树突状细胞疫苗对Walker-256荷瘤大鼠Th1／Th2平衡的调节作用

[目的]通过Walker-256大鼠种植瘤模型，探讨树突状细胞（DC）疫苗对大鼠Th1／Th2平衡的调节作用。[方法]选取25只雌性SD大鼠，在皮下注射Walker-256肿瘤细胞。10d后，将已经成瘤的大鼠按照体重配对，随机分为治疗组和肿瘤组。另外选取10只体重分别相同的雌性SD大鼠作为对照组。治疗组大鼠皮下注射负载Walker-256肿瘤细胞抗原的树突状细胞悬液，肿瘤组和对照组大鼠则皮下注射等量PBS。ELISA分别检测大鼠血细胞因子（包括IL-12、IFN-γ、IL-4和IL-10）。[结果]治疗组与肿瘤组比较，IL-12明显上升（P〈0．01），IFN-γ明显上升（P〈0．01），IL-4明显下降（P〈0．01），IL-10则无统计学意义。以IFN-γ／IL-4代表Th1／Th2，治疗组与肿瘤组比较明显上升（P〈0．05）。[结论]树突状细胞疫苗能够调节荷瘤大鼠Th1／Th2平衡。     

^99Tc^m-Annexin B1探测荷瘤鼠化疗后肿瘤细胞凋亡的实验观察

目的：探讨^99Tc^m-Annexin B1探测化疗后肿瘤细胞凋亡的潜力与可行性。方法：乳腺癌细胞MDA-MB-435荷瘤小鼠经大剂量（30mg／kg）紫杉醇单次化疗后，注射^99Tc^m-Annexin B1，计算化疗后不同时间（0、5、10、15、20和25h）每克肿瘤组织摄取^99Tc^m-Annexin B1的百分注射剂量率（％ID／g）。肉瘤细胞W256荷瘤大鼠经大剂量（200mg／kg）环磷酰胺单次化疗后24h注射^99Tc^m-Annexin B1，对照组荷瘤大鼠注射生理盐水；行SPECT平面显像观察肿瘤摄取情况。结果：乳腺癌荷瘤小鼠化疗后15h，肿瘤摄取^99Tc^m-Annexin B1达高峰，由0h的（0．15±0．013）％ID／g上升至（0．22±0．026）％ID／g。肿瘤对^99Tc^m-Annexin B1的摄取与肿瘤细胞凋亡指数（AI）具有相关性，r=0．88，P〈0．01。W256细胞荷瘤大鼠化疗后24h显像发现，肿瘤对^99Tc^m-Annexin B1的摄取较对照荷瘤大鼠显著升高，对照组的肿瘤与非肿瘤摄取比值（T／B）为1．39±0．21，化疗组为2．57±0．43。结论：^99Tc^m-Annexin B1对探测化疗后肿瘤细胞凋亡具有潜力与可行性。     

