非小细胞肺癌根治术后放射治疗价值的前瞻性研究

目的　评价术后放疗对根治术后N1与N2 非小细胞肺癌的作用。方法　 1982年 2月至 1995年12月收治的 36 6例小于 6 5岁的N1与N2 非小细胞肺癌病例 ,随机分为术后放疗组 (n =184)和单纯手术组 (n= 182 )。结果　术后放疗组和单纯手术组 5年生存率分别为 43 .4%± 5 .1%和 40 .5 %± 4.6 % (P =0 .5 6 ) ,5年无瘤生存率分别为 42 .9%± 5 .2 %和 38.3 %± 4.5 % (P =0 .2 8)。T3 4 N1M0 患者在术后放疗组的 5年生存率和5年无瘤生存率分别为 5 8.1%± 15 .5 %和 6 5 %± 12 % ,单纯手术组则分别为 39.9%± 10 .2 % (P =0 .0 92 )和40 %± 10 % (P =0 .0 5 7)。术后放疗可明显减少胸内复发 (P <0 .0 1)。结论　术后放疗可减少局部复发 ,对总的生存改善不明显 ,但对T3 4 或N1患者有望获得治疗益处     

LMP1通过Survivin抑制60Co诱导鼻咽癌细胞凋亡

目的　研究EB病毒编码的潜伏膜蛋白 1(LMP1)介导凋亡抑制蛋白 (Survivin)表达对辐射效应的影响。方法　利用LMP1可调控表达鼻咽癌细胞系 (Tet on LMP1HNE2 )诱导LMP1表达 ,同时 60 Co照射 5Gy ,采用形态学观察、流式细胞术和半胱氨酸蛋白酶 3(Caspase 3)活性检测等方法 ,分析LMP1表达对60 Co诱导鼻咽癌细胞凋亡的影响。用反义Survivin寡核苷酸阻断Survivin表达 ,观察Sur vivin表达阻断对60 Co辐射效应的影响。结果　LMP1表达抑制60 Co诱导鼻咽癌细胞凋亡 ,LMP1表达60 Co照射组形态学和流式细胞术检测凋亡率 (32 .7%± 2 .1% ,6 .3% )明显低于LMP1表达阴性组 (6 6 .0 %± 3.0 % ,2 9.6 % ) (P <0 .0 5 ) ;转染Survivin反义寡核酸后细胞凋亡率 (5 9.3%± 3.2 % ,3.0 % )明显高于对照组 (2 6 .0 %± 2 .6 % ,8.6 % ) (P <0 .0 5 ) ;同样转染Survivin反义寡核酸组Caspase 3活性 (3.78nmol/ 10 6)高于对照组 (2 .79nmol/ 10 6)。结论　提示LMP1通过介导Survivin表达而抑制60 Co照射诱导凋亡 ,Survivin反义核酸协同辐射诱导肿瘤细胞凋亡 ,Survivin作为增敏放射治疗靶 ,具有潜在的临床意义。     

树突状细胞瘤内注射联合放疗对小鼠肾癌组织Bcl-2和Bax表达的影响

目的:研究放疗增强树突状细胞免疫治疗小鼠肾癌的作用与机制。方法:应用Ren-ca肾癌细胞制作BALB/c小鼠皮下移植瘤模型,分为对照组、单纯放疗组、单纯DC组和DC联合放疗组共4组进行治疗。皮下荷瘤的BALB/c小鼠,在接种瘤细胞后第12~16天,连续5d接受肿瘤局部放射治疗,7Gy6MeV/次,并于第11、15、19和22天分别4次在肿瘤部位直接注射未负载肿瘤抗原的DC细胞,1×106/次,第28天处死小鼠。检测各组肿瘤生长速度和质量。利用免疫印迹法(Westernblot法)检测肿瘤组织的相关凋亡蛋白表达。结果:接受不同治疗的小鼠体内肿瘤质量明显不同,未治疗组为(5·3±0·8)g,单纯DC组(4·5±0·7)g,单纯放疗组(2·8±0·3)g,DC联合放疗组(1·1±0·7)g,经Wilcoxon-Mann-Whitney秩和检验,DC联合放疗组与单纯治疗组和对照组之间差异均有统计学意义,P<0·01。DC联合放疗组肿瘤组织中抗凋亡蛋白Bcl-2表达下调,促凋亡蛋白Bax表达上调。结论:瘤内注射DC联合放疗比单一方法明显提高抑制Renca肾癌细胞在BALB/c小鼠的生长,其增效作用涉及肿瘤细胞的凋亡机制。     

