The Expression of Apoptosis-Related Genes Bcl-2 and Bax Protein and Apoptosis Positivity in Cervical Carcinoma during Irradiation

To evaluate the apoptosis positivity, the expression of Bcl-2, bax proteinsin 30 patients with squamous cell cervix carcinoma before and after radiotherapy. Methods: By usingimmuno-histochemical and TDT-dUTP nick end labelling techniques, 30 cases of squamous cell cervicalcarcinoma were analyzed. Results: The apoptosis positivity before and after irradiation was 76.7%and 100% respectively, with the difference being significant (P 【 0.05); The positive rates of Bcl-2protein before and after irradiation were 73.3% and 46.7% respectively, with the difference beingsignificant (P 【 0.05); The positive rates of bax protein before and after irradiation were 86% and100% respectively, with the difference being significant (P 【 0.05). Conclusion: bax and Bcl-2protein play an important role in apoptosis induced by fractionated radiation therapy. Apoptosisinduced by irradiation is contributed to upregulation of bax protein or downregulation of Bcl-2protein.

Signal transduction mediated by Bid,a pro-death Bcl-2 family proteins, connects the death receptor and mitochondria apoptosis pathways

Two major apoptosis pathways have been defined in mammalian cells, the Fas/TNF-R1 death receptor pathway and the mitochondria pathway. The Bcl-2 family proteins consist of both anti-apoptosis and pro- apoptosis members that regulate apoptosis, mainly by controlling the release of cytochrome c and other mitochondrial apoptotic events. However, death signals mediated by Fas/TNF-R1 receptors can usually activate caspases directly, bypassing the need for mitochondria and escaping the regulation by Bcl-2 family proteins. Bid is a novel pro-apoptosis Bcl-2 family protein that is activated by caspase 8 in response to Fas/TNF-R1 death receptor signals. Activated Bid is translocated to mitochondria and induces cytochrome c release, which in turn activates downstream caspases. Such a connection between the two apoptosis pathways could be important for induction of apoptosis in certain types of cells and responsible for the pathogenesis of a number of human diseases.

Effects of Ethyl Pyruvate on Myocardial Apoptosis and Expression of Bcl-2 and Bax Proteins after Ischemia-reperfusion in Rats

In order to study the effects of ethyl pyruvate on cardiomyocyte apoptosis following ischemia/reperfusion （I/R） in vitro and the expression of Bcl-2 and Bax proteins, isolated rat hearts were perfused in a Langendorff model. Twenty-four rats were randomly divided into 3 groups （n=8 in each group）： control group was perfused for 120 min. In the I/R group, after 30 min stabilization the injury was induced by 30 min global ischemia followed by 60 min reperfusion. Ethyl pyruvate （EP） group was set up with the same protocol as I/R group except that it was supplied with 2 mmol/L EP 15 rain before ischemia and throughout reperfusion. Myocardial malonaldehyde （MDA） content was measured. Myocardial apoptotic index （AI） was tested by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling （TUNEL） method. The expression of anti-apoptotic protein Bcl-2 and pro-apoptotic protein Bax in cardiac myocytes was detected by immunohistochemistry. As compared with control group, the content of MDA, myocardial AI and the expression of Bcl-2, Bax proteins were increased significantly in I/R group, but the content of MDA, myocardial AI and the expression of Bax protein were decreased obviously and the expression of Bcl-2 protein was up-regulated in EP group （P〈0.05）. These results demonstrate that EP could inhibit apoptosis of cardiac myocytes possibly via alleviating oxidative stress, up-regulating Bcl-2 and down-regulating Bax proteins.

Dioscin-induced Apoptosis of Human LNCaP Prostate Carcinoma Cells through Activation of Caspase-3 and Modulation of Bcl-2 Protein Family

Dioscin is a natural steroid saponin derived from several plants, showing potent anti-cancer effect against a variety of tumor cell lines. In the present study, we investigated the anti-cancer activity of dioscin against human LNCaP cells, and evaluated the possible mechanism involved in its antineoplastic action. It was found that dioscin（1, 2 and 4 μmol/L） could significantly inhibit the viability of LNCaP cells in a time- and concentration-dependent manner. Flow cytometry revealed that the apoptosis rate was increased after treatment of LNCaP cells with dioscin for 24 h, indicating that apoptosis was an important mechanism by which dioscin inhibited cancer. Western blotting was employed to detect the expression of caspase-3, Bcl-2 and Bax in LNCaP cells. The expression of cleaved caspase-3 was significantly increased, and meanwhile procaspase-3 was markedly decreased. The expression of anti-apoptotic protein Bcl-2 was down-regulated, whereas the pro-apoptotic protein Bax was up-regulated. Moreover, the Bcl-2/Bax ratio was drastically decreased. These results suggested that dioscin possessed potential anti-tumor activity in human LNCaP cells through the apoptosis pathway, which might be associated with caspase-3 and Bcl-2 protein family.

