高于对照组,但差异无统计学意义(P>0.05)。两组的不良反应主要以Ⅰ~Ⅱ级为主,观察组白细胞减少、血小板减少总发生率显著低于对照组(P<0.05)。随访36个月后,观察组平均生存时间显著长于对照组(P<0.05)。结论免疫调节药物联合R-GemOx方案治疗R/R-DLBCL可降低肿瘤负荷指标、IL-10、TNF-α的表达,减少白细胞减少、血小板减少等不良反应的发生。

新型超滤系统处理的成牛血清在细胞培养的应用及其对产毒效果的影响

为得到符合或优于牛血清质量标准的成牛血清,利用新型超滤系统对细胞培养用成牛血清原料进行处理。经过对3批已处理的成牛血清进行无菌检验、细胞促生长试验及接毒后产毒效果等各项检验,结果表明,经该超滤纯化工艺处理的成牛血清可替代新生牛血清用于细胞培养,且对产毒效果无影响。