介入治疗对肾母细胞瘤瘤细胞凋亡的影响及其机制探讨

目的研究介入治疗对肾母细胞瘤瘤细胞凋亡的影响,并探讨瘤细胞凋亡的相关途径和机制.方法收集在广州中山医科大学附属医院确诊并行术前介入治疗的肾母细胞瘤17例,另收集单纯行手术切除标本22例作为对照.采用原位细胞凋亡(TUNEL法)检测肾母细胞瘤组织中瘤细胞的凋亡,以瘤细胞凋亡指数(apoptoticindex,AI)作为瘤细胞凋亡记数指标;采用免疫组化法检测瘤细胞p53、bcl-2和bax蛋白的表达.结果 (1)94.9%(37/39)的病例中均有不同数量的阳性凋亡瘤细胞出现,其中17例介入治疗组瘤细胞平均AI为50.55士48.05/高倍视野,明显高于22例单纯手术组的19.73士29.07/高倍视野,两者差异具有显著性(P＜0.01);(2)p53和bcl-2蛋白过表达率分别为17.9%(7/39)与82.1%(32/39),与瘤细胞AI均无相关性(P＞0.05);(3)bax蛋白过表达率为97.4%(38/39),介入组瘤细胞表达率(80.0%)明显高于单纯手术组(40.0%),两者差异具有显著性(P＜0.05).结论 (1)术前对肾母细胞瘤行介入治疗可以促进瘤细胞的凋亡;(2)肾母细胞瘤的瘤细胞凋亡可能是一种p53非依赖性的凋亡,bcl-2对瘤细胞的凋亡不起主要的调节作用,而bax过表达可能导致瘤细胞凋亡的主要因素;(3)介入治疗后肾母细胞瘤瘤细胞的凋亡可能是组织缺血、缺氧,以及化疗药物造成的bax过表达,而由bax介导的细胞凋亡.     

丹参酮ⅡA对乳腺癌细胞的影响及其分子机制

目的 观察丹参酮ⅡA(TanⅡA)对乳腺癌细胞增殖和凋亡的影响,并探讨其分子机制.方法 选取处于对数生长期的乳腺癌MCF-7细胞,设对照组(0μg/ml TanⅡA)和处理组(0.25、0.50、0.75μg/ml TanⅡA),处理MCF-7细胞48 h.MTT法检测各组MCF-7细胞的增殖抑制率,流式细胞术检测各组MCF-7细胞的凋亡率,Western Blot和RT-PCR分别检测各组MCF-7细胞中p53、Bcl2的蛋白和mRNA表达水平.结果 与对照组比较,不同剂量TanⅡA处理组的MCF-7细胞增殖抑制率升高(P﹤0.05),且呈剂量-时间依赖性;随着TanⅡA作用剂量的增加,MCF-7细胞的凋亡率逐渐增大,均高于对照组(P﹤0.05).与对照组比较,0.75μg/ml TanⅡA处理组的p53蛋白表达升高,Bcl2蛋白表达水平下降,差异有统计学意义(P﹤0.05);与对照组比较,0.75μg/ml TanⅡA处理组的p53 mRNA表达水平增加,Bcl2 mRNA表达水平降低,分别为对照组的4.88倍和0.42倍(P﹤0.05);0.75μg/ml TanⅡA处理组的p-AKT蛋白表达水平(0.866±0.015)低于对照组的p-AKT蛋白表达水平(1.000±0.020),差异有统计学意义(P﹤0.05).结论 TanⅡA对乳腺癌MCF-7细胞具有抑制增殖和促进凋亡的作用,其凋亡作用与p53和Bcl2蛋白的表达有关,其抗凋亡机制与p-AKT信号通路有关.     