CD80 CD86和CD137L基因联合表达对小鼠肝癌种植模型肿瘤免疫原性的影响

目的探讨CD80、CD86和CD137L基因联合表达对肿瘤免疫原性的影响。方法按接种变异瘤株不同,将BALB／C小鼠随机分成A组（H22．Wt细胞）、B组（H22-neo细胞）、C组（H22-CD80／CD86^＋细胞）、D组（H22．CD137L^＋细胞）、E组（H22-CD80／CD86／CD137L^＋细胞）5组,建立H22．BALB／C小鼠荷肝癌模型,A、B组为对照组。观察小鼠成瘤率、成瘤潜伏期、荷瘤鼠存活率及肿瘤增殖情况。通过复种试验观察转基因对H22变异株免疫原性和机体免疫保护作用的影响。结果E组首次接种成瘤率仅有50．0％,显著低于其余4组（P〈0．01）。首次接种后,C组荷瘤鼠肿瘤生长受到明显抑制,有2只荷瘤鼠肿瘤完全消退。E组肿瘤生长所受抑制较C组更为明显,肿瘤峰值体积显著小于C组,且有3只荷瘤鼠肿瘤完全消退。其余3组荷瘤鼠未见肿瘤完全消退。与A、B、D组相比,C、E组荷瘤鼠生存率显著改善（P〈0．01）,而C、E两组荷瘤鼠生存率差异无统计学意义（P〉0．05）。复种试验表明,C、E组荷瘤鼠再次成瘤率低于对照组,E组与C组差异也有统计学意义（P〈0．01）;第3次接种后,E组成瘤率显著低于C组（P〈0．01）。E组中5只首次接种未成瘤的小鼠,于第21天重复接种H22-Wt细胞,小鼠100％排斥肿瘤,于第56天第3次接种H22／Wt细胞,小鼠仍然100％排斥肿瘤。结论CD80＋CD86和CD137L单独或者联合表达均可显著降低野生型H22细胞株致瘤性,CD80、CD86和CD137L基因联合表达显著改善了野生型H22细胞的免疫原性。     

子宫颈癌患者血浆尿激酶受体检测及其意义

目的研究子宫颈癌患者尿激酶型纤溶酶原激活物受体（uPAR）在血浆中的含量，初步探讨其临床意义。方法通过酶联免疫吸附试验法（ELISA）检测94例子宫颈癌患者及30名健康妇女（对照组）血浆中可溶性uPAR（suPAR）的水平。结果30名健康妇女血浆suPAR水平为（0．5023±0．1724）ng／ml，94例子宫颈癌患者血浆suPAR水平为（1．0433±0．2736）ng／ml，两组相比差异具有统计学意义（P〈0．01）：病理类型、病理分级、生长类型和肿瘤局部大小与血浆suPAR水平变化无显著相关（P〉0．05），临床分期、淋巴结是否转移和侵犯肌层深度与血浆suPAR水平变化相关（P〈0．05）。结论血浆中suPAR水平可能是反映体内整个尿激酶型纤溶酶原（uPA）激活系统活性的指标，它的升高可能与子宫颈癌的发生、发展有密切关系。血浆suPAR可作为子宫颈癌患者疗效判断、临床分期、疾病进展及预后预测的一个重要指标。     

经口给予黄芪提取物对H22肝癌荷瘤小鼠影响的实验研究

目的：综合分析黄芪提取物对H22肝癌荷瘤小鼠肿瘤细胞增殖、凋亡及机体免疫功能的影响。方法：采用病理形态学观察、免疫组化、流式细胞术和免疫学方法研究灌胃不同剂量黄芪提取物（ASA）对H22荷瘤小鼠肿瘤细胞增殖与凋亡、脾脏CD4^＋／CD8^＋T淋巴细胞比例及腹腔巨噬细胞吞噬功能的影响。综合评价ASA对H22荷瘤小鼠的影响。结果：ASA对H22荷瘤小鼠肿瘤重量、肿瘤细胞增殖均无明显影响。除ASA0．031mg／g组外，ASA0．125mg／g、0．500mg／g和2．000mg／g组肿瘤细胞凋亡率和Bax的表达均明显高于对照组（P〈0．01），而实验组Bcl-2表达则明显低于对照组（P〈0．01）。ASA可增加荷瘤小鼠脾脏CD4^＋／CD8^＋比例，提高腹腔巨噬细胞吞噬能力。结论：ASA对H22肝癌荷瘤小鼠肿瘤细胞增殖无明显影响．但可在一定程度上促进肿瘤细胞凋亡，提高机体免疫功能。     