Influence of Tanshinone lla on heat shock protein 70,Bcl-2 and Bax expression in rats with spinal ischemia/reperfusion injury

Tanshinone lla is an effective monomer component of Danshen, which is a traditional Chinese medicine for activating blood circulation to dissipate blood stasis. Tanshinone Ila can effectively improve brain tissue ischemia/hypoxia injury. The present study established a rat model of spinal cord ischemia/reperfusion injury and intraperitoneally injected Tanshinone lla, 0.5 hour prior to model establishment. Results showed that Tanshinone Ila promoted heat shock protein 70 and Bcl-2 protein expression, but inhibited Bax protein expression in the injured spinal cord after ischemia/reperfusion injury. Furthermore, Nissl staining indicated a reduction in nerve cell apoptosis and fewer pathological lesions in the presence of Tanshinone Ila, compared with positive control Danshen injection.

Pretreatment with low-frequency repetitive transcranial magnetic stimulation may influence neuronal Bcl-2 and Fas protein expression in the CA1 region of the hippocampus: A possible anti-epilepsy mechanism in a lithium-pilocarpine-induced epileptic rat mod

BAOKGROUND： Bcl-2 and Fas proteins are well known as anti-apoptotic and pro-apoptotic factors respectively. However, whether the anti-epileptic mechanism of low-frequency repetitive transcranial magnetic stimulation （rTMS） involves an anti-apoptotic effect via regulating Bcl-2 and Fas protein expression remains to be determined. OBJECTIVE： To verify the correlation between the anti-epileptic mechanism following pretreatment of low-frequency rTMS and anti-hippocampal apoptosis. DESIGN, TIME AND SETTING： A randomized controlled animal experiment was performed at Institute of Neurological Disorders, Affiliated Hospital of North Sichuan Medical College between September 2007 and March 2008. MATERIALS： Pilocarpine （053K13011） was provided by Sigma, USA; lithium was provided by Shanghai Biotechnology Co., Ltd., China; Dantec Maglite-r25 rTMS instrument was provided by Dundee, Denmark. METHODS： A total of 21 adult male Wistar rats were randomly divided into control （n = 6）, rTMS pretreatment （n = 9）, and sham-stimulation （n = 6） groups. The rTMS pretreatment group was pretreated with low-frequency rTMS （0.5 Hz, 75% threshold intensity, 20 times/bundle, and 5 bundles/day）, while the sham-stimulation group was sham-stimulated with a similar sound for 7 successive days to establish lithium-pilocarpine-induced epileptic state models. MAIN OUTCOME MEASURES： Epileptic stroke latency; neuronal morphology was observed using hematoxylin and eosin staining; mean positive-reactive cell number and mean absorbance of Bcl-2 and Fas protein in the hippocampal CA1 region was observed using immunohistochemistry. RESULTS： Epileptic latency in the rTMS pretreatment group was significantly enhanced （P 〈 0.01）, and a number of degenerated neurons were observed to be apoptotic. Bcl-2 protein expression increased at each time point, but Fas protein expression decreased （P 〈 0.01）. CONCLUSION： Low-frequency rTMS has an anti-epileptic effect, which may be via regulation of Bcl-2 and Fas protein expression in the hippocampal region.

