Experimental study of the effect of adipose stromal vascular fraction cells on the survival rate of fat transplantation

Objective To investigate the effect of adipose stromal vascular fraction cells(SVFs)on the survival rate of fat ransplantation.Methods 0.5mL autologous fat tissue was mixed with: ① DiI-labeled autologous SVFs (Group A);②

Low dose effects on cultured mammalian cells...

The low dose effects induced by carbon ions on Chinese hamster V79 cells and murine melanoma B16 cells were investigated in this paper. Both cell lines were divided into four groups for irradiation: (1) control, (2) 0.02 Gy or 0.05 Gy(D1), (3) 1 Gy(D2), (4) D1+D2. The survivors and micronuclei were studied as biological endpoints. The results of group (1) and group (2) showed that there were no obvious differences on micronucleus frequency but there were significant increases when irradiation dose was 0.02Gy on colony formation efficiency. Although low dose ion irradiation could not contribute to DNA damages, it could enhance the colony formation efficiency. In the study of group (3) and (4), when the ion dose was 0.02 Gy, there were evident increases on surviving fraction and decreases on micronucleus frequency, but there were no statistical changes on these endpoints when the ion dose was 0.05Gy. This meant that high LET radiation could induce the adaptive response of cultured cells, furthermore, in the range of inducing ion dose , low dose irradiation was more profitable than high dose one.

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 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 N(omega)-nitro-L-arginine methyl ester (L-NAME) and N(omega)-nitro-L-arginine (L-NNA) on nitric oxide (NO) production induced by cytokines (TNF-alpha, IL-1 beta, and IFN-gamma) and bacterial lipopolysaccharide (LPS) mixture (CM) in the cultured rat hepatocytes, and examine their mechanisms action. METHODS: Rat hepatocytes were incubated with AG, L-NAME, L-NNA, Actinomycin D (ActD) and dexamethasone in a medium containing CM (LPS plus TNF-alpha, IL-1 beta, and IFN-gamma) for 24h. NO production in the cultured supernatant was measured with the Griess reaction. Intracellular cGMP level was detected with radioimmunoassy. RESULTS: NO production was markedly blocked by AG and L-NAME in a dose-dependent manner under inflammatory stimuli condition triggered by CM in vitro. The rate of the maximum inhibitory effects of L-NAME (38.9%) was less potent than that obtained with AG(53.7%, P 【 0.05). There was no significant difference between the inhibitory effects of AG and two L-arginine analogues on intracellular cGMP accumulation in rat cultured hepatocytes. Non-specific NOS expression inhibitor dexamethasone (DEX)and iNOS mRNA transcriptional inhibitor ActD also significantly inhibited CM-induced NO production. AG(0.1 mmol x L(-1)) and ActD (0.2 ng x L(-1)) were equipotent in decreasing NO production induced by inflammatory stimuli in vitro, and both effects were more potent than that induced by non-selectivity NOS activity inhibitor L-NAME (0.1 mmol x L(-1)) under similar stimuli conditions (P【0.01). CONCLUSION: AG is a potent selective inhibitor of inducible isoform of NOS,and the mechanism of action may be not only competitive inhibition in the substrate level, but also the gene expression level in rat hepatocytes.

Efficacy of Bee Products(Anzer Honey,Pollen and Propolis)in Detection and Healing of Damage Induced by Antidiabetic Drug Vildagliptin/Metformin Hydrochloride in Healthy Human Pancreatic Cells:Cytotoxic,Genotoxic and Biochemical Studies

Background and Objective Although drugs are powerful therapeutic agents,they have a range of side effects.These side effects are sometimes cellular and not clinically noticeable.Vildagliptin/metformin hydrochloride is one of the most widely used oral antidiabetic drugs with two active ingredients.In this study,we investigated its harmful effects on the metabolic activation system in healthy human pancreatic cells“hTERT-HPNE”,and we aimed to improve these harmful effects by natural products.To benefit from the healing effect,we used the unique natural products produced by the bees of the Anzer Plateau in the Eastern Black Sea Region of Turkey.Methods Cytotoxic and genotoxic effects of the drug were investigated by different tests,such as MTT,flow cytometry-apoptosis and comet assays.Anzer honey,pollen and propolis were analyzed by gas chromatography/mass spectrometry(G/C-MS).A total of 19 compounds were detected,constituting 99.9%of the samples.Results The decrease in cell viability at all drug concentrations was statistically significant compared to the negative control(P<0.05).A statistically significant decrease was detected in the apoptosis caused by vildagliptin/metformin hydrochloride with the supplementation of Anzer honey,pollen and propolis in hTERT-HPNE cells(P<0.05).Conclusion This study can contribute to other studies testing the healing properties of natural products against the side effects of oral antidiabetics in human cells.In particular,Anzer honey,pollen and propolis can be used as additional foods to maintain cell viability and improve heal damage and can be evaluated against side effects in other drug studies.