Bcl-2家族相关基因蛋白在胃癌组织中的表达及意义

目的　通过对胃癌组织中凋亡细胞的原位观察和Bcl 2、Bcl XL、Bcl XS/L、BAX和Mcl 1的表达状态的研究 ,探讨不同病理类型胃癌组织细胞凋亡情况及Bcl 2家族凋亡调控基因蛋白在胃癌组织中的表达对细胞凋亡的影响。方法　 5 8例胃癌手术根治标本 ,分别进行凋亡细胞的原位检测 (TUNEL)和Bcl 2、Bcl XL、Bcl XS/L、BAX和Mcl 1蛋白的免疫组化染色。结果　高、中分化腺癌的细胞凋亡指数明显高于低分化和未分化腺癌 (P <0 .0 5 ) :Bcl 2、Bcl XL、Mcl 1抗原表达阳性的胃癌组织细胞凋亡指数明显低于三种抗原表达阴性的胃癌组织 (P <0 .0 1) ,而BAX、Bcl XS/L抗原表达阳性的胃癌组织细胞凋亡指数明显高于二种抗原表达阴性的胃癌组织 (P <0 .0 1) ;Bcl 2、Bcl XL、BAX和Bcl XS/L在高、中分化腺癌中的表达明显高于低分化腺癌和未分化腺癌 (P <0 .0 1) ,而Mcl 1在低分化腺癌中的表达明显高于高、中分化腺癌(P <0 .0 5 )。结论　高、中分化腺癌的细胞凋亡率高 ,促凋亡基因表达阳性的胃癌组织细胞凋亡率高。Bcl 2、Bcl XL、BAX和Bcl XS/L可能与肠型胃癌的发生有关 ,而Mcl 1主要作用于弥漫型胃癌。     

氟脲嘧啶术前化疗诱导胃癌细胞凋亡的临床研究

目的 :研究 5 氟脲嘧啶 ( 5 FU)术前化疗诱导胃癌细胞凋亡的规律。方法 :37例胃癌患者术前静脉滴入 5 FU 150mg/ (kg·d) ,术中取胃癌组织标本 ,应用 3′ OH末端标记法 (TUNEL)检测细胞的凋亡率 (AI) ,与非化疗组比较。结果 :术前应用 5 FU组总的TUNEL指数为 ( 13.6± 4 .2 ) % ,对照组总的标记指数为 ( 9.4± 6 8) % ,差异有显著性 (P <0 0 5) ;对早期胃癌的诱导作用强于进展期胃癌 (P <0 .0 5)。5 FU诱导胃癌细胞凋亡有剂量依赖性。结论 :术前应用 5 FU辅助化疗可明显诱导胃癌细胞凋亡 ,具有一定的临床应用价值。     

