Influence of norcantharidin on proliferation,proliferation-related gene proteins prolifera-ting cell nuclear antigen and Ki-67 of human gallbladder carcinoma GBC-SD cells

BACKGROUND: Gallbladder carcinoma is a highly lethal and aggressive disease with early metastasis, strong invasion and poor prognosis. Most patients with this disease are at the advanced and un-resectable stage and should be consi- dered for palliative treatment such as chemotherapy and ra- diotherapy. Unfortunately, reports of chemotherapy and radiotherapy for gallbladder carcinoma are disappointing. We investigated the influence of norcantharidin (NCTD) on proliferation, proliferation-related gene proteins PCNA and Ki-67 of human gallbladder carcinoma GBC-SD cells in vitro. METHODS: GBC-SD cell lines of human gallbladder carci- noma were cultured by the cell culture technique. The ex- periment was divided into NCTD group and control group. The tetrazolium-based colorimetric assay was used to evaluate cell growth. The streptavidin-biotin complex method was used to determine the expressions of prolifera- tion-related gene proteins PCNA and Ki-67 of human gall- bladder carcinoma GBC-SD cells. RESULTS: NCTD inhibited the growth and proliferation of GBC-SD cells from 10 mg/L or after 6 hours in a dose- and time-dependent manner, with the IC50 value of 56.18 μg/ ml at 48 hours. After treatment with NCTD, the expression of PCNA (0.932 ±0.031 vs. 0.318 ±0.023, P<0.001) and Ki-67 (0.964 ±0.092 vs. 0.297 ±0.018, P<0.001) proteins were decreased significantly. CONCLUSION: NCTD inhibits the proliferation of human gallbladder carcinoma GBC-SD cells in vitro and the expres- sion of their proliferation-related gene proteins PCNA and Ki-67.

Comparative Analysis of Ki-67 Protein as a Proliferative Expression Index in Cutaneous Basal and Squamous Cell Carcinoma in Federal Medical Centre Umuahia, Nigeria

Background: Evaluating the tumor proliferative index helps predict clinical behavior and provides prognostic insights for cutaneous basal cell carcinoma (cBCC) and squamous cell carcinoma (cSCC). Objective: This study aimed to identify differences in the proliferative indices among variants of cBCC and cSCC diagnosed at a tertiary healthcare center. Method: Skin biopsies histologically diagnosed as cBCC and cSCC between 2012 and 2018 at the Federal Medical Centre (FMC) Umuahia, Abia State, Nigeria, were analyzed. Archival formalin-fixed, paraffin-embedded (FFPE) tissue blocks were retrieved along with clinical data, and were prepared on charged microscope slides and the immunohistochemical staining was carried out. The primary antibody used in this study was clone BioCare CRM325C (RM) and adenotonsillar tissue blocks/slides served as positive controls. Ki-67 immunohistochemistry was performed on fresh 4µm sections of the tumor specimens. Results: The application of Ki-67 immunoperoxidase on both BCC and SCC cohort, yielded an intense observable brownish nuclear stain in areas of dense proliferating tumour cells on both cutaneous tumours. The average Ki-67 index for all cSCC cases was 24.7%, with a range of 2.3% - 80%, while the mean for cBCC was 15.8%, ranging from 1.2% - 45.6%. Variants with high proliferative indices were observed in 11.9% of cBCC cases and 29.1% of cSCC cases. Among the low proliferative index category, cSCC accounted for 5.4%, while cBCC represented 14.3%. For mild proliferative indices, cSCC cases made up 7.3% and cBCC, 11.9%. The majority of cases showed moderate proliferative indices, with 61.9% for cBCC and 58.2% for cSCC. Overall, there was a significant difference in proliferative indices between cSCC, cBCC, and their variants. Conclusion: The study found a significantly higher rate of cell proliferation, measured by Ki-67 immunostaining, in cSCC and its variants compared to cBCC. However, certain variants of cBCC also exhibited high Ki-67 expression, indicating they can be as aggressive as some cSCC variants.