YH-16对宫颈癌Hela细胞及其裸鼠皮下移植瘤作用研究

目的：初步探讨YH-16（重组内皮抑素）对宫颈癌Hela细胞及其荷瘤生长抑制作用及作用机制。方法：用MTY法检测YH-16对Hela细胞生长抑制作用；用透射电镜观察YH-16处理Hela细胞后的凋亡情况、流式细胞仪检测细胞凋亡率及细胞周期；将Hela细胞移植至裸鼠皮下成瘤，观察不同浓度YH-16（0mg／kg、0．4mg／kg、0．75mg／kg和1．5mg／kg）对荷瘤鼠皮下移植瘤生长的影响；TUNEL法观察肿瘤细胞的凋亡；免疫组化方法检测裸鼠移植瘤组织中肿瘤微血管密度（MVD）。结果：YH-16具有体外抑制Hela细胞增殖的作用（P〈0．01）；能诱导Hela细胞凋亡；YH-16能有效抑制裸鼠皮下移植瘤的生长（P〈0.05）；YH-1615mg／kg组的肿瘤MVD计数较对照组和其它治疗组明显降低（P〈0．05）。结论：YH-16具有抑制宫颈癌Hela细胞及其皮下移植瘤生长的作用。     

能量可控陡脉冲对荷瘤小鼠生存转归的影响

目的观察能量可控陡脉冲对接种U14子宫颈癌小鼠的生存转归状况的影响。方法应用陡脉冲作用于40只雌性荷瘤BALB／C小鼠，对照观察实验组和对照组生存期及肿瘤转归状况。结果抑瘤曲线分析结果表明陡脉冲电场能抑制肿瘤细胞的增殖；两组荷瘤小鼠治疗后31天时观察肿瘤转归：实验组20只中完全应答（CR）9只（45．0％），进行性发展（PD）11只（55．0％），其中死亡4只，死亡率为20．0％；而对照组20只全部为PD（100．0％），其中死亡9只，死亡率为45．0％，两组构成比差异有显著性（P〈0．01）。生存期分析结果表明两组差异有显著性（P〈0．01），实验组荷瘤小鼠平均生存天数为52．05天。对照组荷瘤小鼠平均生存天数为33．05天。结论能量可控陡脉冲对恶性肿瘤具有杀灭和抑制作用，并可延长实验组荷瘤小鼠的生存期。     

岩消胶囊对小鼠肝癌抑制作用的实验研究

目的研究岩消胶囊对小鼠肝癌的抑制作用。方法选取40只小鼠，随机分为空白对照组、阳性对照组、实验组，分别观察实体瘤重量、小鼠存活时间、实体瘤的形态学和对腹水癌细胞的直接杀伤死亡率。结果实验组的实体瘤重量显著降低（P〈0．01），抑瘤率达52．0％；小鼠存活时间明显延长，生命延长率81．6％（P〈0．01）；对腹水癌细胞有显著的杀伤作用（P〈0．05）。结论岩消胶囊能显著抑制小鼠肝癌细胞移植性肿瘤的生长，减轻瘤体重量；能显著延长荷瘤小鼠生存期；同时对肿瘤细胞有直接杀伤作用。     

恶性肿瘤患者手术前后血浆纤维蛋白原水平的动态变化

目的研究恶性肿瘤患者手术前后血浆纤维蛋白原（FIB）水平的动态变化及其与疗效及预后的关系。方法对206例行手术治疗的恶性肿瘤患者，前瞻性观察3年，分期取静脉血，应用ACL-8000全自动血凝分析仪检测血浆中FIB的含量，进行FIB水平变化与疾病程度的相关性分析。结果恶性肿瘤患者手术前血浆FIB水平较健康人和良性肿瘤患者均显著升高（P〈0．001）；有淋巴结转移者较无淋巴结转移者显著升高（P〈O．01），且随转移程度增高而升高；手术后缓解的患者明显下降（P〈0．01），未缓解的患者基本维持术前水平，当再度复发后增值更高。结论血浆FIB水平随恶性肿瘤的生长、发展、转移有动态变化，而这一动态变化与疾病的发生、治疗、预后等的进展程度呈正相关，检测FIB可作为肿瘤治疗期间的随访指标。     