THE EXPERIMENTAL STUDY ON THE CELL APOPTOSIS AND EXPRESSION OF BCL-2 PROTEIN IN INTRACEREBRAL HEMORRHAGE IN MODEL OF RATS

Objective To study whether there is the apoptosis of neural cells and the expression of Bcl-2 protein in intracerebral hemorrhage (ICH) in model of rats, for the further understanding the mechanism of the delayed damage of the neural cells around the hematoma after ICH. Methods Fifty SD rats were randomly divided into 5 groups, ten in each. With the Group A as the control, the rest 40 were used to set up intracerebral hemorrhage model. The brains were taken out at 12 th , 24 th , 48 th and 72 th hours, respectively. Apoptosis cells were detected with terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL), and the expression of Bcl-2 protein was detected with immunochemical stainging methed (SP). Results In the control group, no apoptosis cells and Bc1-2 protein were detected. In rest groups, the apoptosis cells and Bc1-2 protein were expressed in different degree. Apoptosis rates verified and corresponded with the time after ICH, with the peak at 48 th -72 th hour after hemorrhage. The peak rate of apoptosis cells was (24.50±2.69)% and Bcl-2 protein expression was (20.76±1.97)% . There was significant difference between the experimental groups and control (P<0.05), and no linear relationship between the apoptosis rate and the expression of Bcl-2 protein. Conclusion Apoptosis may be an important factor in the secondary trauma of ICH. There is a time leg after hemorrhage. All this is instructive to clinical treatment in time. Bcl-2 protein keeps increasing in a certain time after hemorrhage, but not synchronize with the cell apoptosis. This indicates that bcl-2 has the effect to reduce the apoptosis of neural cells.

Regulatory Effect of Bcl-2 Family Proteins in CPB-induced Cardiomyocyte Apoptosis in Dog Hearts

Summary: Whether conventional hypothermic CPB induces myocyte apoptosis in dog hearts and modulation of bcl-2, bcl-xl, bax, bad, and caspase-3 pathways in this setting was investigated. Ten healthy adult dogs were randomized into sham-operated and CPB groups. Samples of left ventricle were obtained before, during and 3 h after CPB. In situ TUNEL was used to detect apoptotic myocytes. Immunohistochemistry and flow cytometry were employed for detection of expressions of bcl-2, bcl-xl, bax and bad proteins. Z-DEVD-AMC substrate cleavage and TBARS methods were used to measure the activity of caspase-3 and the content of lipid peroxide in LV myocardium, respectively. After CPB, the number of apoptotic myocytes in CPB group was significantly increased. The results of immunohistichemistry demonstrated that bcl-2, bcl-xl, bax and bad proteins were constitutionally present on the sarcolemma of the LV myocytes. FACS results showed that, after CPB, expressions of bax and bad in CPB group were significantly upregulated, while the expressions of bcl-2 and bcl-xl were not significantly changed in both groups. The activity of caspase-3 and the content of lipid peroxide in LV myocardium in CPB group were also significantly increased after CPB. The present study shows that there exists myocardiocyte apoptosis in dog hearts undergoing conventional hypothermic CPB and the myocyte apoptosis is initiated by ischemia and performed during reperfusion. Moreover, the CPB-induced myocyte apoptosis was associated with upregulation of expressions of bax and bad proteins, activation of caspase-3 and increase of oxidative stress.

THE QUANTITATIVE MEASUREMENT OF BCL-2, P53 PROTEIN AND PCNA EXPRESSION IN BREAST CARCINOMA AND THEIR CORRELATION WITH PROGNOSIS

To study quantitative index of bci-2, P53, Nroliferating cell nuclear antigen (PCNA),ER and PR in breast carcinoma and their correiation and their relatiousbip with prognosis, the ex expression of bcl-2, P53 and PCNA were studied by immunohistochemical technique. The measurementof ER and PR used enzyme linked affinuity histochemical methods. The quantitative index was analyzed by image technique. All analyses were hased on 60 breast carcinomas. The results were as follows:the more bcl-2 protein, the lower histological graded the longer survival term and the highersurvival rate (P< 0. 05). The quautitative measurement of bcl-2, P53 and PCNA expression were ofvalue in evaluating the degree of differentiation and prognosis in breast carcinoma. The quantitativeand qualitative measurement or p53 protein expression showed a Ⅰwerful evidence in evaluatingprognosis of bcl-2 were more significant in evaluating poor prognosis of breast carcinoma. A relationship between bcl-2 and ER, PR showed a better value for response to endocrine therapy in breastcarcinoma patients.

