Augmentation of cisplatin sensitivity in cisplatin-resistant human bladder cancer cells by modulating glutathione concentrations and glutathione-related enzyme activities

OBJECTIVES: To investigate the roles of glutathione and glutathione-S-transferase (GST) in cisplatin-resistance mechanisms in human bladder cancer, by using glutathione-depleting or GST-blocking agents. MATERIALS AND METHODS: Cisplatin-resistant human bladder cancer cell lines were established by continuous exposure of T24 cells to increasing concentrations of cisplatin. Buthionine sulphoximine (BSO), ethacrynic acid and indomethacin were used to deplete glutathione or block GST. Intracellular glutathione content, GST activity and cisplatin cytotoxicity were determined after exposing parental and drug-resistant cell lines to these agents. RESULTS: Intracellular glutathione content and GST activity were significantly decreased, and cisplatin cytotoxicity significantly enhanced, in both parental and resistant cell lines by glutathione-depleting or GST-blocking agents. However, the resistance of cisplatin-resistant cell lines did not fully recover to that of the parental cells with combined BSO and indomethacin. CONCLUSIONS: Both increased glutathione content and GST activity are significant in the cisplatin resistance of human bladder tumour cells. Because BSO, ethacrynic acid and indomethacin caused a partial recovery of resistance in the cisplatin-resistant cell line, further studies are needed to investigate their efficacy for treating patients with metastatic bladder carcinoma resistant to cisplatin.     

线粒体途径在肿瘤坏死因子凋亡诱导配体诱导结肠癌细胞凋亡中的调节作用

目的探讨线粒体途径在肿瘤坏死因子凋亡诱导配体(TRAIL)诱导结肠癌细胞凋亡过程中的调节作用,为临床合理用药提供理论指导。方法采用流式细胞仪技术、荧光显色技术和Western印迹技术检测TRAIL处理结肠癌细胞SW1116后,在不同时间细胞凋亡情况、线粒体完整性改变(ΔΨm、cardiolipin情况)以及线粒体下游通路细胞色素C和Caspase-9的表达情况。结果TRAIL诱发结肠癌细胞凋亡,于4 h达凋亡高峰,凋亡指数为32．98%；在4 h出现线粒体ΔΨm下降和cardiolipin丢失增加,造成其内膜损伤；细胞色素C表达及Caspase-9酶活性随时间的延长而增加,24 h酶活性达到最大峰值为(48．12±2．21)μmol·L~(-1)·h~(-1)·mg~(-1)蛋白。TRAIL诱导的线粒体损伤可被Caspase抑制剂Z-VAD．fmk所抑制。结论线粒体途径参与TRAIL诱导结肠癌细胞的凋亡过程,以Caspase依赖方式引发线粒体ΔΨm和cardiolipin丢失,造成内膜损伤,导致细胞色素C释放和Caspase-9激活,诱发凋亡。     

Enhanced S100 calcium‐binding protein P expression sensitizes human bladder cancer cells to cisplatin

What’s known on the subject? and What does the study add? So far, several molecules have been reported to be involved in cisplatin resistance. This study revealed that a decreased expression of S100P is implicated in cisplatin resistance. In addition, S100P overexpression rendered bladder cancer cells sensitive to cisplatin.

OBJECTIVE

• ? To investigate the role of S100 calcium‐binding protein P (S100P) in the gain of cis‐diamminedichloroplatinum (II) (cisplatin) resistance in bladder cancer, having previously found, with cDNA microarrays using two pairs of parental (T24, KK47) and their cisplatin‐resistant bladder cancer cell lines (T24/DDP10, KK47/DDP20), that S100P mRNA expression was significantly reduced in cisplatin‐resistant cells.

MATERIALS AND METHODS

• ? S100P mRNA and protein expression levels were investigated by northern and western blot analyses, respectively.
• ? Intracellular S100P localization was examined by immunocytochemistry and immunohistochemistry.
• ? S100P over‐expression, obtained by transfection with S100P expression plasmid, was used to investigate whether or not S100P affected cellular resistance to cisplatin.

RESULTS

• ? S100P mRNA showed increased expression by cisplatin stimulation in parental cell lines.
• ? On the other hand, S100P mRNA and protein expression levels were markedly reduced in cisplatin‐resistant cells.
• ? The over‐expression of S100P in resistant cells resulted in an increased sensitivity to cisplatin.