缩合葡萄糖氯化钠注射液在肝肿瘤手术行急性高容性血液稀释的临床研究

目的：观察缩合葡萄糖氯化钠注射液行急性高容性血液稀释（AHH）对肝肿瘤手术病人血流动力学、凝血功能的影响。方法：肝肿瘤手术患者30例,随机分为对照组（I组,n=15）,研究组（II组,n=15）。麻醉诱导后分别输入林格氏液和缩合葡萄糖氯化钠注射液行扩容治疗（15ml／kg）,扩容速度50ml／min。在AHH前、AHH完毕、AHH完毕后30min记录HR、SBP、DBP、CVP、SPO2并检测红细胞比容（Hct）、血红蛋白计数（Hb）、血小板计数（Plt）和血浆凝血酶原时间（PT）、部分凝血活酶时间（APTT）、凝血酶时间（TT）及血浆纤维蛋白原（FIB）。结果：两组HR、SBP、DBP平稳,CVP在AHH完毕和AHH完毕30rain时增高（P〈0．01）,组间无差异（P〉0．05）。Ⅰ组Hot、Hb、Plt在AHH完毕时明显下降（P〈0．05）,30min后恢复（P〉0．05）。Ⅱ组Het、Hb、Plt在AHH完毕时下降显著（P〈0．05或P〈0．01）,Hct、Hb30min后仍降低（P〈0．05）,但Pit30min后恢复（P〉0．05）。Ⅰ组PT在AHH完毕时延长（P〈0．05）,FIB显著减少（P〈0．01）,但两者30min后恢复（P〉O．05）。Ⅱ组PT在AHH完毕时明显延长（P〈0．01）,FIB明显减少（P〈0．01）,30min后仍未能恢复（P〈0．05）。两组TT和APTT无明显变化。结论：缩合葡萄糖氯化钠注射液在肝肿瘤手术病人行急性高容性血液稀释,可以有效地维持术中循环功能的稳定,但部分病人CVP增高或PT延长及血浆FIB减少。     

Effects of ghrelin on anorexia in tumor-bearing mice with eicosanoid-related cachexia

Ghrelin is a novel brain-gut peptide that stimulates food intake and may secondarily increase body weight via a growth hormone secretagogue receptor (GHS-R). Tumor-bearing mice (MCG101), characterized by anorexia, fat loss and muscle wasting due to increased concentration of PGE2 and proinflammatory cytokines (IL-1beta, IL-6, TNF-alpha), were provided ghrelin i.p. at a low (20 microg/day) and high dose (40 microg/day) to examine the ability of ghrelin to counteract tumor-induced anorexia. Immunohistochemical staining and Western blot analyses were used to identify GHS-R expression in the brain as well as its relationship to NPY expression in hypothalamic neurons. GHS-R mRNA in hypothalamus and ghrelin mRNA in gastric fundus were quantified by RT-PCR. Body composition was determined by carcass extractions. GHS-R expression in hypothalamus and plasma ghrelin levels were significantly increased in freely-fed tumor-bearing mice, while gastric fundus expression of ghrelin was unaltered compared to non-tumor-bearing mice (controls). Ghrelin treatment increased food intake, body weight and whole body fat at both low and high doses of ghrelin in normal controls, while tumor-bearing mice showed improved intake and body composition at the high dose of ghrelin only. Exogenous ghrelin normalized the GHS-R expression in hypothalamus from tumor-bearing mice without alterations in the gastric fundus expression of ghrelin. Tumor growth was not altered by exogenous ghrelin. Our results indicate that MCG 101-bearing mice became ghrelin resistant despite upregulation of hypothalamic GHS-R expression, which confirms similar indirect observations in cancer patients. Thus, other factors downstream of the ghrelin-GHS-R system appear to be more important than ghrelin to explain cancer-induced anorexia.     