Cost-Effectiveness Analysis of Atezolizumab plus Pemetrexed and Platinum in First-Line Treatment of Non-Squamous Non-Small Cell Lung Cancer in China

Objective: To evaluate the cost-effectiveness of atezolizumab plus pemetrexed and platinum-based (APP) in the first-line treatment of non-squamous non- small cell lung cancer (NSCLC). Methods: A partitioned survival model (PSM) was constructed based on the IMpower132 clinical trial. Total cost, quality- adjusted life years (QALY), and incremental cost-effectiveness ratio (ICER) were the main outputs of the model. Deterministic sensitivity analysis and probabilistic sensitivity analysis were adopted to test the uncertainty of the parameters. Results: The results of the base-case analysis illustrated that compared with PP, the incremental cost of APP was CNY 591040.94, the incremental utility was 0.46 QALY, and the ICER was CNY 1291414.83/QALY. Deterministic sensitivity analysis results illustrated that atezolizumab and other parameters have a greater impact on ICER. Probabilistic sensitivity analysis results show that no matter how each parameter changes, under the willingness to pay threshold of 3-times Chinese per capita GDP, the probability of APP has cost-effectiveness is 0. Conclusion: From the perspective of the Chinese health system, APP is not cost-effective for first-line treatment of non-squamous non-small cell lung cancer without sensitizing EGFR or ALK genetic alterations.

Survivin在多发性骨髓瘤患者骨髓细胞中的表达及其临床意义

背景与目的:Survivin是凋亡抑制蛋白家族成员之一,在多种恶性肿瘤中高表达,但在正常成人分化组织无表达。其表达与多种肿瘤的预后及肿瘤对放、化疗的耐受有关。本研究旨在通过检测Survivin在正常人、初治及复发/难治多发性骨髓瘤(multiplemyeloma,MM)患者骨髓细胞及骨髓瘤细胞系KM3中的表达,以揭示Survivin在骨髓瘤中的表达与耐药及疗效的关系。方法:RT-PCR和Westernblot法检测29例MM患者(其中初治17例,复发/难治12例)、9例正常人骨髓标本及KM3细胞系中SurvivinmRNA和蛋白质水平表达。结果:骨髓瘤细胞系KM3高表达Survivin。SurvivinmRNA在正常人、初治和难治/复发MM患者骨髓细胞中阳性率分别为22.2%、70.5%和83.3%,表达水平(Survivin/β-actin比值)分别为0.06±0.04、0.31±0.14和0.69±0.24,骨髓瘤患者表达率和表达水平显著高于正常人(P<0.01),而难治/复发MM组表达水平高于初治组(P<0.05)。所有的正常人标本中均未检测到Survivin蛋白,在初治和难治/复发MM组Survivin蛋白阳性率分别为41.1%和58.3%(P>0.05),表达水平(Survivin/α-tubulin半定量比值)分别为0.11±0.07和0.21±0.12,难治/复发MM组明显为高(P<0.05)。17例初治患者中,7例Survivin阳性者4例部分缓解(partialresponse,PR),1例微小反应(minorresponse,MR),2例无变化(nochange,NC),有效率[完全缓解(completeresponse,CR)+PR+MR]71.4%;10例Survivin阴性者中2例CR,4例PR,2例MR,2例NC,有效率80%,略高于阳性组。但统计学分析未发现两组有效率存在显著性差异。结论:Survivin在骨髓瘤患者中的高表达可能是部分患者对化疗不敏感的原因之一,由于Survivin仅特异性表达于骨髓瘤细胞,Survivin可作为逆转骨髓瘤细胞耐药治疗中的潜在靶点。