大肠癌组织中HSP27和bcl-2及p53蛋白的表达及其临床意义

目的:探讨热休克蛋白27(heatshockprotein,HSP27)、bcl-2和p53蛋白在大肠癌组织中的表达及其临床意义。方法:运用免疫组织化学SP方法检测HSP27、bcl-2和p53在72例大肠癌组织中的表达,并运用多因素COX比例风险模型分析患者的预后。结果:HSP27在大肠癌组织中的阳性率为69·44%(50/72),bcl-2为54·17%(39/72),p53为59·72%(43/72)。HSP27在高分化腺癌组的表达率为84·85%,显著高于低分化组的28·57%,χ2=29·614,P=0·000。bcl-2和p53在高分化腺癌组的表达率也高于低分化腺癌组,χ2=5·771,P=0·016;χ2=4·714,P=0·030。HSP27和bcl-2在大肠癌中的表达具有相关性,r=0·380,P=0·001。COX回归分析提示,HSP27表达与生存期呈负相关。结论:HSP27和bcl-2及p53与大肠癌耐药有关;联合检测对临床制定合理的化疗方案具有指导意义;HSP27可作为判断大肠癌预后的一个独立预测指标。

EGFR、p53、Bcl-2表达,Ki-67标记指数与胸腺瘤WHO组织学分型、分期及预后的关系

目的探讨EGFR、p53、Bcl-2表达,Ki-67标记指数(Ki-67Li)与胸腺瘤WHO组织学分型、分期及预后的关系。方法应用免疫组化染色方法检测46例胸腺瘤患者EGFR、p53、Bcl-2的表达和Ki-67标记指数。结果胸腺瘤EGFR、p53、Bcl-2阳性表达率分别为34.8%、56.5%、54.3%,Ki-67标记指数平均值为11.0%。EGFR、p53、Bcl-2蛋白表达与胸腺瘤WHO组织学分型均无明显关系;B2、B3、C型与A、AB、B1型之间Ki-67标记指数表达差异有显著性(P<0.05);Bcl-2蛋白表达与胸腺瘤Masaoka分期和预后均无关系(P>0.05);EGFR、p53蛋白的过度表达和Ki-67标记指数与胸腺瘤Masaoka分期明显相关(P<0.05);Ki-67标记指数与预后有关(P<0.05)。结论EGFR、p53蛋白的过度表达和Ki-67标记指数与胸腺瘤Masaoka分期明显相关,反应其侵袭性,Ki-67标记指数还与组织学分型相关,并可作为估计胸腺瘤预后的参考指标。

缺氧诱导因子-1α和BCL-2/腺病毒E1B19 kDa相关蛋白3在中耳胆脂瘤表达及意义

目的探讨缺氧诱导因子-1α(hypoxia inducible factor-1,HIF-1α)和BCL-2/腺病毒E1B19KDa相关蛋白3(Bcl2/adenovirus E1B 19 kD interacting protein 3,BNIP3)在中耳胆脂瘤中的表达及胆脂瘤上皮的凋亡情况。方法采用免疫组织化学方法检测30例中耳胆脂瘤标本与18例外耳道皮肤标本中HIF-1α和BNIP3蛋白的表达情况,使用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling,Tunel)检测20例中耳胆脂瘤标本和18例外耳道皮肤标本的凋亡情况。使用Pearson相关分析检验HIF-1α和BNIP3蛋白之间的相关性。结果 HIF-1α在胆脂瘤组和对照组的平均光密度分别为0.16±0.07和0.08±0.03,两组比较差异有统计学意义(t=4.279,P<0.01);BNIP3在胆脂瘤组和对照组的平均光密度分别为0.16±0.08和0.11±0.06,两组比较差异有统计学意义(t=2.463,P=0.0185);经pearson相关分析,在胆脂瘤上皮中,HIF-1α和BNIP3之间呈正相关(r=0.418,P=0.003);Tunel染色中,凋亡指数在胆脂瘤组和对照组分别为(52.8±12.5)%和(9.99±2.97)%,两组比较差异有统计学意义(t=14.166,P<0.01)。结论 HIF-1α和BNIP3在中耳胆脂瘤中的异常表达可能与胆脂瘤的高凋亡特性有关。

Specific COX-2 inhibitor NS398 induces apoptosis in human liver cancer cell line HepG2 through BCL-2