Effects of Peptide Nucleic Acids against Ki-67 Gene on the Proliferation and Apoptosis of Human Renal Carcinoma Cell Line

To investigate the effects of anti-sense peptide nucleic acids （PNAs） targeting Ki-67 gene on modulation of the proliferation and apoptosis of human renal carcinoma cell lines, human renal carcinoma cell line 786-0 cells were treated with anti-sense PNAs at different concentrations （1.0 μmol/L, 2.0 μmol/L, 10.0 μmol/L）. The Ki-67 expression of 786-0 cells was detected by immunohistochemical technique and Western blot method respectively. The proliferation of 786-0 cells was studied by cell growth curves and ^3H-thymidine incorporation. The apoptosis of 786-0 cells was detected by TUNEL assay. The control groups were treated with anti-sense oligonucleotide （ASODNs） targeting Ki-67 gene. Our results showed that the Ki-67 expression of 786-0 cells treated with anti-sense PNAs （16.9±0.7） was significantly inhibited as compared with that of the control groups （28.6±0.4） （P〈0.01）. The Ki-67 protein rate of 786-0 cells treated with anti-sense PNAs （42.1 ±2.2） was significantly reduced when compared with that of the control groups （83.6± 1.4） （P〈0.01）. Proliferation of 786-0 cells treated with anti-sense PNAs （20.7 ± 1.5） was significantly inhibited as compared with that of the control groups （58.6± 1.4） （P〈0.01）. The apoptosis rate of 786-0 cells treated with anti-sense PNAs （28.7 ± 2.3） was significantly increased higher compared with that of the control groups （13.8 ±1.0） （P〈0.01）. From these finds we are led to conclude that anti-sense PNAs targeting Ki-67 gene have stronger effects on the inhibition of the proliferation and induction of apoptosis of human renal carcinoma cells than ASODNs targeting Ki-67 gene. The strategies using anti-sense PNAs targeting Ki-67 gene may be a promising approach for the treatment of renal cell carcinoma.

P53、P16及Ki-67与早期食管癌患者ESD术后复发的关系分析

目的 分析研究抑制蛋白基因P53(P53)、抑制蛋白基因P16(P16)及细胞增殖核抗原Ki-67(Ki-67)与早期食管癌患者内镜黏膜下剥离术(ESD)术后复发的关系。方法 选取2019年1月至2023年1月三门峡市中心医院收治80例的早期食管癌患者作为研究对象,均进行ESD治疗。比较所有患者癌组织与癌旁组织(距肿瘤边缘>3 cm,镜下未见肿瘤组织或不典型增生组织)P53、P16、Ki-67蛋白表达。ESD术后对患者随访1年,根据有无术后复发食管癌,将患者分为复发组(n=20)与无复发组(n=60)。比较两组癌组织P53、P16、Ki-67蛋白表达。采用多因素Logistic回归分析早期食管癌患者ESD术后复发的影响因素,并绘制ROC曲线分析P53、P16、Ki-67蛋白表达与早期食管癌患者ESD术后复发。结果 与癌旁组织相比,癌组织P53、Ki-67蛋白表达升高,P16蛋白表达降低(t=9.276、13.987、10.595,均P<0.05);复发组的癌组织P53、Ki-67蛋白表达均高于无复发组,P16蛋白表达低于无复发组(t=5.086、4.648、5.139,均P<0.05);多因素Logistic回归分析显示,肿瘤低分化(OR=1.870)、肿瘤浸润侵犯黏膜下层(OR=1.808)、有淋巴结转移(OR=2.089)、P53蛋白高表达(OR=2.046)、P16蛋白低表达(OR=1.988)及Ki-67蛋白高表达(OR=1.761)均是早期食管癌患者ESD术后复发的独立危险因素(P<0.05);ROC曲线分析显示,P53、P16、Ki-67蛋白表达及联合检测的曲线下面积(AUC)分别为0.803、0.828、0.834、0.942,联合检测优于单一检测(P<0.05)。结论 P53、P16及Ki-67蛋白与早期食管癌患者ESD术后复发情况相关,可以作为辅助预测的相关诊断指标。

Effect of norcantharidin on proliferation and invasion of human gallbladder carcinoma GBC-SD cells