基因对胃癌MGC 803细胞的抑制作用及其可能的机制

目的:研究沉默乳腺癌相关抗原1（breast cancerassociated antigen 1,BRCAA1)基因对胃癌细胞株MGC803的抑制作用及其可能的机制。方法：构建BRCAA1基因shRNA载体，将构建的shRNABRCAA1质粒与阴性对照质粒shRNAN转染胃癌MGC803细胞，24 h后用荧光显微镜观察转染效率，实时定量PCR检测 BRCAA1和GAPDH基因mRNA表达水平。MTT法检测转染后24、48与72 h的细胞增殖水平，AnnxinV PE/7AAD检测转染24 h后的细胞凋亡水平，Western blotting检测转染48 h后细胞的凋亡相关蛋白表达水平。结果：BRCAA1 siRNA表达质粒转染MGC803细胞24 h 的转染效率为（81.2±2.6）％ 。转染后48 h MGC803细胞的BRCAA1 mRNA水平下降了61.4％，MGC803细胞增殖的抑制率达45.0%，转染siRNA细胞的凋亡率明显高于未转染细胞和对照质粒转染细胞\[（14.4±１.6）% vs（5.4±2.0）％，（4.4±2.5）％，P<0.05\]。转染siRNA细胞的凋亡相关蛋白Rb与Bax的表达量显著增加（P<0.05），Bcl2的表达量显著减少（P<0.05）。结论：BRCAA1基因的沉默可有效抑制人胃癌MGC803细胞的增殖和诱导细胞凋亡，其机制与其促进Rb和Bax蛋白表达、抑制Bcl2蛋白表达有关。     

榄香烯乳区域动脉灌注对乳腺癌细胞凋邙和增殖的影响

目的观察中药提取物榄香烯乳术前区域动脉灌注对乳腺癌细胞凋亡和增殖的影响。方法应用末端转移酶介导的脱氧核苷酸末端标记法(TUNEL法)和增殖细胞核抗原(PCNA)、凋亡抑制基因蛋白(bcl-2)免疫组化检测方法,观察术前榄香烯乳治疗组14例和Ⅰ期手术组17例乳腺癌标本的凋亡指数,增殖指数和bcl-2蛋白表达强度的差异。结果榄香烯乳治疗组凋亡指数(7.97±1.50)明显高于Ⅰ期手术对照组(2.26±0.49);bcl-2蛋白表达(分值0.50±0.67)明显低于对照组(1.38±0.87),P值均<0.01;榄香烯乳治疗组增殖细胞核抗原指数(44.54±9.99)与对照组(42.80±6.78)差异无显著性,P>0.05;14例术前榄香烯乳治疗组等级相关分析凋亡指数与bcl-2分值呈中度负相关(rs=-0.508)。结论乳腺癌患者术前区域动脉灌注榄香烯乳可降低乳腺癌细胞bcl-2基因蛋白的表达,诱导乳腺癌细胞凋亡。     

榄香烯乳区域动脉灌注对乳腺癌细胞凋亡和增殖的影响

目的：观察中药提取物榄香烯乳术前区域动脉灌注对乳腺癌细胞凋亡和增殖的影响。方法：应用末端转移酶介导的脱氧核苷酸末端标记法（TUNEL法）和增殖细胞核抗原（PCNA）、凋亡抑制基因蛋白（bcl－2）免疫组化检测方法,观察术前榄香烯乳治疗组14例和Ⅰ期手术组17例乳腺癌标本的凋亡指数,增殖指数和bcl－2蛋白表达强度的差异。结果：榄香烯乳治疗组凋亡指数（7．97±1．50）明显高于Ⅰ期手术对照组（2．26±0．49）;bcl－2蛋白表达（分值0．50±0．67）明显低于对照组（1．38±0．87）,P值均＜0．01;榄香烯乳治疗组增殖细胞核抗原指数（44．54±9．99）与对照组（42．80±6．78）差异无显著性,P＞0．05;14例术前榄香烯乳治疗组等级相关分析凋亡指数与bcl－2分值呈中度负相关（rs＝－0．508）。结论：乳腺癌患者术前区域动脉灌注榄香烯乳可降低乳腺癌细胞bcl－2基因蛋白的表达,诱导乳腺癌细胞凋亡。     