AIM: To evaluate the effects of NS-398, a cyclooxygenase-2 (COX-2) inhibitor, on the proliferation and apoptosis of HepG2 cells. METHODS: The effects of NS-398 on the proliferation of HepG2 cells were evaluated by MTT. DNA fragmentation gel analysis was used to analyze the apoptotic cells. DNA ploidy and apoptotic cell percentage were calculated by flow cytornetry. The expression of COX-2 and Bcl-2 mRNA was identified by competitive RT-PCR. Furthermore, expression level of Bcl-2 was detected using Western blot in HepG2 after treated with NS-398. RESULTS: NS-398 inhibited cell proliferation and induced apoptosis of HepG2 cells in a concentration-dependent manner. DNA ploidy analysis showed that S phase cells were significantly decreased with increase of NS-398 concentration. The quiescent GO/G1 phase was accumulated with decrease of Bcl-2 mRNA. Whereas NS-398 had no effect on the expression of COX-2 mRNA, and no correlations were found between COX-2 mRNA and HepG2 cell proliferation and apoptosis induced by NS-398 (r=0.056 and r=0.119, respectively). Bcl-2 protein level was inhibited after treated with NS-398. CONCLUSION: NS-398 significantly inhibits the proliferation and induces apoptosis of HepG2 cells. Mechanisms involved may be accumulation of quiescent GO/G1 phase and decrease of Bcl-2 expression.

THE EXPRESSION AND CLINICAL VALUE OF APOPTOSIS CONTROL GENE Bcl-2 AND Bax IN BREAST CANCER

Objective: To study the expression and clinical value of apoptosis control gene bcl-2 and bax in breast cancer. Methods: Protein bax and bcl-2 in 41 breast cancers obtained from operations in our hospital in 1996 were detected using ABC immunohistochemical stain assay and compared with 10 cases with normal breast tissues. Results: The positive rate of bax in normal breast tissue was 90% and in breast cancer was 59%, with a significant statistical difference between them (P<0.05), but there was no statistical difference in bcl-2 protein expression. Among the 41 breast cancer, the group with lymph node metastasis (21 cases) had obviously low bax expression (43%) and high bcl-2 expression (76%), showing significant difference to the group without lymph node metastasis (P<0.05). Conclusion: The antiapoptosis function of bcl-2 was stronger than bax in breast cancer. Protein bax and bcl-2 assay may be useful in understanding the biological behaviors of breast cancer.

THE OVEREXPRESSION OF APOPTOSIS-RELATED GENES OF P_53 AND BCL-2 IN CERVICAL CARCINOMA

Objective To investigate the significance of overexpression of p5s and bcl-2 protein in carcinogene- sis of cervix. Methods 10 cases of cervical intraepithelial neoplasis(CIN) and 57 cases of invasive cancer were in- vestigated with immunohistochemistry technique. Results The overexpresion or P53 protein ir CIN and cervical can- cer was significantly higher than that or control, respectively (P<0.01). But there was no significant difference be- tween CIN and cervical cancer(P>0.05). The immunoreactivity of bcl-2 in CIN was much more higher than that of control (P<0.05). The positive rate and immunoreactivity of bcl-2 in cervical carcinoma were both remarkably high- er than those of control (P<0.0l),but there was no significant difference between CIN and cervical carcinoma (P> 0.05). It was also found that there was a remarkably positive correlation between the overexpression of bcl-2 and P53 (P<0.01). Conclusion Because of the loss of wtP53 function,the expression of bcl-2 can not be down-reguated, which is associated with the pathogenesis and development of cervical carcinoma.

c-erbB-2、VEGF-c及激素受体在乳腺癌中的表达

目的 :探讨 c- erb B- 2、VEGF- c、ER、PR在乳腺癌组织中的表达及与临床病理特征之间的关系。方法 :采用PV- 90 0 0二步法分别检测 12 8例乳腺癌、2 5例乳腺良性病变中 c- erb B- 2、VEGF- c、ER、PR的表达。结果 :c- erb B- 2、VEGF- c、ER、PR的表达在乳腺良、恶性病变之间均有显著性差异 (P<0 .0 1) ,c- erb B- 2、VEGF- c的表达与乳腺癌淋巴结转移密切相关 (P<0 .0 1) ;ER、PR与 c- erb B- 2、VEGF- c的表达呈负相关 (P<0 .0 5 ) ;四种蛋白的表达均与乳腺癌发病年龄、肿瘤大小、是否浸润无关 (P>0 .0 5 )。结论 :c- erb B- 2、VEGF- c的过度表达预示着乳腺癌具有较强的转移能力 ,二种蛋白可能在乳腺癌的浸润转移过程中起协同作用。联合检测 c- erb B- 2、VEGF- c、ER、PR对预测乳腺癌的淋巴结转移、判断预后、指导临床治疗具有十分重要的意义。