AIM: To investigate the effect of norcantharidin on proliferation and invasion of human gallbladder carcinoma GBC-SD cells in vitro and its anticancer mechanism. METHODS: Human gallbladder carcinoma GBC-SD cells were cultured by cell culture technique. The growth and the invasiveness of GBC-SD cells in vitro were evaluated by the tetrazolium-based colorimetric assay and by the Matrigel experiment and the crossing-river test. Expression of PCNA, Ki-67, MMP2 and TIMP2 proteins of GBC-SD cells was determined by streptavidin-biotin complex method. RESULTS: In vitro norcantharidin inhibited the growth and proliferation of GBC-SD cells in a dose- and time-dependent manner, with the IC50 value of 56.18 μ/mL at 48 h. Norcantharidin began to inhibit the invasion of GBC-SD cells at the concentration of 5 μg/mL, and the invasive action of GBC-SD cells was inhibited completely and their crossing-river time was prolonged significantly at 40 μg/mL. After treatment with norcantharidin, the expression of PCNA, Ki-67, and MMP2 was significantly decreased. With the increase in TIMP2 expression, the MMP2 to TIMP2 ratio was decreased significantly (P<0.05). CONCLUSION: Norcantharidin inhibits the proliferation and growth of human gallbladder carcinoma cells in vitro at relatively low concentrations by inhibiting PCNA and Ki-67 expression. Its anti-invasive activity may be the result of decrease in MMP2 to TIMP2 ratio and reduced cell motility.

Effect of preoperative transcatheter arterial chemoembolization on proliferation of hepatocellular carcinoma cells

AIM： To evaluate the effect of preoperative transcatheter arterial chemoembolization （TACE） on proliferation of hepatocellular carcinoma （HCC） cells. METHODS： A total of 136 patients with HCC underwent liver resection. Of 136 patients, 79 patients received 1 to 5 courses of TACE prior to liver resection （TACE group）, who were further subdivided into four groups： Group A （n = 11） who received i to 4 courses of chemotherapy alone; Group B （n = 33） who received i to 5 courses of chemotherapy combined with iodized oil; Group C （n = 23） who received i to 3 courses of chemotherapy combined with iodized oil and gelatin sponge; and Group D （n = 12） who received 1 to 3 courses of chemotherapy combined with iodized oil, ethanol and gelatin sponge. The other 57 patients only received liver resection （non- TACE group）. The expressions of Ki-67 and proliferating cell nuclear antigen （PCNA） protein were detected in the liver cancer tissues by immunohistochemical method. RESULTS： The Ki-67 protein expression was significantly lower in Groups C and D as compared with non-TACE group （31.35% ± 10.85% vs 44.43% ± 20.70%, 30.93% ± 18.10% vs 44.43% ± 20.70%, respectively, P 〈 0.05）. The PCNA protein expression was significantly lower in Groups C and D as compared with non-TACE group （49.61% ± 15.11% vs 62.92% ± 17.21%, 41.16% ± 11.83% vs 62.92% ± 17.21%, respectively, P 〈 0.05）. The Ki-67 protein expression was significantly higher in Group A as compared with non-TACE group （55.44% ± 13.72% vs 44.43% ± 20.70%, P 〈 0.05）. The PCNA protein expression was significantly higher in Groups A and B as compared with non-TACE group （72.22% ± 8.71% vs 62.92% ± 17.21%, 69.91% ± 13.38% vs 62.92% ± 17.21%, respectively, P 〈0.05）. CONCLUSION： Preoperative multi-material TACE suppresses the proliferation of HCC cells, while a single material embolization and chemotherapy alone enhance the proliferation of HCC cells.

Molecular biomarkers of cell proliferation in ameloblastomas

Cell proliferation is a vital biological process that is important for all living organisms because of its role in growth and the maintenance of tissue homeostasis.The control of this important process differs greatly among benign and malignant neoplasms,and the evaluation of cell proliferation in neoplasms has become a common tool used by pathologists to provide useful information pertaining to diagnosis,clinical behavior,and treatment.The usefulness of information regarding cell proliferation has led to numerous studies on the value of these methods for diagnosing different types of tumors and for clinical decision making.Ameloblastomas are no exception.This review discusses the use of several classical molecular proliferation markers,including Ki-67,proliferating cell nuclear antigen,cyclin D1 and DNA topoisomeraseⅡalpha,to characterize ameloblastomas and proposes the use of new proliferation markers used previously to characterize other neoplasms.The use of these biomark-ers offers valuable opportunities to evaluate the biological behavior of this type of odontogenic tumor.

