异体DBM骨粒复合rhBMP-2及骨水泥材料修复骨缺损的实验研究

目的探讨异体脱钙骨基质（DBM）骨粒、骨水泥（BC）及重组人骨形态发生蛋白-2（rhBMP-2）复合材料修复实验性骨缺损的能力。方法复合材料植入兔实验性尺骨骨缺损部位（A组），B组植入纯骨水泥棒材作为对照。不同时间行组织学、印度墨汁动脉血管灌注及材料自然断面扫描电镜观察。结果材料植入第2周表面纤维组织样完整包膜形成，材料外周及两端血管形成密集，并向材料中长入；第4、8、12周新生血管明显增多，且深入至材料中央，新生间充质组织继续大量长入；包绕DBM骨粒的间充质组织部分4周转化为软骨。第8、12周软骨趋于成熟，可见含有造血骨髓的新生骨组织形成，其间可见较多的哈佛氏系统；同时，可见明显DBM骨粒被新生组织爬行吸收现象。第4周原自然裂隙部分已被结构紊乱的胶原纤维束充填。第8至12周，可见大量排列紊乱的矿化骨结构沿多方向长入，新生骨组织附于脱钙骨基质骨粒及骨水泥表面，原自然裂隙几近消失。植入B组材料者除外被纤维膜外余无变化。结论脱钙骨基质骨粒、骨形态发生蛋白、骨水泥复合材料具有良好的骨诱导及骨引导生成作用，是良好的骨缺损修复材料。     

MNNG诱发新生大鼠腺胃癌模型的建立及其在胃癌发病机制研究上的应用

通过给新生Ｗｉｓｔａｒ大鼠连续１０次（每日１次）１－甲基－３－硝基－１亚硝基肌（ＭＮＮＧ）灌胃，成功地诱发出腺胃癌、腺瘤和异型增生等病变。在０．４ｍｇ／只剂量组，这三种病变的诱发率分别为３９％、５０％和１００％，腺胃癌的诱发率与ＭＮＮＧ剂量成正比，雄性大鼠高于雌性（Ｐ＜０．０２），７０％病变发生在胃窦部。本模型具有致癌物用量小、易定量、给药期短、省时省力和不易污染环境等优点。研究还发现６个腺胃癌中有４个ＤＮＡ具有使ＮＩＨ／３Ｔ３发生恶性转化的作用，这种转化表现为对Ｂａｌｂ／ｃ裸鼠有致瘤性，提示在这种腺胃癌ＤＮＡ中存在转化基因。     

DNA甲基化抑制剂诱导Kasumi-1细胞分化和凋亡作用

目的：探讨DNA甲基化抑制剂5—氮—2′—脱氧胞苷(5—Aza—CdR)体外诱导Kasumi-1细胞分化和凋亡作用。方法：应用MTT比色法观察5—Aza—CdR对细胞的生长抑制作用，普通光学显微镜观察细胞形态和结构改变，流式细胞术检测髓系分化抗原的表达，DNA凝胶电泳分析细胞凋亡。结果：5—Aza—CdR明显抑制Kasumi-1细胞的生长，半数抑制浓度(IC50)约为0.65μmol/L。5—Aza—CdR可诱导Kasumi-1细胞髓系分化抗原CDllb和CDl3表达增加。5—Aza—CdR诱导Kasumi-1细胞凋亡。用5—Aza—CdR处理后的细胞出现单核细胞样分化和凋亡细胞形态改变。结论：5--氮—2′—脱氧胞苷抑制Kasumi-1细胞生长，并能诱导细胞部分分化与凋亡。     

肿瘤伴发贫血及其对肿瘤患者生活质量影响的调查

目的 :探讨肿瘤伴发贫血及其对患者生活质量的影响。方法 :应用简明健康状况调查表 (SF 36简表 )对 2 6 3例恶性肿瘤患者进行生活质量调查评定 ,并分析这些患者的贫血情况与其他一些临床因素之间的关系及对生活质量的影响。结果 :1)在 2 6 3例患者中总贫血发生率为 4 8 3% ,其中泌尿生殖系统肿瘤贫血的发生率最高 ,为 70 6 % ;血液系统肿瘤发生 3、4级贫血的比例最高 ,为 2 9 2 %。不同病种发生贫血的比例之间差异有显著意义。 2 )随肿瘤分期的升高 ,贫血发生率逐渐升高 ,且存在统计学差异 ,说明进展期肿瘤更易发生贫血。 3)不同性别、年龄和病程发生贫血的比例差异无显著意义。 4 )贫血对生活质量影响的单因素分析显示 ,贫血对体能状态、精神状态和总体生活质量均有显著影响 ,随贫血的加重生活质量下降。 5 )对生活质量影响因素进行多元逐步回归 ,显示贫血对于体能状态、精神状态和总体生活质量均存影响。结论 :轻、中、重度贫血对患者的生活质量、体能状态和精神状态均有影响 ,且随着贫血的加重而加重 ,必须充分重视纠正贫血的重要性。     

Chemosensitivity and radiosensitivity profiles of four new human epithelial ovarian cancer cell lines exhibiting genetic alterations in BRCA2, TGFbeta-RII, KRAS2, TP53 and/or CDNK2A