两种ErbB2/Neu阳性-PTEN缺失乳腺癌基因工程小鼠模型的建立及其生物学特征比较

目的：建立两种ErbB2／Neu阳性-PTEN缺失的乳腺癌基因工程小鼠模型并比较其生物学特征。方法：利用先前建立的由鼠乳腺肿瘤病毒（MMTV）启动子同时驱动活化型ErbB2／Neu基因和重组酶Cre表达的FVB／N—MMTV—NIC小鼠与Flox-PTEN小鼠交配；或将由内源性启动子驱动活化型ErbB2／Neu基因表达的FVB／N-ErbB2^KI、FVB／N—MMTV—Cre及Flox—PTEN三种基因工程小鼠交配；PCR分别扩增Neu、Cre和PTEN基因，对其子代小鼠进行基因型鉴定；免疫组织化学法检测乳腺组织ErbB2／Neu和PTEN蛋白表达。对两种模型的成瘤时间、肿瘤数目、肺转移等生物学特征进行比较，观察肿瘤组织病理学形态，免疫组织化学法检测肿瘤细胞Ki-67表达，TUNEL法检测肿瘤细胞凋亡水平。结果：经基因型鉴定和组织蛋白表达分析，获得了两种ErbB2／Neu阳性-PTEN纯合型缺失的乳腺癌基因工程小鼠模型；一是由MMTV外源性启动子同时驱动活化型ErbB2／Neu和Cre表达，抑癌基因PTEN条件性敲除的NIC／PTEN^-/-模型；二是由MMTV-Cre使内源性启动子驱动ErbB2／Neu基因表达，PTEN条件性敲除的ErhB2^KI／PTEN^-/-模型。NIC／PTEN^-/-模型的平均成瘤时间低于ErbB2^KI／PTEN^-/-模型（30d与368d，P〈0．01）；肿瘤数目、肺转移率均高于ErbB2^KI／PTEN^-/-模型（分别为10个与1～2个，75．0％与37．5％，均P〈0．01）；两种模型肿瘤呈现不同的组织病理形态，肿瘤细胞凋亡水平相当（P〉0．05）；NIC／PTEN^-/-模型Ki-67阳性细胞百分率高于ErhB2^KI／PTEN^-/-模型（86．9％±2．8％与37．4％±7．2％，P〈0．01）。结论：两种不同表型的ErbB2／Neu阳性-PTEN缺失的乳腺癌基因工程小鼠为探索ErbB2／HER2阳性乳腺癌的发生、发展规律及更有效的防治方案提供了理想的动物模型。

青年结直肠癌c-erbB-2蛋白高表达的病理学意义

目的 :探讨青年结直肠癌c erbB 2表达与临床病理特点之间的联系。方法 :采用流式细胞术对c erbB 2蛋白在青、老年结直肠癌中的表达加以定量检测和对比分析。结果 :青年组 62例中共有 46例c erbB 2阳性表达 ,而老年组 3 2例中有 15例阳性表达 ,二者之间差异有统计学意义 ,P <0 0 5。c erbB 2高表达与青年患者肿瘤组织学类型和浸润深度无明显关系 ,但与肿瘤分级和淋巴结转移密切相关 ,P <0 0 5 ,即分级高或有局部淋巴结转移的多呈高表达 ;反之 ,则几乎均为低表达或无表达。与老年组对比 ,青年组分化程度低、浸润周围软组织或局部淋巴结发生转移的c erbB 2表达量显著升高 ,P <0 0 5。结论 :c erbB 2蛋白的表达对于判断青年结直肠癌恶性程度及预后具有重要病理学意义。

p^(53)蛋白及c-erbB-2蛋白在胆囊癌中的表达

目的：研究ｐ５３及ｃｅｒｂＢ２蛋白在胆囊良恶性病变中的表达及意义，探讨它们在胆囊癌早期诊断和鉴别诊断中的潜在价值。方法：采用免疫组化ＳＰ法及微波抗原修复法检测２９例胆囊癌及２１例胆囊良性病变的ｐ５３蛋白的表达，同时仅用ＳＰ法检测ｃｅｒｂＢ２蛋白的表达。结果：ｐ５３蛋白在胆囊癌中表达的阳性率为５１７％，而在良性病变中无表达（Ｐ＜００５）；ｐ５３蛋白的表达在早晚期胆囊癌中无显著性差异（Ｐ＞００５）；仅３例胆囊癌ｃｅｒｂＢ２阳性表达，其中１例ｐ５３亦阳性。