p53、Ki-67、PCNA的表达与食管鳞癌放疗近期疗效及预后的关系

目的:探讨食管鳞癌组织中p53、Ki-67及增殖细胞核抗原(PCNA)的表达与食管癌患者放疗近期疗效及预后的关系。方法:收集接受放疗的食管癌患者83例,采用免疫组化方法检测活检癌组织中p53、Ki-67及PCNA的表达,并分析其与临床病理特征、放疗疗效和预后的关系。结果:p53、Ki-67及PCNA在食管鳞癌中高表达率分别为57.8%、72.3%、67.5%。p53、Ki-67及PCNA表达与性别、年龄、侵犯部位、肿瘤长度等各临床病理因素无关(P>0.05),p53与肿瘤分化程度、临床分期、淋巴结转移、放疗近期疗效明显相关(P<0.05),Ki-67与肿瘤分化程度、淋巴结转移、放疗近期疗效明显相关(P<0.05),PCNA与临床分期、淋巴结转移、放疗近期疗效明显相关(P<0.05)。p53低、高表达组食管癌患者3年总生存率分别为57.14%、27.08%。结论:p53、Ki-67及PCNA可作为评价食管癌恶性程度、放射敏感性的生物学指标,p53可作为评价食管癌预后的有效指标。

LRIG3基因沉默对神经胶质瘤细胞系GL15增殖及PCNA和Ki-67表达的影响

背景与目的:富含亮氨酸重复序列免疫球蛋白样蛋白3(leucine-rich repeats and immunoglobin-like domains3,LRIG3)是LRIG基因家族成员之一,在多种肿瘤中均有表达下调,但其作用尚不明了。本研究旨在探讨RNA干扰沉默LRIG3基因表达对神经胶质瘤细胞系GL15增殖及增殖细胞核抗原(proliferating cell nuclear antigen,PCNA)和Ki-67表达的影响及其机制。方法:用携带U6启动子和LRIG3特异性短发夹RNA(short hairpin RNA,shRNA)序列的质粒载体pGenesil2-LRIG3-shRNA1、pGenesil2-LRIG3-shRNA2及含非特异性shRNA编码序列的对照质粒pGenesil2-negative shRNA(neg)转染胶质瘤细胞系GL15,G418筛选出稳定株,逆转录聚合酶链反应(RT-PCR)和Western blot法检测LRIG3表达的改变,应用噻唑蓝(MTT)法检测稳定转染后对GL15细胞增殖的影响,应用免疫组化SABC法检测对照组和实验组GL15细胞中PCNA和Ki-67的表达。结果:shRNA1及shRNA2组细胞LRIG3 mRNA水平与对照组相比分别下降了52.4%和63.8%,LRIG3蛋白水平分别下降了50.9%和67.4%。MTT结果显示实验组细胞增殖率高于对照组。对照组细胞PCNA阳性率为(35.40±5.69)%,shRNA1及shRNA2组细胞PCNA阳性率分别为(72.13±5.64)%和(81.93±5.23)%,差异均有统计学意义(P<0.01)。Ki-67阳性率在对照组细胞为(49.73±5.73)%,shRNA1及shRNA2组细胞分别为(82.27±5.50)%和(88.67±3.52)%,差异均有统计学意义(P<0.01)。Ki-67表达与PCNA表达呈正相关(r=0.932,P<0.001)。结论:下调LRIG3基因表达可促进胶质瘤细胞的增殖。

脑肿瘤细胞PCNA和Ki-67表达的对比观察

观察45例（4组）原发性脑肿瘤的免疫组化研究发现：增殖细胞核抗原（PCNA）和Ki67抗原（Ki－67）阳性率均为100％，两种阳性细胞密度均随肿瘤恶性程度增加而升高，并与肿瘤体积呈正相关，两种阳性细胞密度间也呈正相关，各肿瘤组PCNA阳性细胞密度均高于同组Ki－67阳性细胞密度。提示PCNA和Ki－67表达水平均能较客观地反应脑肿瘤的增殖速度和恶性程度。PCNA能用于石蜡切片是检测增殖期细胞更实用的标记物。