肝癌细胞Survivin的表达及其与化疗药物顺铂敏感性的关系

目的对临床肝癌标本生存素(Suvivin)基因蛋白的表达进行研究,并分析其与化疗药物敏感性的关系。方法免疫组化SP法检测肝癌标本Survivin表达。对原代培养的肝癌细胞进行顺铂(cisplation,DDP)化学药物处理后检测细胞活性,建立肝癌细胞Survivin表达与化疗药物敏感性的关系。结果Survivin在肝癌中阳性表达率达66.7%(14/21),明显高于癌旁肝组织的9.5%(2/21)。对原代培养的肝癌细胞经过1.0 mg/L DDP处理,24 h后行MTT检测,Survivin阳性组的细胞存活率为47.6%,明显高于Survivin阴性组22.5%,两组间差异有统计学意义(P=0.0014)。结论肝癌细胞高表达Survivin,且Survivin阳性的癌细胞对DDP有一定耐受性,而Survivin阴性的癌细胞对DDP的敏感性较好。Survivin的检测有可能成为预测肝癌化疗敏感性的重要指标。

Survivin shRNA增强人卵巢癌耐药细胞OVCAR3对泰素敏感性的研究

背景与目的:耐药是目前恶性肿瘤治疗急需解决的难题。最近研究显示,卵巢癌组织及细胞中均有Survivin高表达,可能与其抑癌耐药有关。本研究探讨Survivin的短发夹状RNA(shorthairpinRNA,shRNA)对人卵巢癌耐药细胞OVCAR3Survivin基因表达、凋亡及其对泰素、顺铂敏感性的影响。方法:脂质体介导SurvivinshRNA转染OVCAR3。转染空载体或脂质体的细胞及未转染细胞作为对照。逆转录聚合酶链反应(reversetranscription-polymerasechainreaction,RT-PCR)检测SurvivinmRNA的表达,流式细胞仪分析Survivin蛋白的表达及细胞凋亡率。四甲基偶氮唑蓝法(MTT法)测定SurvivinshRNA转染后OVCAR3细胞对泰素的敏感性。结果:与未转染组、空脂质体组、空载体组相比较,SurvivinshRNA处理24h后细胞SurvivinmRNA及蛋白表达水平均明显下调。SurvivinshRNA转染12、24、36、48h后的细胞凋亡率分别为20.7%、31.9%、39.0%、46.7%,呈时间依赖性。MTT结果显示,泰素对未转染组、空脂质体组、空载体组、转染组OVCAR3细胞的IC50分别为(0.305±0.032)μmol/L、(0.157±0.031)μmol/L、(0.175±0.010)μmol/L、(0.019±0.001)μmol/L;顺铂对4组OVCAR3细胞的IC50依次为(9.410±0.796)μmol/L、(6.675±1.739)μmol/L、(6.930±1.273)μmol/L、(7.862±0.081)μmol/L,SurvivinshRNA使OVCAR3对泰素的敏感性提高16倍(P<0.01),但是对顺铂的影响不大(P>0.05)。结论:靶向Survivin的序列特异性shRNA可有效抑制OVCAR3细胞中Survivin基因的表达,同时可以增强OVCAR3对泰素的敏感性,但不增加其对顺铂的敏感性。

Autophagy and multidrug resistance in cancer

Multidrug resistance(MDR) occurs frequently after long-term chemotherapy, resulting in refractory cancer and tumor recurrence.Therefore, combatting MDR is an important issue. Autophagy, a self-degradative system, universally arises during the treatment of sensitive and MDR cancer. Autophagy can be a double-edged sword for MDR tumors: it participates in the development of MDR and protects cancer cells from chemotherapeutics but can also kill MDR cancer cells in which apoptosis pathways are inactive. Autophagy induced by anticancer drugs could also activate apoptosis signaling pathways in MDR cells, facilitating MDR reversal. Therefore, research on the regulation of autophagy to combat MDR is expanding and is becoming increasingly important. We summarize advanced studies of autophagy in MDR tumors, including the variable role of autophagy in MDR cancer cells.

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.