CONCLUSIONS

• ? In bladder cancer cells, S100P was expressed and localized mainly in the nucleus.
• ? S100P expression was also involved in cisplatin sensitivity.
• ? S100P might thus represent a molecular marker predicting cisplatin sensitivity and a molecular therapeutic target for cisplatin‐based chemotherapy.

     

Identification of effective retinoids for inhibiting growth and inducing apoptosis in bladder cancer cells

PURPOSE: Retinoids modulate the growth and differentiation of normal and malignant epithelial cells in vitro and in vivo, and inhibit bladder carcinogenesis in animal models. Retinoid analogs have been used in several clinical chemoprevention trials of superficial bladder cancer recurrence. There is a clear need to identify new effective retinoids and develop novel approaches for the chemoprevention and treatment of superficial bladder cancer. We investigated the effects of various retinoids on growth inhibition and apoptosis induction in bladder cancer cell lines. MATERIALS AND METHODS: Ten grades 1 to 3 bladder cancer cell lines and the 4 retinoids all-trans-retinoic acid, 9-cis retinoic acid, 4-(N-hydroxyphenyl) retinamide (4HPR) and LGD1069 were used in the study. We compared the ability of these retinoids to inhibit growth, induce apoptosis, affect the expression of nuclear retinoid receptors and modulate apoptosis related genes. RESULTS: Most bladder cancer cell lines did not express retinoic acid receptor beta and were resistant to the effect of all-trans-retinoic acid and 9-cis retinoic acid on growth inhibition and apoptosis induction, even at a concentration of 10(-5) M. The 2 cell lines that expressed retinoic acid receptor beta were constitutively sensitive to the growth inhibitory effect of all-trans-retinoic acid. 4HPR inhibited cell growth by about 90% in all but 1 cell line and induced apoptosis at a concentration of 10(-5) M after a 24-hour treatment. LGD1069 had virtually no effect. All-trans-retinoic acid and 4HPR induced retinoic acid receptor beta expression in 1 bladder cancer cell line. However, the effect of 4HPR on cell growth and apoptosis were not related to the constitutive expression of retinoic acid receptor beta. 4HPR decreased bcl-2 expression in 6 of 8 bladder cancer cell lines but did not change p53 gene expression. CONCLUSIONS: The results demonstrate that 4HPR is the most potent growth inhibitor and apoptosis inducer of the retinoids tested. Lack of retinoic acid receptor beta expression may be responsible for cell resistance to all-trans-retinoic acid but not to the other retinoids.     

Adjuvant chemotherapy with paclitaxel and carboplatin in patients with advanced bladder cancer: a study by the Hellenic Cooperative Oncology Group

PURPOSE: Radical cystectomy represents the treatment of choice for muscle infiltrative bladder carcinoma. Adjuvant chemotherapy has been used to improve outcome after cystectomy. We report results in a prospective cohort of patients at high risk for relapse who were treated with the combination of paclitaxel and carboplatin as adjuvant treatment following cystectomy for muscle invasive bladder cancer. MATERIALS AND METHODS: A total of 92 patients with extravesical tumor extension (pT 3b or greater) or lymph node involvement (N+) were treated with 4 cycles of paclitaxel at 175 mg/m and carboplatin (area under the curve 5 according to the Calvert formula) every 3 weeks following radical cystectomy. Patients were followed every 6 months thereafter. RESULTS: Median followup was 36.6 months. Chemotherapy was well tolerated with 62% of patients receiving 100% of the expected chemotherapy doses without delays. Grade 3 or 4 neutropenia was reported in 19% of patients, while neutropenic fever was reported in 7%. Five-year overall, cause specific and disease-free survival was 28.9% (95% CI 14.8 to 43.0), 36.6% (95% CI 24.4 to 49.7) and 29% (95% CI 16.3 to 42.4), respectively. CONCLUSIONS: Adjuvant chemotherapy with paclitaxel and carboplatin is feasible and could be used as adjuvant treatment for high risk bladder carcinoma. Its true value should be assessed in prospective, randomized trials.     