子宫颈鳞状细胞癌组织中细胞凋亡及相关调控基因蛋白的表达

目的：通过对细胞凋亡及部分相关蛋白表达进行检测,探讨子宫颈鳞状细胞癌组织中凋亡细胞的调控机制。方法：应用原位末端标记法（ＴＵＮＥＬ）和双重免疫荧光染色技术对正常子宫颈及不同分化程度的鳞状细胞癌组织中凋亡细胞和Ｂａｘ、Ｂｃｌ－２、ｃａｓｐａｓｅ－３蛋白表达进行检测,利用共聚焦显微镜观察结果。结果：ＴＵＮＥＬ法检测发现,每例标本均有不同程度的细胞凋亡,但数量及分布区域不完全相同,低分化鳞状细胞癌凋亡细     

Role of Bcl-2 family of proteins in malignancy

B cell lymphoma gene-2 (Bcl-2) is the prototypic member of a growing family of proteins that play evolutionarily conserved, key regulatory roles in apoptosis. The Bcl-2 family members are characterized by the presence of one or more Bcl-2 homology domains and are comprised of both the prosurvival and proapoptotic proteins. Bcl-2 itself is a prosurvival member of the family and its aberrant expression has been linked to a variety of different cancers, including several hematological malignancies. Although the exact mechanism of action of Bcl-2 family of proteins in regulating apoptosis is still a matter of some debate, these proteins appear to act upstream of caspase activation. Many recent studies have shown the therapeutic potential of targeting Bcl-2 family members for the treatment of cancer. This article summarizes what is currently known about Bcl-2-like proteins and how the evolving understanding of the biology of these proteins is paving way for the development of novel cancer therapeutics.     

Evaluation of Effects of Metformin in Primary Ovarian Cancer Cells

Background: Ovarian cancer is the third most common cause of cancer in Indian women. Despite an initial70-80% response rate, most patients relapse within 1-2 years and develop chemoresistance. Hence, identificationor repositioning of drugs to resensitise ovarian cancer cells to existing chemotherapy is needed. Traditionallyimmortalized cell lines have been used in research, but these may contain genetic aberrations and chromosomalabnormalities serving as poor indicators of normal cell phenotype and progression of early-stage disease. Theuse of primary cells, maintained for only short periods of time in vitro, may serve as the best representative forstudying in vivo conditions of the tissues from which they are derived. In this study we have attempted to evaluatethe effect of metformin (an antidiabetic drug) in primary ovarian cancer cells because of its promising effectin other solid tumours. Materials and Methods: Primary cultures of epithelial ovarian cancer cells establishedfrom ascitic fluid of untreated ovarian cancer patients were used. The cells were treated with metformin at dosesstandardized by MTT assay and its ability to induce apoptosis was studied. The cells were analysed for apoptosisand apoptosis related proteins by flow cytometry and western blotting respectively. Results: Metformin inducedapoptosis in ovarian cancer cells, provoking cell cycle arrest in the G0/G1 and S phase. It induced apoptosis inovarian cancer cells by, down-regulating Bcl-2 and up-regulating Bax expression. Conclusions: Metformin wasable to induce apoptosis in primary ovarian cancer cells by modulating the expression of Bcl-2 family proteins.These data are relevant to ongoing translational research efforts exploring the chemotherapeutic potential ofmetformin.     

Bcl-X expression in esophageal squamous cell carcinoma: association with tumor progression and prognosis

BACKGROUND AND OBJECTIVES: Bcl-2 family proteins are regulators of programmed cell death and important in the development and progression of human various tumors. The role of these proteins in the development, progression and differentiation of esophageal squamous cell carcinoma (ESCC) is unclear. METHODS: We investigated the expression of Bcl-2, Bcl-X, and Bax using immunohistochemistry in 86 ESCCs, and scored the expression by the weighted score. RESULTS: Bcl-2 expression related to pT category (P=0.043) and histological grade (P = 0.001). Bcl-X expression related to pT category (P = 0.003), pN category (P = 0.041) and the number of positive nodes (P = 0.036), and had a tendency to relate to histological grade (P = 0.086). Bax expression had a tendency to relate to pN category (P = 0.081). The inverse relationship between Bcl-2 and Bcl-X expression was detected (P = 0.001), while the positive one between Bcl-X and Bax expression was detected (P = 0.014). Patients with low Bcl-X weighted score had a significantly longer survival compared with those with high Bcl-X weighted score. Multivariate analysis revealed Bcl-X expression as the independent prognostic factors (P = 0.022). CONCLUSION: These results imply that Bcl-2 family proteins, especially Bcl-X, may contribute to the progression in ESCC.     