骨肉瘤P21^(WAF1)蛋白、PCNA与Ki-67的表达及其意义

目的 :研究骨肉瘤组织中P2 1WAF1 蛋白、增殖细胞核抗原 (PCNA)、Ki 6 7蛋白的表达 ,及其与骨肉瘤的发生、发展之间的关系及对预后的影响。方法 :用免疫组化LSAB法检测P2 1WAF1 蛋白、增殖细胞核抗原 (PCNA)、Ki 6 7蛋白在骨肉瘤中的表达。结果 :45例骨肉瘤中 ,P2 1WAF1 有 8例阳性表达 ,阳性率为 17.77% ;PCNA均有表达 ,阳性率为 10 0 % ;Ki 6 7有 2 7例阳性表达 ,阳性率为 6 0 %。结论 :P2 1WAF1 的低表达、PCNA、Ki 6 7的高表达 ,从一个侧面反映了骨肉瘤的恶性程度较高 ,检测P2 1WAF1 蛋白、增殖细胞核抗原 (PCNA)、Ki 6 7蛋白等多个指标可较全面反映骨肉瘤的恶性程度的高低及患者的预后情况。

肝细胞癌和肝硬化组织中增殖细胞核抗原及Ki-67抗原的表达及意义

为探讨肝细胞癌 (HCC)和肝硬化组织中增殖细胞核抗原 (PCNA)及 Ki- 67抗原的表达及意义 ,采用免疫组织化学技术检测 PCNA和 Ki- 67抗原在 HCC和肝硬化组织中的标记指数 (L I)。结果显示 , 、 、 级 HCC的 PCNA L I分别为 (2 6.9± 17.4) %、 (3 3 .1± 2 2 .7) %、 (73 .8± 16.3 ) % ,各级之间差异均有显著性(P均 <0 .0 5 ) ;Ki- 67L I分别为 (2 5 .8± 15 .6) %、 (5 8.2± 18.6) %、 (75 .3± 2 0 .2 ) % ,各级之间差异均有显著性 (P均 <0 .0 5 ) ;但各级 HCC中的 PCNA L I和 Ki- 67L I差异均无显著性 (P均 >0 .0 5 )。肝硬化组织中 PCNAL I为 (8.8± 5 .2 ) % ,Ki- 67L I为 (7.9± 4.4) % ,两者之间差异无显著性 (P>0 .0 5 )。提示 HCC及肝硬化组织中 PCNA和 Ki- 67抗原的阳性率基本一致 ,HCC的分化程度与 PCNA或 Ki- 67密切相关 ;原位检测 HCC组织中PCNA或 Ki- 67抗原的表达 ,有助于判断

拓扑异构酶Ⅱα和Ki-67表达与子宫肉瘤预后的相关性研究

目的通过检测DNA拓扑异构酶Ⅱα(TopoⅡα)、细胞核相关抗原-67(Ki-67)的表达水平,评价子宫肉瘤细胞增殖的生物学行为,寻找其预后相关因素。方法回顾性分析解放军总医院因子宫肉瘤行肿瘤切除手术的患者48例。按照国际妇产科联盟(FIGO)分期标准,分为Ⅰ期22例,Ⅱ期12例,Ⅲ期8例,Ⅳ期6例。按照美国妇科肿瘤组(GOG)病理组织学分类,包括子宫平滑肌肉瘤(LMS)19例,子宫内膜间质肉瘤(ESS)21例,子宫恶性中胚叶混合瘤(MMMT)8例。应用免疫组织化学(IHC)方法检测TopoⅡα、Ki-67在子宫肉瘤中的表达水平并分析其与子宫肉瘤预后的相关性。结果TopoⅡα和Ki-67的高增殖(LI)组(阳性表达细胞数>25%)患者的2年、5年生存率与低LI组(阳性表达细胞数≤25%)患者比较均无明显差别,但总体生存率高LI组均明显低于低LI组(分别为P=0.002,P=0.004)。TopoⅡα和ki-67低LI组患者的复发包块体积均大于高LI组(P=0.005,P=0.000),且复发时间均明显长于高LI组(P=0.000,P=0.000)。TopoⅡα与Ki-67表达呈明显正相关(r=0.9355,P=0.000)。COX多因素分析表明,除病理类型及分期外,TopoⅡα和Ki-67的表达与患病年龄、初潮年龄、孕产次、月经周期及经期、是否绝经均无关。结论TopoⅡα与Ki-67均可作为细胞增殖的特异性标记物,但TopoⅡα在反映细胞精确的增殖状态方面较Ki-67可能有更好的特异性,结合病理类型及分期,可能对判断子宫肉瘤的预后具有重要指导意义。

