草苁蓉提取物对大鼠肝癌前病变模型血清抗氧化酶活性及肿瘤坏死因子的影响

目的 :探讨草苁蓉甲醇提取后进一步分离的水层提取物在大鼠肝脏化学致癌初期对血清抗氧化酶活性和肿瘤坏死因子的影响 ,从而进一步探索其抗致癌作用的可能机制。方法 :按略改良的 Solt- Farber方法建立大鼠肝脏癌前病变模型 ,用草苁蓉提取物 (BR)饲养大鼠 6周后 ,取血测定超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶(GSH - PX)、谷胱甘肽 - S-转移酶 (GST)、过氧化氢酶 (CAT)的活性和血清中的丙二醛 (MDA )及肿瘤坏死因子(TNF-α)含量。结果 :草苁蓉提取物在大鼠肝脏化学致癌初期对血清 SOD、GSH - PX、CAT的活性及 TNF-α含量有回升作用 ,并能降低由于癌前病变的形成所增高的 GST活性及 MDA含量。结论 :草苁蓉水层提取物具有抗氧化作用和调节机体免疫功能的作用 ,而这可能是草苁蓉的抗致癌机制之一     

前列腺癌组织中ILK和E-Cadherin的表达及其意义

目的　探讨整合素连接激酶 (ILK )、上皮细胞钙黏素 (E cad)在前列腺癌组织中的表达及其意义。方法　应用免疫组织化学 (S P)方法检测 5 0例前列腺癌及 16例良性前列腺增生组织中ILK、E cad蛋白的表达。结果　前列腺癌组织中ILK、E cad阳性表达率分别为 46.0 % (2 3 /5 0 )、5 0 .0 % (2 5 /5 0 )。随肿瘤细胞病理分级、临床分期程度的增高 ,ILK阳性表达率增高而E cad表达降低 ,各组间均有显著性差异 (P <0 .0 5或P <0 .0 1)。与良性前列腺增生组织中的阳性表达率 10 0 .0 % (16/16)和 6.2 % (1/16)比较 ,均有显著性差异 (P <0 .0 5 )。结论　ILK、E cad蛋白异常表达在前列腺癌的恶性进展中起重要作用 ,ILK高表达或激活可能是E cad低表达或缺失的原因之一 ,联合检测ILK、E cad表达有利于判断病期及预后。     

立体适形放射治疗前列腺癌29例临床分析

目的:分析立体适形放射治疗(3D-CRT)前列腺癌的疗效.方法:采用3D-CRT治疗前列腺癌29例,26例放疗前行双侧睾丸切除,22例同时服用内分泌治疗药物.采用3D-CRT技术,5次/周,1.8～2Gy/次,DT 60～72Gy,中位剂量68Gy.结果:中位随访18个月,生存率82.8%,肿瘤特异生存率93.1%.1、2、3级急性胃肠道不良反应发生率分别为44.8%,6.9%,3.4%,1、2级急性泌尿生殖系统不良反应发生率分别为34.5%,6.9%.结论:3D-CRT治疗前列腺癌疗效满意,不良反应小.     

前列腺癌的诊断(附159例分析)

回顾性分析18年间159例前列腺癌的诊断结果，其发病率近9年明显增高。发病率与年龄是正相关。直肠指诊（DRE）诊断阳性率为72．96％（116／159），经腹B超69．23％（18／26），CT90．32％（28／31），ACP45．71％（32／70），PSA85．92％（61／71），穿刺活检89．32％（92／103）。作者建议：DRE、PSA可作为60岁以上男性排尿困难患者的常规检查，期望早期检出前列腺癌。     

Dose-Volume Histograms for bladder and rectum

: A careful examination of the foundation upon which the concept of the Dose-Volume Histogram (DVH) is built, and the implications of this set of parameters on the clinical application and interpretation of the DVH concept has not been conducted since the introduction of DVHs as a tool for the quantitative evaluation of treatment plans. The purpose of the work presented herein is to illustrate problems with current methods of implementing and interpreting DVHs when applied to hollow anatomic structures such as the bladder and rectum.

: A typical treatment plan for external beam irradiation of a patient with prostate cancer was chosen to provide a data set from which DVH curves for both the bladder and rectum were calculated. The two organs share the property of being shells with contents that are of no clinical importance. DVHs for both organs were computed using a solid model and using a shell model. Typical treatment plans for prostate cancer were used to generate DVH curves for both models. The Normal Tissue Complication Probability (NTCP) for these organs is discussed in this context.

: For an eight-field conformal treatment plan of the prostate, a bladder DVH curve generated using the shell model is higher than the corresponding curve generated using the solid model. The shell model also has a higher NTCP. A six-field conformal treatment plan slo results in a higher DVH curve for the shell model. A treatment plan consisting of bilateral 120-degree arcs, results in a higher DVH curve for the shell model, as well as a higher NTCP.

: The DVH concept currently used in evaluation of treatment plans is problematic because current practices of defining exactly what constitutes “bladder” and “rectum.” Commonly used methods of tracing the bladder and rectum imply use of a solid structure model for DVHs. In reality, these organs are shells and the critical structure associated with NTCP is obviously and indisputably the shell, as opposed to its contents. Treatment planning algorithms for DVH computation should thus be modified to utilize the shell model for these organs.     