肿瘤坏死因子凋亡诱导配体诱导结肠癌细胞凋亡的机制

目的探讨肿瘤坏死因子凋亡诱导配体(TRAIL)诱导结肠癌细胞发生凋亡的机制。方法流式细胞仪技术、酶联免疫吸附技术、荧光显色技术检测500μg／L TRAIL和／或Caspase抑制剂Z-VAD．fmk处理后,结肠癌细胞SW1116在不同时点(0、2、4、6、24 h)凋亡情况、Caspase-3酶活性及4 h线粒体△ψm、cardiolipin、细胞ROS变化。结果 TRAIL可引起结肠癌细胞凋亡,并于 4 h达凋亡高峰,凋亡指数为32．98％;并出现线粒体△ψm下降、cardiolipin丢失增加及Caspase-3酶活性增加,4 h达到最大峰值为(37．56±2．572)μmol／L·hr-1·mg-1蛋白。但TRAIL所诱导的细胞凋亡作用可被Caspase抑制剂Z-VAD．fmk所抑制。同时证实TRAIL所诱导的结肠癌细胞凋亡与细胞氧自由ROS的生成无关。结论 TRAIL通过Caspase依赖方式引起线粒体△ψm下降、cardi- olipin丢失增加导致线粒体内膜损伤,从而诱导细胞发生凋亡。     

Role of mitochondria in ciprofloxacin induced apoptosis in bladder cancer cells

PURPOSE: In our earlier series we showed that ciprofloxacin inhibits bladder tumor cell growth with concomitant S/G2M cell cycle arrest and reported an increased Bax-to-Bcl-2 ratio in cells undergoing cell death. In the current series we elucidated the molecular mechanisms by which ciprofloxacin induces apoptotic processes. MATERIALS AND METHODS: Ciprofloxacin mediated mitochondrial depolarization was detected by flow cytometry in HTB9 cells. Mitochondrial permeability transition was measured by spectrophotometry in isolated mitochondria treated with ciprofloxacin in the presence and absence of cyclosporin. The consequential decrease in mitochondrial calcium, cytochrome c release and Bax translocation to mitochondria, which resulted in the activation of caspase 3 leading to apoptotic cell death, was measured by biochemical and confocal microscopy. RESULTS: Mitochondrial depolarization was observed during ciprofloxacin induced apoptotic processes. Cyclosporin A, a known inhibitor of the mitochondrial permeability transition pore, protected cells against decreased mitochondrial potential. Also, ciprofloxacin induced an alteration of mitochondrial calcium as early as 5 minutes and this disruption of intracellular calcium homeostasis was prevented by cyclosporin. Ciprofloxacin also had a direct effect on swelling of isolated mitochondria, which was absent in the presence of cyclosporin. Mitochondrial changes were accompanied by cytochrome c release and caspase 3 activation. Our findings also showed Bcl-2 dependent subcellular redistribution of Bax to the mitochondrial membrane in ciprofloxacin treated bladder tumor cells. CONCLUSIONS: The disruption of calcium homeostasis, mitochondrial swelling and redistribution of Bax to the mitochondrial membrane are key events in the initiation of apoptotic processes in ciprofloxacin treated bladder cancer cells.     

BAK基因过表达对膀胱癌细胞的诱导凋亡作用及其分子机制

目的：探讨BAK基因过表达对膀胱癌的诱导凋亡效应及机制。方法：脂质体介导BAK基因转染膀胱癌EJ细胞1－7d后，逆转录聚合酶链反应检测BAK基因表达，细胞计数法检测癌细胞生长活性，DNA Ladder法、吖啶橙－溴化乙锭荧光染色法及原位末端转移酶标记技术检测癌细胞凋亡，免疫组织化学法检测癌细胞Caspase-3、Bcl-2,p53表达。结果：转染1－7d后，癌细胞BAK基因表达显著增强（P＜0．01），体外生长抑制20．66％－35．58％（P＜0．01），部分癌细胞呈现凋亡形态学变化，凋亡率为18．0％－20．6％（P＜0．01），癌细胞Caspase-3表达增强6．6倍（P＜0．01）Bcl．2和P53表达差异无显著性（P＞0．05）。结论：BAK基因表达能显著诱导膀胱癌细胞凋亡，其中Caspase-3激活是其作用机制之一。     