Paclitaxel-etoposide-carboplatin/cisplatin versus etoposidecarboplatin/cisplatin as first-line treatment for combined small-cell lung cancer: a retrospective analysis of 62 cases

Objective: To compare the efficacy and adverse effects of paclitaxel-etoposide-carboplatin/cisplatin(TEP/TCE) regimen with those of etoposide-carboplatin/cisplatin(EP/CE) regimen as first-line treatment for combined small-cell lung cancer(CSCLC).Methods: A retrospective study was conducted on 62 CSCLC patients who were treated at Tianjin Medical University Cancer Institute and Hospital from July 2000 to April 2013 and administered with TEP/TCE regimen(n=19) or EP/CE regimen(n=43) as first-line CSCLC treatment. All patients received more than two cycles of chemotherapy, and the response was evaluated every two cycles. The primary endpoint was overall survival(OS), and the secondary endpoints were progression-free survival(PFS), objective response rate(ORR), disease control rate(DCR), and adverse effects. Results: ORR between the TEP/TCE and EP/CE groups showed a statistical difference(90% vs. 53%, P=0.033). Both groups failed to reach a statistical difference in DCR(100% vs. 86%, P=0.212). The median PFS and OS of the TEP/TCE group were slightly longer than those of the EP/CE group, although both groups failed to reach a statistical difference(10.5 vs. 8.9 months, P=0.484; 24.0 vs. 17.5 months, P=0.457). However, stratified analysis indicated that the PFS of patients with stages III and IV CSCLC showed marginally significant difference between the TEP/TCE and EP/CE groups(19.5 vs. 7.6 months; P=0.071). Both rates of grade IV bone marrow depression and termination of chemotherapy in the TEP/TCE group were significantly higher than those in the EP/CE group(26.3% vs. 7.0%, P=0.036; 31.6% vs. 14.7%, P=0.004). Conclusion: The TEP/TCE regimen may not be preferred for CSCLC, and this three-drug regimen requires further exploration and research. To date, the EP/CE regimen remains the standard treatment for CSCLC patients.

Targeting autophagic pathways for cancer drug discovery

Autophagy , an evolutionarily conserved lysosomal degradation process , has drawn an increasing amount of attention in recent years for its role in a variety of human diseases, such as cancer. Notably, autophagy plays an important role in regulating several survival and death signaling pathways that determine cell fate in cancer. To date, substantial evidence has demonstrated that some key autophagic mediators, such as autophagy-related genes (ATGs), PI3K, mTOR, p53, and Beclin-1, may play crucial roles in modulating autophagic activity in cancer initiation and progression. Because autophagy-modulating agents such as rapamycin and chloroquine have already been used clinically to treat cancer, it is conceivable that targeting autophagic pathways may provide a new opportunity for discovery and development of more novel cancer therapeutics. With a deeper understanding of the regulatory mechanisms governing autophagy, we will have a better opportunity to facilitate the exploitation of autophagy as a target for therapeutic intervention in cancer. This review discusses the current status of targeting autophagic pathways as a potential cancer therapy.

Overexpression of heme oxygenase-1 protects smooth muscle cells against oxidative injury and inhibits cell proliferation

To investigate whether the expression of exogenous heme oxygenase-1 (HO-1) gene within vascular smooth muscle cells (VSMC) could protect the cells from free radical attack and inhibit cell proliferation, we established an in vitro transfection of human HO-1 gene into rat VSMC mediated by a retroviral vector. The results showed that the profound expression of HO-1 protein as well as HO activity was 1.8- and 2.0-fold increased respectively in the transfected cells compared to the non-transfected ones. The treatment of VSMC with different concentrations of H2O2 led to the remarkable cell damage as indicated by survival rate and LDH leakage. However, the resistance of the HO-1 transfected VSMC against H2O2 was significantly raised. This protective effect was dramatically diminished when the transfected VSMC were pretreated with ZnPP-IX, a specific inhibitor of HO, for 24 h. In addition, we found that the growth potential of the transfected cells was significantly inhibited directly by increased activity of HO-1, and this effect might be related to decreased phosphorylation of MAPK. These results suggest that the overexpression of introduced hHO-1 is potentially able to reduce the risk factors of atherosclerosis, partially due to its cellular protection against oxidative injury and to its inhibitory effect on cellular proliferation.