沙苑子黄酮抗肝癌生长作用及对免疫功能的影响

目的:探讨中药提取物沙苑子黄酮(flavonoids extracts from semen Astragali complanati,FAC)对小鼠肝癌H22细胞生长的影响及其机制.方法:建立H22荷瘤小鼠模型,观察FAC对H22肝癌移植瘤生长的抑制作用及其对荷瘤小鼠免疫器官、巨噬细胞吞噬功能、淋巴细胞转化功能及生存期的影响.结果:高、中、低剂量组FAC对荷瘤小鼠肝癌细胞生长具有显著抑制作用,与正常对照模型组比较差异具有统计学意义(P<0.05);其中环磷酰胺(cyclophosphamide,CTX)对照组的抑瘤率与FAC高剂量组相近(P>0.05). FAC可以明显延长荷瘤小鼠的存活期,高、中、低剂量组的生命延长率分别为64.9%、56.7%和28.1%,与CTX对照组比较差异具有统计学意义(P<0.01).另外,高、中、低剂量组FAC明显提高荷瘤小鼠的胸腺指数和脾指数,与正常对照模型组比较差异具有统计学意义(P<0.05);且高、中剂量组能显著提高巨噬细胞吞噬功能和淋巴细胞转化能力,与正常对照模型组比较差异具有统计学意义(P<0.01);而CTX的作用方向相反,与正常对照模型组比较差异也具有统计学意义(P<0.01).结论:FAC可抑制肝癌H22细胞生长,延长荷瘤小鼠存活期,并能提高荷瘤小鼠的非特异性免疫功能.FAC可能通过调节机体免疫功能来发挥抗肿瘤作用.     

Effect of 7,12-dimethylbenz[a]anthracene-induced mammary carcinogenesis on the opioid peptide levels in the rat central nervous system

Mammary tumors were induced in female Sprague-Dawley rats by giving a single oral dose of 20 mg 7,12-dimethylbenz[a]anthracene (DMBA). Animals were killed after full development of tumors 4 months after the ingestion of DMBA. Opioid peptides in various tissues were estimated by radioimmunoassay (RIA). Tumor-bearing rats (n = 5) had higher (P less than 0.05) contents of beta-endorphin in pituitary (+60%), striatum (+52%) and midbrain (+85%) compared to animals with no tumors. However, tumor-bearing rats showed a decrease of 35% in striatal met-enkephalin content. Dynorphin level decreased (P less than 0.05) in pituitary (-49%) and hypothalamus (-29%) of tumor-bearing rats. Thus for the first time, we report the alteration in the level of these neuropeptides during the process of chemical carcinogenesis.     

Amino acid profiles in tumor-bearing and pair-fed nontumor-bearing malnourished rats

To investigate the metabolic and organ changes accompanying growth of a malignant tumor, ten male Fisher 344 rats weighing 150 to 200 g were inoculated subcutaneously with 10(6) viable MCA sarcoma cells (tumor-bearing). Ten other rats (controls) were similarly inoculated with saline. Both groups were allowed food and water ad libitum. An additional ten rats (pair-fed) were inoculated with saline and fed the same mean daily food intake as the tumor-bearing rats. Thirty-five days after inoculation the rats were killed by exsanguination. Livers, spleens, and tumors were weighed, and amino acid profiles and biochemical parameters were measured. Liver and spleen weights in tumor-bearing rats were significantly greater than control rats (P less than 0.05 and P less than 0.01, respectively). Liver weight in pair-fed rats was significantly less than control rats (P less than 0.01), but spleen weight was greater (P less than 0.01). Amino acid profiles of tumor-bearing rats and pair-fed rats were different from each other and from those of control rats. Branched-chain amino acids were lowest in tumor-bearing rats and significantly different from control and pair-fed rats. Lysine was significantly higher (P less than 0.01) and arginine significantly lower (P less than 0.05) in tumor-bearing rats compared with control rats. These different plasma amino acid profiles and changes in serum biochemistry of cachectic tumor-bearing rats compared with malnourished pair-fed rats suggest specific tumor effects on host metabolism not mediated solely by anorexia.     