槐耳清膏联合肿瘤坏死因子相关凋亡诱导配体对肝癌细胞生长的影响

目的探讨肿瘤坏死因子相关凋亡诱导配体（TRAIL）联合中药槐耳清膏对肝癌细胞株HepG2及肝癌耐阿霉素（ADM）细胞株（HepG,．ADM）的作用。方法通过培养液中ADM的浓度梯度递增法筛选培养,建立肝癌细胞HepG2-ADM耐药细胞株;TRAIL,TRAIL＋ADM,TRAIL＋槐耳清膏分别处理肝癌细胞株HepG2、HepG,-ADM及正常肝细胞株L02,噻唑蓝（MTT）比色法检测细胞增殖,采用流式细胞仪检测细胞凋亡情况。结果联合用TRAIL（100ng／L）和槐耳清膏（1．0g／L）处理肝癌细胞株HepG2-ADM及肝细胞株L02,MTT显示对前者增殖有明显抑制作用,而对后者无明显作用;流式细胞仪检测TRAIL联合槐耳清膏处理HepG2、HepG2-ADM,可诱导细胞凋亡,与其他组相比,差异有统计学意义（P〈0．05）。结论槐耳清膏可显著增强TRAIL对HepG2及HepG2-ADM的杀伤作用,而对正常胎肝细胞株L02杀伤作用轻微,TRAIL和槐耳清膏联合应用可望克服肿瘤细胞中存在的化学治疗药物耐药和TRAIL耐受问题。     

Update on chemotherapy for advanced bladder cancer

PURPOSE: Recent years have seen several advances in the treatment of locally advanced and metastatic bladder cancer. We summarize the current state of the art for advanced bladder cancer treatment. MATERIALS AND METHODS: A comprehensive review of published, prospective phase II/III clinical trials and retrospective analyses of patients with advanced bladder cancer was performed. RESULTS: Adjuvant and neoadjuvant chemotherapeutic strategies around the time of radical cystectomy have been used to decrease the risk of subsequent metastatic disease. Although the benefit of adjuvant chemotherapy remains unproven, neoadjuvant chemotherapy is associated with a modest 5% to 6% absolute survival benefit in 2 meta-analyses of the available data. Chemoradiation is feasible and effective in some patients, allowing bladder preservation with an acceptable risk of progression. Randomized, phase III data comparing methotrexate, vinblastine, doxorubicin and cisplatin chemotherapy to gemcitabine/cisplatin showed similar response proportions and overall survival with less toxicity in the gemcitabine/cisplatin arm. This has led to the widespread use of gemcitabine/cisplatin as first line chemotherapy for metastatic bladder cancer. The optimal agents and regimens for second line chemotherapy remain undefined. Similarly biological and targeted therapies for advanced bladder cancer remain investigational. CONCLUSIONS: Combination cisplatin based neoadjuvant chemotherapy may benefit patients with locally advanced bladder cancer. Gemcitabine/cisplatin has replaced methotrexate, vinblastine, doxorubicin and cisplatin as the regimen of choice in patients with good renal function. The optimal regimens for the medically unfit patient and second line chemotherapy remain undefined. The development of targeted therapies, less toxic regimens and improved cytotoxic agents are necessary to improve outcomes.     

干扰素对膀胱肿瘤细胞膜TNFR表达的影响

目的：探讨用干扰素治疗膀胱肿瘤时对膀胱肿瘤细胞膜肿瘤坏死因子受体（ＴＮＦＲ）表达的影响。方法：用放射配基结合分析法检测α和γ干扰素分别作用于膀胱癌ＢＩＵ－８７细胞前后细胞膜ＴＮＦＲ的变化。结果：膀胱肿瘤细胞膜存在的ＴＮＦＲ，受体的特异性结合量与干扰素深度和作用时间关系密切；γ干扰素对受体表达的影响大于α干扰素。结论：干扰素可以使膀胱肿瘤细胞膜ＴＮＦＲ的表达增加，从而使免疫治疗后高表达的ＴＮＦ可以与     

Paclitaxel and cisplatin as intravesical agents against non-muscle-invasive bladder cancer

OBJECTIVES

To investigate the effects of cisplatin and paclitaxel against human bladder cancer cells in vitro, and to obtain both pharmacokinetic and pharmacodynamic data after intravesical administration in mice.

MATERIALS AND METHODS

Six bladder cancer cell lines (J82, KU7, RT4, SW780, T24, UMUC3) were treated with various combined doses of both drugs and cell proliferation was evaluated 3 days later. In vivo, solutions of cisplatin and micellar paclitaxel were instilled transurethrally in female mice and pharmacokinetic data were acquired using high‐performance liquid chromatography‐mass spectrometry and atomic absorption methods. To obtain efficacy data, mice with orthotopic KU7‐luc tumours were administered cisplatin and/or micellar paclitaxel intravesically, and the tumour burden quantified using bioluminescence imaging.