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

AIM: To evaluate antihepatoma effect of antisense phosphorothioate oligodeoxyribonucleotides (S-ODNs) targeted to alpha-fetoprotein (AFP) genes in vitro and in nude mice. METHODS: AFP gene expression was examined by immunocytochemical method or enzyme-linked immunosorbent assay. Effect of S-ODNs on SMMC-7721 human hepatoma cell growth in vitro was determined using microculture tetrazolium assay. In vitro antitumor activities of S-ODNs were monitored by measuring tumor weight differences in treated and control mice bearing SMMC-7721 xenografts. Induction of cell apoptosis was evaluated by fluorescence-activated cell sorter (FACS) analysis. RESULTS: Antisense S-ODN treatment led to reduced AFP gene expression. Specific antisense S-ODNs, but not control S-ODNs, inhibited the growth of hepatoma cells in vitro. In vitro, only antisense S-ODNs exhibited obvious antitumor activities. FACS analysis revealed that the growth inhibition by antisense S-ODNs was associated with their cell apoptosis induction. CONCLUSION: Antisense S-ODNs targeted to AFP genes inhibit the growth of human hepatoma cells and solid hepatoma, which is related to their cell apoptosis induction.

Adeno-associated virus mediated endostatin gene therapy in combination with topoisomerase inhibitor effectively controls liver tumor in mouse model

AIM:rAAV mediated endostatin gene therapy has been examined as a new method for treating cancer.However, a sustained and high protein delivery is required to achieve the desired therapeutic effects.We evaluated the impact of topoisomerase inhibitors in rAAV delivered endostatin gene therapy in a liver tumor model. METHODS:rAAV containing endostatin expression cassettes were transduced into hepatoma cell lines.To test whether the topoisomerase inhibitor pretreatment increased the expression of endostatin,Western blotting and ELISA were performed.The biologic activity of endostatin was confirmed by endothelial cell proliferation and tube formation assays. The anti-tumor effects of the rAAV-endostatin vector combined with a topoisomerase inhibitor,etoposide,were evaluated in a mouse liver tumor model. RESULTS:Topoisomerase inhibitors,including camptothecin and etoposide,were found to increase the endostatin exPression level in vitro.The over-expressed endostatin, as a result of pretreatment with a topoisomerase inhibitor, was also biologically active.In animal experiments,the combined therapy of topoisomerase inhibitor,etoposide with the rAAV-endostatin vector had the best tumor- suppressive effect and tumor foci were barely observed in livers of the treated mice.Pretreatment with an etoposide increased the level of endostatin in the liver and serum of rAAV-endostatin treated mice.Finally,the mice treated With rAAV-endostatin in combination with etoposide showed the longest survival among the experimental models. CONCLUSION:rAAV delivered endostatin gene therapy in combination with a topoisomerase inhibitor pretreatment is an effective modality for anticancer gene therapy.

Ruxolitinib add-on in corticosteroid-refractory graft-vs-host disease after allogeneic stem cell transplantation:Results from a retrospective study on 38 Chinese patients

BACKGROUND Graft-vs-host disease (GVHD) is a major cause of mortality after allogeneic hematopoietic stem cell transplantation.Some patients have steroid-refractory(SR) GVHD.AIM To evaluate the effect and safety of ruxolitinib add-on in the treatment of patients with SR acute (a) and chronic (c) GVHD.METHODS We retrospectively analyzed 38 patients administered ruxolitinib add-on to standard immunosuppressive therapy for SR-aGVHD or SR-cGVHD following allogeneic hematopoietic stem cell transplantation.Ruxolitinib was administered5-10 mg/d depending on disease severity,patient status,and the use of antifungal drugs.Overall response rate,time to best response,malignancy relapse rate,infection rate,and treatment-related adverse events were assessed.RESULTS The analysis included 10 patients with SR-aGVHD (gradeⅢ/Ⅳ,n=9) and 28patients with SR-cGVHD (moderate/severe,n=24).For the SR-aGVHD and SRcGVHD groups,respectively:Median number of previous GVHD therapies was 2(range:1-3) and 2 (1-4);median follow-up was 2.5 (1.5-4) and 5 (1.5-10) mo;median time to best response was 1 (0.5-2.5) and 3 (1-9.5) mo;and overall response rate was 100%(complete response:80%) and 82.1%(complete response:10.7%) with a response observed in all GVHD-affected organs.The malignancy relapse rates for the SR-aGVHD and SR-cGVHD groups were 10.0%and 10.7%,respectively.Reactivation rates for cytomegalovirus,Epstein-Barr virus,and varicella-zoster virus,respectively,were 30.0%,10.0%,and 0%for the SR-aGVHD group and 0%,14.3%,and 7.1%for the SR-cGVHD group.CONCLUSION Ruxolitinib add-on was effective and safe as salvage therapy for SR-GVHD.

