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.

Relationship between Fas/ FasL expression and apoptosis of colon adenocarcinoma cell lines

INTRODUCTIONFas/ FasL system has been identified as a keymediator of apoptosis in tumor cells[1-4]. Theoccurrence and development of neoplasm are closelyrelated to apoptosis[5-7] Most chemotherapeuticdrugs kill cancer cells mainly by inducingapoptosis[8-14].'

Multimodality treatment in hepatocellular carcinoma patients with tumor thrombi in portal vein

AIM: To compare the therapeutic effect and significances of multimodality treatment for hepatocellular carcinoma (HCC) with tumor thrombi in portal vein (PVTT). METHODS: HCC patients (n=147) with tumor thrombi in the main portal vein or the first branch of portal vein were divided into four groups by the several therapeutic methods. There were conservative treatment group in 18 out of patients (group A); and hepatic artery ligation(HAL) and/or hepatic artery infusion (HAI) group in 18 patients (group B), in whom postoperative chemoembolization was done periodically; group of removal of HCC with PVTT in 79 (group C) and group of transcatheter hepatic arterial chemoembolization (TACE) or HAI and/or portal vein infusion (PVI) after operation in 32 (group D). RESULTS: The median survival period was 12 months in our series and the 1-,3-, and 5-year survival rates were 44.3%, 24.5% and 15.2%, respectively. The median survival times were 2, 5, 12 and 16 months in group A, B, C and D, respectively. The 1-, 3- and 5-year survival rates were 5.6%, 0% and 0% in group A; 22.2%, 5.6% and 0% in group B; 53.9%, 26.9% and 16.6% in group C; 79.3%, 38.9% and 26.8% in group D, respectively. Significant difference appeared in the survival rates among the groups (P 【 0.05). CONCLUSION: Hepatic resection with removal of tumor thrombi and HCC should increase the curative effects and be encouraged for the prolongation of life span and quality of life for HCC patients with PVTT, whereas the best therapeutic method for HCC with PVTT is with regional hepatic chemotherapy or chemoembolization after hepatic resection with removal of tumor thrombi.

Intensify standardized therapy for esophageal and stomach cancer in tumor hospitals

INTRODUCTIONCancer treatment situation in tumor hospitals inChina has its own unique characteristics which arenot found in other parts of the world. Because ofthe huge population and high incidence rates ofesophageal and stomach cancer[1-5], the number ofcancer patients waiting for admission isinconceivably large.

Mechanical properties of hepatocellular carcinoma cells

AIM: To study the viscoelastic properties of human hepatocytes and hepatocellular carcinoma (HCC) cells under cytoskeletal perturbation, and to further to study the viscoelastic properties and the adhesive properties of mouse hepatoma cells (HTC) in different cell cycle. METHODS: Micropipette aspiration technique was adopted to measure viscoelastic coefficients and adhesion force to collagen coated surface of the cells. Three kinds of cytoskeleton perturbing agents, colchicines (Col), cytochalasin D (CD) and vinblastine (VBL), were used to treat HCC cells and hepatocytes and the effects of these treatment on cell viscoelastic coefficients were investigated. The experimental results were analyzed with a three-element standard linear solid. Further, the viscoelastic properties of HTC cells and the adhesion force of different cycle HTC cells were also investigated. The synchronous G(1) and S phase cells were achieved through thymine-2-desoryriboside and colchicines sequential blockage method and thymine-2-desoryriboside blockage method respectively. RESULTS: The elastic coefficients, but not viscous coefficient of HCC cells (K(1)=103.6+/-12.6N.m(-2), K(2)=42.5 +/ 10.4N.m(-2), mu=4.5 +/- 1.9Pa.s), were significantly higher than the corresponding value for hepatocytes (K(1)=87.5 +/- 12.1N.m(-2), K(2)=33.3+/-10.3N.m(-2), mu=5.9+/-3.0Pa.s, P【0.01). Upon treatment with CD, the viscoelastic coefficients of both hepatocytes and HCC cells decreased consistently, with magnitudes for the decrease in elastic coefficients of HCC cells (K(1): 68.7 N.m(-2) to 81.7N.m(-2), 66.3% to 78.9%; K(2): 34.5N.m(-2) to 37.1N.m(-2), 81.2% to 87.3%, P【0.001) larger than those for normal hepatocytes (K(1): 42.6N.m(-2) to 49.8N.m(-2), 48.7% to 56.9%; K(2): 17.2N.m(-2) to 20.4N.m(-2), 51.7% to 61.3%, P【0.001). There was a little decrease in the viscous coefficient of HCC cells (2.0 to 3.4Pa.s, 44.4 to 75.6%, P【0.001) than that for hepatocytes (3.0 to 3.9Pa.s, 50.8 to 66.1% P【0.001). Upon treatment with Col and VBL, the elastic coefficients of hepatocytes generally increased or tended to increase while those of HCC cells decreased. HTC cells with 72.1% of G(1) phase and 98.9% of S phase were achieved and high K(1), K(2) value and low mu value were the general characteristics of HTC cells. G(1) phase cells had higher K(1) value and lower mu value than S phase cells had, and G(1) phase HTC cells had stronger adhesive forces ((275.9 +/- 232.8) x 10(-10)N) than S phase cells ((161.2 +/- 120.4) x 10(-10)N, P【0.001). CONCLUSION: The difference in both the pattern and the magnitude of the effect of cytoskeletal perturbing agent on the viscoelastic properties between HCC cells and hepatocytes may reflect differences in the state of the cytoskeleton structure and function and in the sensitivity to perturbing agent treatment between these two types of cells. Change in the viscoelastic properties of cancer cells may affect significantly tumor cell invasion and metastasis as well as interactions between tumor cells and their micro-mechanical environments.