RESULTS

In vitro, both cisplatin and paclitaxel potently decreased the proliferation of all cell lines tested, and in combination had an additive but not a synergistic effect. After intravesical instillation, mouse serum concentrations of cisplatin and paclitaxel were in the low microgram/millilitre range and bladder tissue concentrations achieved were 82 and 241 µg/g, respectively. Similar drug levels were reached using combined therapy. In vivo, all chemotherapeutic agents significantly inhibited bladder tumour growth, with the best results for combined therapy and micellar paclitaxel alone. However, there was toxicity in the combined treatment arm.

CONCLUSIONS

Both cisplatin and paclitaxel were absorbed at effective amounts into bladder tissues. As intravesical agents, paclitaxel had slightly stronger anticancer potency than cisplatin. Due to increased adverse events, caution should be exercised when combining both cisplatin and paclitaxel intravesically.     

γ-干扰素加强肿瘤坏死因子相关凋亡诱导配体抑制胆管癌细胞的作用

目的　探讨肿瘤坏死因子 (TNF)相关凋亡诱导配体 (TRAIL)对人胆管癌的作用及γ 干扰素 (IFN γ)对TRAIL抗瘤活性的影响。方法　应用透射电镜、琼脂糖凝胶电泳和流式细胞仪 (FCM ) ,研究TRAIL对人胆管癌细胞的抑制作用及IFN γ对TRAIL抗瘤活性的影响。结果　透射电镜和DNA琼脂糖凝胶电泳可见到典型细胞凋亡特征。FCM分析显示 :浓度为 0、1、10、10 0、10 0 0 μg/L的TRAIL 2 4h引起QBC93 9细胞的凋亡率分别为 (1.66± 0 .73 ) %、(8.83± 0 .5 4) %、(2 2 .3 0± 0 .64 ) %、(4 2 .5 0± 0 .47) %、(4 9.0 6± 0 .72 ) % ,与对照组比较差异有显著性 (P <0 .0 1)。IFN γ与TRAIL 10 0 μg/L联合应用 ,当IFN γ浓度大于 5 0U /ml或 10 0U /ml时 ,IFN γ作用时间超过 2 4h分别与单用TRAIL组比较 ,明显加强QBC93 9细胞凋亡 (P <0 .0 1)。结论　TRAIL通过诱导胆管癌细胞凋亡而起到抑癌作用 ,IFN γ能加强TRAIL诱导胆管癌细胞的凋亡。     

Combination chemotherapy with paclitaxel,estramustine and carboplatin for hormone refractory prostate cancer

PURPOSE: The activity of estramustine phosphate is synergistic with paclitaxel against hormone refractory prostate cancer. Moreover, the single agent activity of carboplatin has demonstrated a 17% response rate in measurable disease. Therefore, we conducted a prospective trial to establish more effective chemotherapy consisting of paclitaxel, estramustine phosphate and carboplatin for hormone refractory prostate cancer. MATERIALS AND METHODS: The study included 32 patients with hormone refractory prostate cancer. Prior chemotherapy was accepted. Patients were treated with 100 mg./m.2 paclitaxel intravenously weekly, 10 mg./kg. estramustine phosphate orally daily and carboplatin intravenously to an area under the curve of 6 on day 1 of every 4-week cycle. Treatment was continued until disease progression or excessive toxicity. RESULTS: Of the 32 patients 30 were assessable for response. A median of 7 consecutive cycles was administered per patient. Ten patients had received prior cytotoxic chemotherapy. Levels of prostate specific antigen decreased by greater than 50% in 100% of patients and by greater than 90% in 56.7%. Partial response was obtained in 61.1% of measurable lesions. Consumption of medication for cancer induced pain was reduced in 89.5% of patients. Tumor volume reduction and/or antitumor therapeutic effects were exhibited in 81.0% of patients with positive biopsy. At a median followup of 48 weeks median time to progression was 48 weeks and median overall survival was 95 weeks. Two patients suffered myocardial infarction and hepatic insufficiency, respectively, and discontinued treatment during the first cycle. Major toxicities were grade 3 or 4 anemia in 59.4% of patients, leukopenia in 37.5%, thrombocytopenia in 28.1% and neuropathy in 12.5%. However, all toxicity was temporary and reversible with dose reduction or temporary cessation of chemotherapeutic agents. CONCLUSIONS: Paclitaxel, estramustine phosphate and carboplatin chemotherapy was extremely effective for hormone refractory prostate cancer. Although hematological and neurotoxicity were modest, this therapy may be more manageable with lower doses.     