Functional characteristics of transplantable rat pituitary tumor MtT SA5 inducing pronounced adrenal hyperplasia

Transplantable rat pituitary tumor MtT SA5 is characterized by the induction of pronounced adrenal enlargement. In spite of remarkable elevation of plasma ACTH levels, serum corticosterone levels in hypophysectomized tumor-bearing rats were lower than those in intact control rats. No immunohistochemical alterations were seen in corticotrophs of the pituitary in tumor-bearing rats. Ratio of bioactive ACTH (Bio-ACTH) to immunoreactive ACTH (Ir-ACTH) in the tumor tissues was 0.2%, being extraordinarily lower than in the pituitary tissues (23%). Gel chromatography of the tumor tissue showed large molecular weight forms of Ir-ACTH, which seem to result from abnormal processing of proopiomelanocortin, and are responsible for the lower levels of Bio-ACTH compared to Ir-ACTH. The MtT SA5 tumor is suggested to secrete ACTH-related peptides which induce pronounced adrenal enlargement with little or no stimulation of glucocorticoid production.     

Studies on estrogen induced pituitary tumor in the rat with special reference to the relationship of the tuberoinfundibular dopamine neuron system

Pituitary tumors were experimentally induced in female Wistar rats by repeated injections of estradiol dipropionate. The hypothalamus and pituitary tumors were studied simultaneously by fluorescence histochemistry and immunohistochemistry. The pituitary gland became larger with a concomitant increase of serum prolactin in proportion to the dose of estrogen. Estrogen-induced pituitary tumor exhibited a proliferating prolactin cells by the peroxidase immunohistochemical method. Ultramicroscopical findings showed that these tumor cells were in an extremely hyperfunctional state. The dopamine neuronal perikarya in the hypothalamic arcuate nucleus and their terminals in the external layer of the median eminence were examined by fluorescence histochemistry in the rats bearing estrogen induced pituitary tumor and it was concluded that in our experimental conditions, estrogen effected directly on pituitary rather than on the hypothalamus and consequently dopamine synthesis in the arcuate neurons and its release into portal capillaries were accerelated simultaneously in order to inhibit prolactin secretion from tumor cells.     

Stimulatory effects of retinoic acid on tumor growth and serum insulin-like growth factor-1 in rats bearing estrogen-responsive pituitary tumor MtT/Se

MtT/Se is one of 4 cell lines derived from an estrogen-dependent pituitary tumor, MtT/F84. The main difference between these tumor types is that MtT/F84 secretes both growth hormone (GH) and prolactin (PRL) whereas MtT/Se secretes only GH. MtT/Se grew slowly in ovariectomized (ovex) rats, but tumor growth was much faster in estrogen-treated ovex rats. Effects of dietary retinoic acid (RA) on tumor growth, serum GH and insulin-like growth factor-1 (IGF-1) levels were examined in ovex rats. Latency of tumor growth was shortened, and tumor take and weight were promoted by all-trans RA both in the presence and absence of exogenous estrogen. Serum GH and IGF-1 levels became increased in tumor-bearing rats whereas PRL levels remained unchanged. Serum IGF-1 levels exhibited a good correlation with tumor weights (r = 0.84). Our results suggest a close relationship between increase of tumor weight and stimulation of serum IGF-1 level by RA in tumor-bearing rats.     