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.

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.

Effect of heparin on apoptosis in human nasopharyngeal carcinoma CNE2 cells

In order to study the mechanism of the effect of heparin on apoptosis in carcinoma cells, the nasopharyngeal carcinoma cell line CNE2 was used to identify the effect of heparin on apoptosis associated with the expression of c-myc, bax, bcl-2 proteins by use of Hoechst 33258 staining, terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), agarose gel electrophoresis, and flow cytometry, as well as Western blot analysis. The results showed that heparin induced apoptosis of CNE2 cells including the morphologic changes such as reduction in the volume, and the nuclear chromatin condensation, as well as the 'ladder pattern' revealed by agarose gel electrophoresis of DNA in a concentration-dependent manner. The number of TUNEL-positive cells was dramatically increased to 33.6+/-1.2% from 2.8+/-0.3% by treatment with heparin in different concentrations (10 to approximately 40 kU/L). The apoptotic index was increased to 32.5% from 3.5% by detecting SubG1 peaks on flow cytometry. Western blot analysis showed that levels of bcl-2, bax and c-myc were significantly overexpressed by treatment with the increase of heparin concentrations. These results suggest that heparin induces apoptosis of CNE2 cells, which may be regulated by differential expression of apoptosis-related genes.

Transretinoic acid inhibits rats gastric epithelial dysplasia induced by N-methyi-N-nitro-N-nitrosoguanidine:influences on cell apoptosis and expression of its regulatory genes

INTRODUCTIONGastric epithelial dysplasia (GED) hypothetically is a straight-forward concept: dysplastic epithelium replacing the normal gastric epithelium of the stomach [1].In the stomach ,like any other segment of the gut ,it is defined as an unequivocal non-invasive epithelial change[2,3].The observation of gastric dysplasia as a cancerous lesion was recognized over a century ago ,but it is only after the advent of gastroscopy that its clinical significance has been stressed[4-7].

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.

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].

前列腺癌间歇性内分泌治疗的临床观察及其疗效影响因素分析

目的:观察间歇性内分泌治疗在不同分期及分级的前列腺癌患者中的效果,并分析影响疗效的可能相关因素。方法:对45例不同分期及分级的前列腺癌患者进行间歇性内分泌治疗:首先行激素诱导治疗即药物去势和/或抗雄激素治疗,停止治疗的时机为保持前列腺特异抗原(prostate specific antigen,PSA)≤0.2μg/L(ng/mL)水平持续3个月,以后根据每月PSA的检测结果决定是否再行内分泌治疗。随访观察患者治疗的轮数和治疗期及间歇期的时间。根据治疗效果将上述患者分为治疗耐受较好和治疗耐受较差两组,单因素分析比较两组患者在人口统计学、临床、生化、影像、病理等方面的差异,并使用非条件Logistic回归分析探讨影响治疗耐受的独立相关因素。结果:平均随访时间为40.7±13.4个月。45例患者中,41名患者进入第2轮治疗,其中8例患者在第2轮治疗期间进展为雄激素非依赖性前列腺癌;8例中7例患者均为T3-4M0或M1期且Gleason评分≥8分。16名患者进入第3轮治疗,其中有14名分期为Ⅲ期以内,有13名患者Gleason评分≤7分。第1到第4周期平均间歇期(分别占第1到第4疗程时间的百分比)分别为8.7±5.4个月(47.1%),8.4±4.9个月(49.3%),7.0±3.4个月(43.7%),3.7±0.6个月(42.5%)。5例患者在治疗过程中出现骨转移,目前没有患者死亡。按照评价标准将患者分为治疗耐受较好(n=16)与治疗耐受较差两组(n=29),与治疗耐受较差的患者相比,治疗耐受较好的患者Gleason评分较低(P=0.002),PSA值较低(P=0.053),Ⅳ期患者较少(P=0.001)。相反,年龄、有无骨转移、淋巴结转移及有无复发等差异均无统计学意义。非条件Logistic回归分析显示Ⅳ期患者所占比例是唯一影响治疗的独立相关因素(OR=12.113,95%CI1.330～110.312,P=0.027)。结论:能坚持较多治疗周期的患者多为肿瘤分化较好的Ⅲ期及以内的病患,而较快进展为激素非依赖性的患者多为分化较差的Ⅳ期患者,间歇性内分泌治疗可能更适合于Ⅲ期以内患者。