TRAIL受体在膀胱癌中的表达及意义

目的：了解肿瘤坏死因子相关诱导凋亡配体（TRAIL）受体在膀胱癌组织中的表达及意义。方法：采用RT－PCR及Northern blot方法检测TRAIL受体在膀胱癌组织及正常膀胱粘膜中的表达。结果：死亡受体DR4、DR5在膀胱癌组织及正常膀胱粘膜中呈强表达,候受体DcR-1在正常膀胱粘膜呈强表达,假受体DcR-2未见表达。结论：TRAIL基因在膀胱移行上皮细胞癌凋亡机制中可能发挥重要作用。     

阿霉素协同TRAIL真核表达载体诱导前列腺癌细胞凋亡的研究

目的探讨阿霉素与肿瘤坏死因子相关凋亡诱导配体（TRAIL）真核表达载体诱导前列腺癌细胞凋亡的协同作用.方法 RT-PCR方法克隆人TRAIL全长基因,并插入真核表达载体pLXIN多克隆位点,经酶切和测序鉴定.将pLXIN-TRAIL质粒转染PC3-M细胞,RT-PCR方法检测外源性TRAIL表达率,TUNEL染色和流式细胞术比较单独表达TRAIL和联合应用阿霉素对PC3-M细胞凋亡率的影响,Western blot法检测经阿霉素诱导前后PC-3M细胞死亡受体-5（DR5）的表达变化.结果成功构建pLXIN-TRAIL真核表达载体,外源性TRAIL表达可以诱导PC-3M细胞凋亡,阿霉素能够增强TRAIL的凋亡诱导效应,6μg pLXIN-TRAIL质粒DNA组,加入1 mg/L阿霉素前后平均凋亡率分别为11.8%和20.7%,同时可提高PC-3M细胞DR5的表达. 结论 TRAIL真核表达载体介导的细胞凋亡是治疗前列腺癌的新途径,阿霉素可以通过提高DR5表达而增强PC-3M细胞对TRAIL诱导的凋亡敏感性.     

Human complement factor H related protein test for monitoring bladder cancer

PURPOSE: The BTA stat test is a rapid, noninvasive, qualitative urine test that detects bladder tumor associated antigen (human complement factor H related protein) in urine. We compared BTA stat test to voided urine cytology in patients monitored for bladder cancer in a prospective trial, and determined whether this test is effective in detection of recurrence not seen by regular cystoscopy. MATERIALS AND METHODS: A total of 445 consecutive patients with bladder cancer were studied. A voided urine sample was obtained before cystoscopy and divided for culture, cytology and BTA stat testing. In cases of a positive BTA stat test but negative cystoscopy, excretory urography or renal ultrasound, random biopsies and collected ureteral urine samples for ureteral cytology were obtained. The overall sensitivity and specificity as well as positive and negative predictive values for BTA stat test, cytology and their combination were calculated. RESULTS: Of the 445 patients 118 (26.5%) had bladder cancer recurrence on cystoscopy, which was detected by BTA stat test and cytology in 63 (53.4%) and 21 (17.8%), respectively. Of the remaining 327 patients not having recurrent tumor on cystoscopy 81 (24.8%) had a positive BTA stat test. Excretory urography or renal ultrasound and random biopsies in 48 (59.3%) of these patients revealed 7 recurrences, making the total number of recurrent tumors 125 of 412 (30.3%). The overall sensitivities and specificities for the BTA stat test, cytology and their combination were 56.0%, 19.2%, 60.0% and 85.7%, 98.3% and 85.0%, respectively. CONCLUSIONS: The sensitivity for detection of recurrent tumor on BTA stat test is superior to that of voided urine cytology in all bladder cancer categories, whereas the specificity of voided urine cytology is higher than that for BTA stat test. However, a sixth of the patients with apparent false-positive BTA stat test results chosen for further investigation had recurrent tumors that were not found on routine cystoscopy. Although the sensitivity and specificity were highest when both tests were used, the differences were not significant overall. Therefore, the BTA stat test could potentially replace urine cytology for followup of superficial bladder cancer.     

蒲葵子提取物对膀胱癌细胞增殖凋亡的影响及其相关机制

目的:探讨蒲葵子提取物对膀胱癌细胞增殖、凋亡的影响及其相关机制。方法:将T24细胞分别用含蒲葵子提取物且终浓度分别为0、25、50、100 mg/L的培养液培养,分别记为对照组和蒲葵子低、中、高剂量组。用细胞计数试剂盒8(CCK-8)检测细胞存活率;克隆形成实验检测细胞克隆形成数量;流式细胞术检测细胞凋亡;蛋白质印迹法...