雄黄抑制卵巢癌细胞株SKOV3增殖和诱导凋亡的体外研究

目的 研究中药雄黄主要成分As₄S₄对卵巢癌细胞株SKOV3细胞的增殖抑制和诱导凋亡的作用及其机制。方法 不同浓度As₄S₄(20 μmol/L、40 μmol/L、60 μmol/L、80 μmol/L),处理SKOV3细胞24 h,48 h,72 h后,透射电镜观察细胞形态变化;MTT法测定细胞增殖抑制率;流式细胞仪检测细胞凋亡率和细胞周期变化;RT-PCR法和Westernblot法检测As₄S₄对卵巢癌细胞株SKOV3细胞Bcl-2和Bax mRNA和蛋白的表达影响。结果 不同浓度As₄S₄处理的卵巢癌细胞株SKOV3,细胞增殖受到抑制,作用呈明显的浓度、时间依赖性,差异有统计学意义(P＜0.01);流式细胞仪进行细胞周期DNA成分分析结果显示,随着As₄S₄浓度的增加SKOV3细胞G₀/G₁期细胞百分比明显降低,S期细胞百分比上升;Bcl-2的表达随药物作用浓度的增加而递减,Bax的表达随药物作用浓度的增加而增强。结论 四硫化四砷具有抑制SKOV3细胞生长增殖的作用,其作用机制与诱发细胞凋亡和调节Bcl-2与Bax表达有关。     

Survivin在胃癌组织中的表达及其与Bcl-2、Bax表达的关系

目的: 探讨Survivin在胃癌组织中的表达及其与Bcl2、Bax表达的关系,并讨论它们相关的临床意义。 方法：选择临床及病理资料完整的中国医科大学附属盛京医院2005-2007年手术切除并经病理证实为胃腺癌术前均未行化放疗的蜡块标本54例,另取良性胃黏膜组织15例。应用免疫组化SP法检测54例胃癌组织中Survivin、Bcl2、Bax的表达,并检测15例正常胃黏膜组织中Survivin的表达。 结果：54 例胃癌组织中有39例Survivin 表达阳性,阳性率为72.2%;15例正常胃黏膜组织中无Survivin 阳性表达。 Survivin的表达与胃癌的浸润深度、淋巴结转移和TNM分期密切相关（P<0.05或P<0.01),而与患者的性别、年龄、肿瘤大小、远隔转移及分化程度无相关性。Bcl2阳性表达者中Survivin阳性表达率为81.8%,Bcl2阴性表达者中Survivin阳性表达率为57.1%,Survivin与Bcl2的表达呈正相关（P<0.01);而Survivin与Bax的表达无明显相关性。结论：胃癌组织中Survivin的表达与肿瘤的浸润深度、淋巴结转移和临床分期密切相关;Bcl2的表达呈正相关,而与Bax的表达无明显相关性     

An association of Bcl-2 phosphorylation and Bax localization with their functions after hyperthermia and paclitaxel treatment