促性腺激素释放激素及其受体在肿瘤治疗中的应用

促性腺激素释放激素(GnRH)是由下丘脑神经元分泌的一种十肽类激素,其生理功能是调节垂体前叶促性腺激素的分泌,进而刺激黄体生成素及卵泡刺激素的分泌以调节性激素的水平。GnRH对垂体外的多种外周组织的生理功能也有调节作用。近年研究发现,乳腺、卵巢、子宫内膜、前列腺、胰腺、肺、肝脏发生的肿瘤细胞上均有GnRH受体分布,GnRH类似物可抑制这些肿瘤细胞生长。GnRH及其类似物的抗肿瘤效应是通过调节垂体促性腺激素水平来实现的。本文对GnRH及其受体在肿瘤治疗中的应用进展进行综述。

抗肿瘤药物对肾上腺机制影响的研究进展

多种抗肿瘤药物如激素类、化疗、靶向药物和免疫检查点抑制剂在发挥抗癌作用的同时对内分泌腺具有毒性作用,其中对肾上腺的影响逐渐受到临床重视。药物治疗相关的肾上腺功能不全若无法及时诊治,可导致肾上腺危象的发生甚至危及生命。本文将就抗肿瘤药物对肾上腺机制影响进行综述,为临床防治肿瘤患者的肾上腺功能异常提供指导。

Adjuvant therapy in pancreatic cancer

The outlook for patients with pancreatic cancer has been grim. There have been major advances in the surgical treatment of pancreatic cancer, leading to a dramatic reduction in post-operative mortality from the development of high volume specialized centres. This stimulated the study of adjuvant and neoadjuvant treatments in pancreatic cancer including chemoradiotherapy and chemotherapy. Initial protocols have been based on the original but rather small GITSG study first reported in 1985. There have been two large European trials totalling over 600 patients (EORTC and ESPAC-1) that do not support the use of chemoradiation as adjuvant therapy. A second major finding from the ESPAC-1 trial (541 patients randomized) was some but not conclusive evidence for a survival benefit associated with chemotherapy. A third major finding from the ESPAC-1 trial was that the quality of life was not affected by the use of adjuvant treatments compared to surgery alone. The ESPAC-3 trial aims to assess the definitive use of adjuvant chemotherapy in a randomized controlled trial of 990 patients.

托瑞米芬治疗乳腺囊性增生症临床疗效的初步观察

为了观察托瑞米芬(枢瑞)治疗乳腺囊性增生症的临床疗效。选取临床症状及体征均明显的乳腺囊性增生 症100例,试验组(50例)给予托瑞米芬40mg口服,1次/d,连用3个月,并根据乳腺活检后ER结果分成ER(+)及 ER(-)两个亚组观察其临床疗效。对照组(50例)给予中成药(乳癖散结胶囊)对症治疗,连用3个月。托瑞米芬治 疗乳腺囊性增生症的临床有效率为80%(40/50),对ER(+)患者疗效更高,有效率92.9%(26/28)。无明显的毒副 反应。乳癖散结胶囊对照组临床有效率为58%(29/50),两组比较差异有统计学意义,0.01<P<0.025。初步研究 结果提示,托瑞米芬治疗乳腺囊性增生症临床疗效确切、不良反应小,是目前较为理想的药物选择之一。

Apoptosis susceptibility of tumor cells to arsenic trioxide and the inherent cellular level of reactive oxygen species