Ki-67、PCNA及HPV在宫颈癌和宫颈上皮内瘤变的表达及意义

目的:研究Ki-67,增殖细胞核抗原(PCNA)在早期宫颈癌(IA^IIA期高分化)、宫颈上皮内瘤变(CINI、CINII、CINIII)及慢性宫颈炎中的表达,及其与HPV感染的关系,探究3者联合应用的诊断价值。方法:应用免疫组织化学S-P法检测宫颈病变中Ki-67、PCNA抗原的表达,PCR反应检测HPV感染,结合临床病理特点分析。结果:慢性宫颈炎、CIN、宫颈鳞癌中Ki-67阳性表达率分别为33.33%、89.19%、100%。PCNA阳性表达率分别为66.67%、97.30%、100%。HPV阳性率分别是13.33%、54.05%、1000%。CINI和CINII/III中Ki-67阳性表达率分别为85.00%、94.12%;PCNA阳性表达率分别为95.00%、100.00%。HPV阳性率分别是30%、82.35%。CIN和宫颈癌中的Ki7、PCNA及HPV的阳性表达与宫颈炎相比,差异均有显著性(P<0.05)。Ki-67及PCNA过表达率在CINII/III组与CINI组间差异显著(P<0.05)。HPV阳性率在CINII/III与CINI之间差异显著(P<0.01)。Ki-67及PCNA表达与HPV感染有相关性(P<0.05)。结论:Ki-67、PCNA抗原过表达与CINII/III和早期宫颈癌显著相关。Ki-67、PCNA表达与HPV感染率相关,联合检测宫颈组织中Ki-67、PCNA的过表达及HPV感染,有助于判断细胞的增殖活性,可作为诊断早期宫颈癌和CINII/III的标记物。

Ki-67在急性髓系白血病中的研究进展

Ki-67抗原表达与细胞周期密切相关,几乎表达于整个细胞周期的分裂期,检测Ki-67抗原可以反映血液肿瘤的细胞增殖活性。Ki-67的检测已广泛应用于淋巴瘤的疾病分期,疗效监测和预后判断,并已有大量研究探讨了Ki-67表达在急性淋巴细胞白血病(acute lymphocytic leukemia,ALL)和慢性淋巴细胞白血病(chronic lymphocytic leukemia,CLL)中的表达及与治疗疗效、预后的相关性,而在急性髓系白血病(acute myeloid leukemia,AM L)中Ki-67表达的相关研究较少,研究结果也不一致。本文就Ki-67的结构、细胞内定位、表达调控、生理功能及其在AM L中的应用现状做一综述,旨在了解Ki-67可否在AM L的诊断以及预后评估中发挥作用。

联合检测FHIT、Ki-67及PCNA在皮质醇增多症肾上腺皮质不同病变中的意义

目的探讨皮质醇增多症肾上腺皮质不同病变中脆性组氨酸三联体(FHIT)、Ki-67及增殖细胞核抗原(PCNA)的表达水平及其在鉴别诊断中的作用。方法应用免疫组织化学方法检测49例皮质醇增多症肾上腺皮质病变(腺癌14例、腺瘤26例、皮质增生9例)患者FHIT、Ki-67及PCNA的表达。结果 FHIT在肾上腺皮质增生表达最高,腺瘤次之,腺癌最低(分别为100.00%、96.15%、42.86%);Ki-67与PCNA在肾上腺皮质腺癌的表达最高,腺瘤次之,皮质增生最低(分别为85.71%、7.69%、0和100.00%、96.15%、77.78%)。FHIT、Ki-67及PCNA在皮质醇增多症肾上腺皮质病变中的表达两两相关,其中FHIT与Ki-67表达呈负相关(r=-0.718,P=0.00),FHIT与PCNA表达呈负相关(r=-0.449,P=0.001),Ki-67与PCNA表达呈正相关(r=0.387,P=0.006)。联合检测FHIT、Ki67及PCNA结果显示,腺癌表现为FHIT阴性或弱阳性、Ki-67强阳性、PCNA强阳性;腺瘤表现为FHIT阳性、Ki-67阳性、PCNA阳性;皮质增生表现为FHIT强阳性、Ki-67阴性、PCNA阴性。结论联合检测FHIT、Ki-67及PCNA对肾上腺皮质腺癌、腺瘤及增生的鉴别诊断具有重要的价值。