Dietary retinoids and carotenoids in rodent models of mammary tumorigenesis

In this review of the scientific literature the relationship between retinoids, carotenoids, and mammary carcinogenesis is examined. Several retinoids have shown promise as chemopreventive agents against chemically induced mammary carcinogenesis in mice and especially in rats. The most promising retinoids are retinyl acetate (RA) and N-(4-hydroxyphenyl)retinamide (4-HPR, fenretinide). In rats, dietary administration of these retinoids reduced tumor incidence and multiplicity, and increased the latency of DMBA or MNU-induced mammary cancers. In mice, 4-HPR reduced the number of hyperplastic alveolar nodules and the number of tumors in MTV- and MTV+ mice, respectively. Among retinoids, 4-HPR is at present the most promising analogue, due to its ability to concentrate in the mammary gland. The combination of 4-HPR with tamoxifen not only is more effective in suppressing breast cancer than either agent alone, but also inhibits the appearance of subsequent cancers following the surgical removal of the first tumor. These studies suggest that retinoids, like tamoxifen, may be applicable to the prevention of contralateral breast cancer in women who underwent breast cancer surgery. It is also becoming evident that differentiation therapy and chemoprevention can become attractive alternative approaches to intensive cytotoxic chemotherapy. The role of carotenoids in the prevention of mammary carcinogenesis, however, is ambiguous. Poor absorption and low levels of carotenoids that reach the target tissues complicate interpretation of data in rodent models of mammary carcinogenesis. Very few animal studies are presently available in which purified carotenoids were found effective against mammary carcinogenesis. These results do not justify undertaking clinical evaluation of individual carotenoids against breast cancer at this time.     

Increased risk of salivary gland tumors after low-dose irradiation

Objective: To assess the risk of neoplastic development among persons exposed to scalp irradiation. Study Design: Historical cohort study initially; prospective follow-up subsequently. Method: Two control groups—population and siblings—matched for age, sex, ethnic origin, and year of immigration. Follow-up from time of irradiation (1950s) until the end of 1991. Linkage with nationwide cancer registry. Results: A 4.5–fold incidence of cancer (P < .01) and a 2.6–fold increase of benign tumors were noted. The mean length of latency period until tumor development was 11 years for malignant tumors and 21.5 years for benign. A clear dose response effect for both cancer and benign tumors was demonstrated. Conclusions: The study confirms the role of radiation in salivary gland carcinogenesis. It indicates a need for better awareness, a comprehensive examination, and long-term follow-up of patients who have been subjected to head and neck radiation.     

The 1.5 GHz Electromagnetic Near-field Used for Cellular Phones Does Not Promote Rat Liver Carcinogenesis in a Medium-term Liver Bioassay

We have recently established that local exposure to a 929.2 MHz electromagnetic near-field, used for cellular phones, does not promote rat liver carcinogenesis in a medium-term bioassay system. In the present study, a 1.439 GHz electromagnetic near-field (EMF), another microwave band employed for cellular phones in Japan, was similarly investigated. Time division multiple access (TDMA) signals for the Personal Digital Cellular (PDC) Japanese cellular telephone standard system were directed to rats through a quarter-wavelength monopole antenna. Numerical dosimetry showed that the peak SARs within the liver were 1.91–0.937 W/kg, while the whole-body average specific absorption rates (SARs) were 0.680–0.453 W/kg, when the time-averaged antenna radiation power was 0.33 W. Exposure was for 90 min a day, 5 days a week, over 6 weeks, to male F344 rats given a single dose of diethylnitrosamine (200 mg/kg, i.p.) 2 weeks previously. At week 3, all rats were subjected to a two-thirds partial hepatectomy. At week 8, the experiment was terminated and the animals were killed. Carcinogenic potential was scored by comparing the numbers and areas of the induced glutathione S-transferase placental form (GST-P)-positive foci in the livers of exposed (48) and sham-exposed rats (48). Despite increased serum levels of corticosterone, adrenocorticotropic hormone (ACTH) and melatonin, the numbers and the areas of GST-P-positive foci were not significantly altered by the exposure. These findings clearly indicated that local body exposure to a 1.439 GHz EMF, as in the case of a 929.2 MHz field, has no promoting effect on rat liver carcinogenesis in the present model.     

Enhancing Effects of Quinacrine on Development of Hepatopancreatic Lesions in N-Nitrosobis(2-oxopropyl)amine-initiated Hamsters

The modifying effects of quinacrine administration during the post-initiation phase of carcinogenesis were investigated in hamsters treated with N -nitrosobis(2-oxopropyl)amine (BOP). Female Syrian hamsters were given three weekly s.c. injections of BOP at a dose of 10 mg/kg and then 300 or 100 ppm quinacrine in their diet for 37 weeks. Additional groups of animals received the BOP injection alone, or only the 300 ppm quinacrine treatment as BOP-negative controls. At week 40 of the experiment, all surviving animals were killed and development of proliferative lesions was assessed histopathologically. The multiplicity of pancreatic adenocarcinomas and dysplastic lesions per hamster was significantly higher ( P <0.01 and P <0.05) in the BOP/Q100 group (1.92 and 1.78) than in the BOP-alone group (1.07 and 0.79). The incidence of hepatocellular adenomas plus carcinomas was also significantly elevated ( P <0.05) in the BOP/Q300 and BOP/Q100 groups. In contrast, the multiplicity of lung adenomas plus adenocarcinomas was significantly decreased ( P <0.05) by the Q300 treatment. Neither the incidence nor the multiplicity of renal cell tumors (adenomas and carcinomas) or nephroblastomas significantly differed between the BOP-treated groups. Electron microscopic examination revealed an abundance of myeloid lamellar bodies filling the cytoplasm of hepatocytes and pancreatic ductular and acinar cells, and epithelial cells of the gallbladder in the quinacrine-treated animals, the degree being dose-dependent. Our results indicate that quinacrine enhances pancreatic and hepatic carcinogenesis in hamsters induced by BOP.