OBJECTIVE: To explore the association of inherent cellular reactive oxygen species (ROS) levels with susceptibility of the tumor cells to apoptosis induction by arsenic trioxide (As(2)O(3)). METHODS: Low concentration (2 micromol/L) of As(2)O(3) was administered to two cultured leukemic cell lines, NB4 and U937, and two esophageal carcinoma cell lines, EC1.71 (also named EC/CUHK1) and EC1867, to confirm the difference in apoptosis susceptibility of NB4 versus U937 and of EC1.71 versus EC1867. Dihydrogenrhodamine 123 (DHR123), used as a ROS capture agent, was incubated with cells in the absence of As(2)O(3). Fluorescence intensity of rhodamine 123, the product of cellular oxidation of DHR123, was detected by flow cytometry and ROS was measured. RESULTS: Low concentration of As(2)O(3) induced apoptosis was more likely to occur in NB4 and EC1.71 cells than in U937 and EC1867 cells, or NB4 was more sensitive than U937, and EC1.71 more sensitive than EC1867 to As(2)O(3). The inherent cellular ROS level is higher in NB4 than in U937, and also higher in EC1.71 than in EC1867. CONCLUSIONS: The difference in cellular ROS level is positively associated with cellular susceptibility to apoptosis induction by As(2)O(3). The inherent ROS level might be important in defining apoptotic susceptibility to As(2)O(3).

Plating densities, alpha-difluoromethylornithine effects and time dependence on the proliferation of IEC-6 cells

OBJECTIVE: To characterize the role of plating densities and alpha-difluoromethylornithine (DFMO) on the proliferation of IEC-6 cells in vitro. METHODS: IEC-6 cells were seeded in 96-well microplates at various densities in the presence or absence of DFMO. Cells were counted and their proliferative capability was monitored Days 1 to 7 with MTT assay at an optical density of 570 nm. RESULTS: There was a positive relationship between cell number and OD value (r = 0.954, P 0.5 x 10(4) cells/well) inhibited the growth of cells on Day 2. When the density reaches 4 x 10(4) cells/well, the OD value increased gradually and reached a peak on Day 5. After that, the OD value began to fall. The growth of IEC-6 cells was limited at a low density (0.2 x 10(4) cells/well) on Day 4. DFMO caused a complete inhibition of proliferation of IEC-6 cells on Days 1 to 3. CONCLUSION: Proliferation of IEC-6 cells is related to plating density and incubation time. It is inhibited by DFMO, but is reversible when the incubation time is prolonged.

Arsenic trioxide induces multiple myeloma cell apoptosis via disruption of mitochondrial transmembrane potentials and activation of caspase-3

OBJECTIVE: To investigate the response of multiple myeloma (MM) cells to arsenic trioxide (As2O3) and their possible mechanisms. METHODS: Two MM-derived cell lines RPMI8226 and U266 cells were used as in vitro models. Cell apoptosis was assessed by morphology, flow cytometry, and DNA gel electrophoresis. Mitochondrial transmembrane potentials (delta psi m) were evaluated by measuring cellular Rhodamine 123 staining intensity. Protein expression was analyzed using Western blot. RESULTS: Zero point one to 0.5 mumol/L As2O3 inhibited cell proliferation and 2.0 mumol/L As2O3 induced cell apoptosis, while 1.0 mumol/L As2O3 inhibited proliferation with a weak degree of apoptosis induction in RPMI8226 and U266 cell lines. As2O3-induced apoptosis was accompanied by mitochondrial transmembrane potentials (delta psi m) collapse and caspase-3 activation in the presence of intact membrane. Glutathione depleter buthionine sulfoximine enhanced, while disulfide bond-reducing agent dithiothreitol partially antagonized As2O3-induced delta psi m collapse and apoptosis in MM cells. All-trans retinoic acid (ATRA) could also induce apoptosis in RPMI8226 cells, but it did not show any cooperative effects with As2O3. CONCLUSION: As2O3 exerts apoptosis-inducing and growth-inhibiting effects on MM cells, and mitochondrium is a pivotal and common target of As2O3 for apoptosis induction.

短期新辅助治疗对前列腺癌组织内聚集素蛋白表达的影响

目的 探讨短期新辅助治疗(NHT)后前列腺癌组织学及癌细胞内聚集素蛋白表达的变化及其临床意义。方法 采用免疫组织化学方法,对未行雄激素阻断治疗的 26例前列腺癌患者前列腺癌根治术(RP)标本(26份,无NHT组 ), 19例行 3个月NHT患者NHT前穿刺活检标本及NHT后的RP标本(NHT组),行前列腺癌组织内聚集素蛋白表达水平的测定,观察NHT对癌组织中聚集素蛋白表达水平的影响。结果 聚集素主要存在于前列腺癌细胞的细胞浆中,部分存在于细胞外间质。NHT组NHT前癌组织中聚集素表达较弱,染色强度平均值为 1 .42±0 .51,NHT后表达较强,染色强度平均值为 2 .16±0. 60(t=7. 10,P<0. 01);NHT组NHT后聚集素表达高于无NHT组 (染色强度平均值为 1 .57±0. 70,t=2 91,P<0 .01)。结论 雄激素阻断治疗可使前列腺癌细胞内聚集素适应性上调,针对聚集素的辅助治疗可提高激素阻断治疗的效果。