Apoptosis is induced by many kinds of therapy-related inducers, such as hyperthermia and chemotherapeutic agents. However, differences in apoptotic pathways between these inducers remain unclear, although knowing the differences is important to map out a therapeutic strategy. Therefore, we focused on the localization and phosphorylation of Bcl-2 and Bax, key mediators of the apoptotic pathway, after hyperthermia and paclitaxel treatment of PC-10 squamous cell carcinoma cells that excessively expressed Bcl-2 and Bax in the cytoplasm. Paclitaxel treatment markedly induced qualitative changes in Bcl-2, whereas hyperthermia did only quantitative changes in Bax. The levels of Bax increased gradually with the duration of hyperthermia, whereas Bcl-2 levels slightly decreased. On the other hand, paclitaxel treatment induced dose- and time-dependent phosphorylation of Bcl-2. Interestingly, phosphorylated Bcl-2 was observed in the specific subcellular sites, mitochondria- and lysosome-rich fractions. Both treatments disturbed the heterodimerization of Bax with Bcl-2. Hyperthermia, but not paclitaxel treatment, induced a gradual Bax translocation from the cytoplasm to the nucleus. Although both treatments induced a prominent cell cycle disturbance in the G2M phase, paclitaxel treatment induced typical apoptosis, and hyperthermia hardly induced apoptosis. Our results suggest that the subcellular redistribution of Bax and the phosphorylation of Bcl-2 depend on the type of apoptosis inducers, such as hyperthermia and paclitaxel, and Bcl-2 has a central role in the decision of apoptotic outcome. Our data may afford new insights in apoptosis from the aspect of an association of Bcl-2 phosphorylation with intracellular Bax localization.     

胃液对膀胱癌细胞系Bcl-2/Bax表达的影响

 目的　为了探讨胃液诱导膀胱癌细胞系细胞凋亡的机制。方法　采用流式细胞术及免疫组化方法观察了胃液对膀胱癌细胞系BIU-87细胞凋亡及Bcl-2/Bax表达的影响。结果　显示胃液处理后AI值升高,Bcl-2表达降低,Bax表达升高,Bcl-2/Bax比值为0.71。结论　提示胃液诱导BIU-87细胞凋亡可能是通过降低Bcl-2,升高Bax而实现的。     

甘草多糖的体内抑瘤作用及其机制的研究

目的：探讨甘草多糖对于S-180荷瘤小鼠体内肿瘤的抑制作用及其机制。方法：Balb/c小鼠接种S-180肉瘤瘤株后，分别给予甘草多糖和对照药物12天，然后处死。将荷瘤小鼠的肿瘤取出称重，并进行比较；免疫组织化学方法和HE染色对肿瘤中的bcl-2、p53和bax蛋白进行比较分析。结果：给予甘草多糖的小鼠的肿瘤明显小于对照组，而对照组的bcl-2和p53蛋白的表达率明显高于甘草多糖的小鼠组，bax蛋白的表达率则低于后。结论：甘草多糖对于S-180肿瘤具有抑制作用，并有可能影响bcl-2、p53及bax基因蛋白的表达。     

Predictive value of p53, Bcl2 and bax in the radiotherapy of head and neck cancer

Radiation is known to induce DNA damage resulting in the onset of apoptosis. The apoptosis is modulated by p53, Bcl2 and Bax proteins. High level of wild type p53 is required for radiation induced apoptosis. The p53 status, therefore, may be a crucial determinant of radiosensitivity of tumor cells. Overexpression of Bcl2, however, inhibits apoptosis via hetero- and homodimeric interaction. Bax might function as a cell death effector molecule that is neutralized by Bcl2. The aim of the present study is to investigate the correlation between p53, Bcl2, Bax and c-myc levels and the clinical response of head and neck cancer patients to radiation. The base line and 30 GY gamma radiation induced values of p53, Bcl2, Bax and c-myc were estimated by Western blot in 40 biopsies of head and neck cancers. We found that the radiosensitivity of head and neck cancer patients depends on the ratio of p53, Bcl2 and Bax protein levels. High Bcl2 levels resulted in radioresistance of cancer patients. Overexpression of Bax and c-myc may ensure the radiosensitivity of head and neck cancer patients. Our studies indicate that prediction of radiation sensitivity of tumors could be based on the simultaneous evaluation of p53, Bax and Bcl2 levels.