To address the cellular basis for the response to ovarian cancer treatment, we characterized the chemosensitivity and radiosensitivity of four human epithelial ovarian cancer cell lines that harbor different genetic alterations. The TOV-21G, TOV-81D, OV-90, and TOV-112D cell lines were derived from ovarian tumors (TOV) or ascites (OV) from chemotherapy- and radiotherapy-naive patients and were characterized by their mutation spectrum of BRCA2, TGF-RII, KRAS2, TP53, and CDKN2A. Cells were monitored for survival following exposure at various concentrations to different cytotoxic agents including cisplatin, camptothecin or paclitaxel or to different doses of -irradiation. At the lowest doses, the TGF-RII-mutated and KRAS2-mutated cell line, TOV-21G, and the BRCA2-mutated cell line, TOV-81D, demonstrated a significantly higher sensitivity to cisplatin and -irradiation than the TP53-mutated cell lines, TOV-112D and OV-90. At higher doses, differences between the TP53-mutated lines were observed with TOV-112D being less sensitive to cisplatin than OV-90 that also harbors a CDNK2A mutation. All cell lines were similarly sensitive to high doses of -irradiation. In contrast, sensitivity to camptothecin or paclitaxel was not significantly different between all cell lines, irrespective of the mutation status of BRCA1, BRCA2, TGF-RII, KRAS2, TP53, and CDKN2A. The observed responses to treatment are consistent with the current knowledge concerning BRCA2, TGF-RII, KRAS2, TP53, and/or CDKN2A aberrant function.The first and second authors contributed equally to this work.     

On the application of data on mode of action to carcinogenic risk assessment.

In the Forum article in this issue of Toxicological Sciences,Cohen et al. (2004) discuss a framework for systematic analysisof data on modes of carcinogenic action of chemicals in experimentalanimals, and its application to cancer risk assessment. Thissummarizes an exercise recently completed by the ILSI Risk ScienceInstitute (Cohen et al., 2003), which builds on a harmonizationinitiative of the International Programme on Chemical Safety(Sonich-Mullin et al., 2001). The framework approach is basedfundamentally on advances that have been achieved in recentdecades in understanding the pathogenesis of neoplasia. It isnow recognized that     

全反式维甲酸激活人肺腺癌细胞系GLC-82中-PIG-B高度同源基因-PIGB1

目的：探讨全反式维甲酸（all-trans retinlic acid,ＡＴＲＡ）诱导肿瘤细胞分化的分子机制。方法：采用Ｓouthern和Ｎorthern杂交方法对本室用ＡＴＲＡ诱导人肺腺癌细胞ＧＬＣ－８２,经消减杂交所构建的cＤＮＡ消减文库ＰＩＧＢ１,该基因与人ＰＩＧ－Ｂ（phosphaidylinlsitol glycan of clmplementaion class Ｂ）基因高度同源,在多种胎儿组织中均有表达。结论：ＰＩＧＢ１基因可能参与ＡＴＲＡ诱导肿瘤细胞分化过程。     

中线外周T细胞淋巴瘤长期随访结果(附56例临床分析)

目的　分析中线外周T细胞淋巴瘤( 原中线恶网) 的诊断、治疗结果及预后因素。方法　56 例中27 例进行免疫组化检查,所有病例均经过放射治疗,其中13 例配合化疗。结果　27 例免疫组织化学检查中19 例为T 细胞来源,1 例为B细胞来源,7 例不能分型。3,5,10 年生存率分别为59.2% ,51 .1% 和46 .0% 。全身(B) 症状、颈淋巴结侵犯及放射治疗剂量是影响生存率的重要因素。结论　原中线恶网多为结外侵犯的外周T 细胞淋巴瘤,放射治疗是局部首选的治疗方法,影响预后的重要因素为B症状,颈淋巴结侵犯及放射治疗剂量     

Results of a cohort of 200 hormone-naïve consecutive patients with prostate cancer treated with iodine 125 permanent interstitial brachytherapy by the same multidisciplinary team

PurposeTo report survival and morbidity of a cohort of 200 hormone-naïve consecutive patients with localized prostate cancer, treated by low-dose rate brachytherapy within the frame of multidisciplinary approach.Patients and methodsBetween 2001 and 2011, 200 patients were treated by the same team with 125 iodine seeds: 167 low-risk and 33 intermediate risk according to the d’Amico classification; eligible patients had clinical stage T1/T2a-b, Gleason score 3+3 or 3+4, baseline prostate-specific antigen level below 15 ng/mL, prostate volume less than 60 cm³. The median number of random biopsies was 12 (range 6–32) and the breakdown of positive cores was as follows: 1 (29%), 2 (35%), 3 or more (36%). Acute morbidity was assessed according to the Common Terminology Criteria for Adverse Events and late toxicity according to the EORTC/RTOG scale. Data were prospectively collected.ResultsThe median follow-up was 69 months (range 16 to 135). The 5- and 10-year biochemical relapse free survivals were 95.6% (95% confidence interval [CI]: 91–98) and 89.7% (95% CI: 79.4–95.0). The 5-year and 10-year overall survival were respectively 96.4% (95% CI: 92–98.4) and 89.7% (95% CI: 80.8–94.6%) and the 10-year disease specific survival, 99.1% (95% CI: 93.0–99.9). The 5- and 10-year grade 3 acute toxicity cumulative rate were respectively 3.3% (95% CI: 1.4–6.6) and 4% (95% CI: 1.4–6.6) and the 5- and 10-year grades 3 cumulative late toxicity 2.5% (95% CI: 2.0–5.9) and 4% (95% CI: 2.0–5.9).ConclusionBrachytherapy managed within the frame of a multidisciplinary approach – from diagnosis to evaluation – may offer optimized results with a reduced late toxicity rate, while remaining opened to dosimetry and technical improvements.