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 beta-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 beta-tubulin isotype II, III expressions in S-2/TXT were increased remarkably. CONCLUSION: The both intrinsic and acquired TXT-related drug resistance in these PAC cell lines is mainly mediated by P-gp, but had no relationship to MRP and LRP expressions. The increases of beta-tubulin isotype II, III might be collateral changes that occur when the SUIT-2 cells are treated with TXT.

原代肿瘤细胞化疗药物敏感性检测指导下治疗对晚期癌症患者生存预后及肿瘤标志物的影响

目的探讨原代肿瘤细胞化疗药物敏感性检测指导下治疗对晚期癌症患者生存预后及肿瘤标志物的影响。方法以2022年1月至2023年4月在华南大学第一附属医院就诊的107例晚期癌症患者为研究对象,按不同化疗方案分为观察组(n=41例)和对照组(n=66例)。观察组:原代肿瘤细胞化疗药物敏感性检测指导下进行化疗;对照组:接受FOLFOX4(奥沙利铂+5⁃氟尿嘧啶+亚叶酸钙)方案化疗,随访12个月。比较两组完全缓解(CR)、部分缓解(PR)、稳定性疾病(SD)、病情进展(PD),计算有效缓解率(ORR)和疾病控制率(DCR);比较两组肿瘤标志物[鳞状上皮细胞癌抗原(SCC)、癌胚抗原(CEA)、糖类抗原125(CA125)、细胞角蛋白片段19(CYFRA21⁃1)];采用Kaplan⁃Meier生命曲线进行生存分析。结果观察组ORR率与DCR率均显著高于对照组,差异有统计学意义(P<0.05)。经治疗,两组血清SCC、CEA、CA125与CYFRA21⁃1水平均相应下降(P<0.05),且观察组低于对照组,差异有统计学意义(P<0.05)。Kaplan⁃Meier生命曲线分析结果显示,观察组PFS、OS与对照组比较差异有统计学意义(P<0.05)。结论原代肿瘤细胞化疗药物敏感性检测指导下治疗晚期癌症,改善患者预后,对癌症晚期个体化治疗方案具有一定的指导价值。

载药微球对比碘化油肝动脉化疗栓塞联合局部热消融治疗巨块型肝癌的疗效分析

目的 对比碘化油肝动脉化疗栓塞(C-TACE)与载药微球肝动脉化疗栓塞(D-TACE)联合局部热消融治疗巨块型肝癌的疗效。方法 选择2018年4月至2021年6月在南阳市第一人民医院就诊的巨块型肝癌患者72例,以随机数字表法分为研究组36例,对照组36例。对照组采用局部热消融联合C-TACE治疗,研究组采用局部热消融联合D-TACE治疗。对比2组临床疗效、肿瘤标志物、肝功能、血清学指标、血流灌注指标、不良反应,术后随访2年,对比2组无进展生存期(PFS)。结果 研究组疾病控制率(DCR)、客观缓解率(ORR)比对照组高(P<0.05)。术后3个月,2组甲胎蛋白(AFP)、异常凝血酶原(PIVKA-Ⅱ)水平均降低(P<0.05),且研究组更低;2组丙氨酸转氨酶(ALT)均升高(P<0.05),而研究组低于对照组;2组白蛋白(ALB)均降低(P<0.05),而研究组高于对照组(P<0.05);2组表皮生长因子受体(EGFR)、血管内皮生长因子(VEGF)、胸腺激酶1(TK1)水平均降低(P<0.05),且研究组更低;2组血容量(BV)、血流量(BF)均降低(P<0.05),且研究组更低;2组对比剂平均通过时间(MTT)均升高(P<0.05),且研究组更高。研究组不良反应总发生率比对照组低(P<0.05)。术后随访2年,2组各失访1例,随访率为97.22%,研究组中位PFS为15.41个月(95%CI:7.02~23.19),对照组中位PFS为12.34个月(95%CI:6.16~22.30),研究组PFS曲线优于对照组(P<0.05)。结论 局部热消融联合D-TACE可改善巨块型肝癌患者肝功能、血流灌注情况,疗效显著,降低肿瘤标志物,调节血清EGFR、VEGF、TK1表达,安全可靠,且可延长中位PFS。