松针叶绿素-胡萝卜素软膏对S180荷瘤小鼠的抗肿瘤作用及其对免疫功能的影响

目的探讨松针叶绿素-胡萝卜素软膏对S180荷瘤小鼠的抗肿瘤作用及其对免疫功能的影响,为其进一步研发提供实验依据。方法采用小鼠移植性S180肉瘤模型,观察和测定松针叶绿素-胡萝卜素软膏(400、600、800 mg/kg)单独给药和联合环磷酰胺给药时的抑瘤率和免疫器官指数,并通过测定荷瘤小鼠血清半数溶血值、廓清指数以及吞噬系数来评价其对免疫功能的影响。结果松针叶绿素-胡萝卜素软膏中、高剂量组有显著抑瘤效果(P<0.05,P<0.01),低、中剂量组对环磷酰胺有显著的协同增效作用(P<005,P<0.01)。松针叶绿素-胡萝卜素软膏可显著提高荷瘤小鼠以及环磷酰胺化疗导致的血清半数溶血值(P<0.01)、廓清指数K和吞噬系数α值下降(P<0.05)。结论松针叶绿素-胡萝卜素软膏能抑制小鼠移植性S180肉瘤生长,提高环磷酰胺化疗效果,其机制可能与增强机体免疫功能有关。     

肝动脉阻断结合外放射治疗大鼠肝移植瘤的初步观察

[目的]观察肝动脉阻断法结合外放射治疗肝肿瘤的效果。[方法]采用大鼠肝内移植Walker256肿瘤模型,以肝动脉结扎(HAL)的方法阻断肝动脉血供。荷瘤大鼠分为对照组、HAL组、HAL 外放射(RT)组。观察治疗后肝内肿瘤的大小变化,原位杂交法检测肿瘤组织VEGFmRNA表达水平,免疫组化法检测肿瘤组织PCNA表达。[结果]对照组、HAL组、HAL RT组肿瘤体积分别为(0.88±0.33)cm3、(0.53±0.43)cm3、(0.33±0.32)cm3,HAL组和HAL RT组的肿瘤生长抑制率分别为39.8%、62.5%。HAL RT组的肿瘤体积较对照组明显缩小(P<0.01),而且,HAL RT组PCNA及VEGFmRNA表达水平与对照组相比明显下降(P<0.05)。[结论]肝动脉阻断结合外放射综合治疗较单独的动脉阻断治疗可提高治疗效果。     

Local treatment of mixed osteolytic/osteoblastic spinal metastases: is photodynamic therapy effective?

The widespread use of systemic and local therapies aimed at spinal metastatic lesions secondary to breast cancer has increased the incidence of mixed osteolytic/osteoblastic patterns of bony disease. The complex structure of these lesions requires novel therapeutic approaches to both reduce tumor burden and restore structural stability. In photodynamic therapy (PDT), a minimally invasive approach can be used to employ light to activate a photosensitizing agent that preferentially accumulates in tumor tissue, leading to cell toxicity and death. Previous work in an osteolytic rat model (MT-1) demonstrated that PDT effectively ablates tumor and improves vertebral structural properties. The aim of this study was to assess the efficacy of PDT in a rat model of mixed osteolytic/osteoblastic spinal metastases. Mixed spinal metastases were generated through intracardiac injection of Ace-1 canine prostate cancer cells into female athymic rats (day 0). A single PDT treatment was applied to lumbar vertebra L2 of tumor-bearing and healthy control rats (day 14). PDT-treated and untreated control rats were euthanized and excised spines imaged with μCT to assess bone quality (day 21). Spines were mechanically tested or histologically processed to assess mechanical integrity, tumor burden, and remodelling properties. Untreated tumor-bearing vertebrae showed large areas of osteolysis and areas of immature, new bone formation. The overall bone quality resulting from these lesions consisted of decreased structural properties but without a significant reduction in mechanical integrity. PDT was shown to significantly decrease tumor burden and osteoclastic activity, thereby improving vertebral bone structural properties. While non-tumor-bearing vertebrae exhibited significantly more new bone formation following PDT, the already heightened level of new bone formation in the mixed tumor-bearing vertebrae was not further increased. As such, the effect of PDT on mixed metastases may be more influenced by suppression of osteoclastic resorption as opposed to the triggering of new bone formation.