乳腺癌18F-FDG PET/CT代谢参数与TNM分期及Ki-67表达的关系

目的探讨乳腺癌治疗前18F-FDG PET/CT显像中的3种代谢参数最大标准摄取值(maximum standardized uptake value,SUVmax)、肿瘤代谢体积(metabolic tumor volume,MTV)以及糖酵解总量(total lesion glycolysis,TLG)与肿瘤TNM分期及增殖细胞核抗原Ki-67的关系。方法回顾性分析52例乳腺癌患者治疗前的18F-FDG PET/CT显像。在影像工作站手动勾画病灶感兴趣区(region of interest,ROI),提取病灶SUVmax、MTV和TLG。采用Mann-Whitney秩和检验方法,分析3种PET/CT显像的代谢参数与TNM分期及Ki-67之间的关系。结果SUVmax、MTV和TLG这3种代谢参数在T分期T0~1组和T2~4组间比较,差异均具有统计学意义(均P<0.05)。MTV和TLG在N分期N0组和N1~3组间比较,差异均具有统计学意义(均P<0.05),而SUVmax在两组间比较,差异无统计学意义(P>0.05)。3种代谢参数在M分期M0组和M1组间比较,差异均无统计学意义(均P>0.05)。以20%作为Ki-67高低表达的阈值,3种代谢参数在Ki-67高表达组和低表达组间比较,差异均具有统计学意义(均P<0.05)。结论 18F-FDG PET/CT代谢参数MTV和TLG可以作为评估乳腺癌治疗前T、N分期及Ki-67指标的临床评价参数。

组织芯片技术研究食管胃黏膜病变中Ki-67的表达及其与细胞增殖和凋亡的关系

背景：近20年来食管和食管胃连接处（EGJ）腺癌发生率呈上升趋势,Barrett食管（BE）被认为是其发生的重要危险因素。目的：应用组织芯片技术研究Ki-67在各类食管胃黏膜病变中的表达及其与细胞增殖和凋亡的关系。方法：制作140例各类食管胃黏膜组织的组织芯片,结合免疫组化方法检测Ki-67和增殖细胞核抗原（PCNA）表达。以原位末端标记技术（TUNEL法）检测BE、食管腺癌和贲门癌的细胞凋亡情况。结果：BE、食管腺癌和贲门癌组Ki-67阳性率分别为40.9%、69.6%和61.9%,均显著高于正常贲门组织（0.0%,P〈0.01）和贲门肠化生（IM）组（11.5%,P〈0.05）。BE、贲门IM、胃窦IM、食管腺癌和贲门癌组PCNA阳性率均显著高于正常贲门组织（45.5%、42.3%、39.3%、52.2%和42.9%对10.0%,P〈0.05）。BE、食管腺癌和贲门癌中Ki-67表达弱阳性和阳性者细胞凋亡指数均较表达阴性者显著降低（P〈0.05）,而PCNA仅表达阳性者凋亡指数较表达阴性者显著降低（P〈0.05）。结论：BE和EGJ处肿瘤的发生与Ki-67表达异常有关,Ki-67较PCNA更能反映EGJ处细胞凋亡状态。

PCNA和Ki-67在子宫内膜癌中的表达及其临床意义

目的 探讨增殖细胞核抗原 (PCNA)和Ki-67在子宫内膜癌组织中的表达及其与临床病理参数之间的关系。方法 采用免疫组化S -P法检测 10例正常子宫内膜、3 0例单纯性增生、3 0例复杂性增生、3 0例非典型增生和47例子宫内膜癌组织中PCNA和Ki-67的表达。结果 PCNA和Ki-67标记指数 (LI)在非典型增生组高于正常子宫内膜、单纯性增生和复杂性增生组 ,子宫内膜癌组高于非典型增生组 ,差异有显著性 (P <0 .0 5 ) ,PCNA和Ki-67LI均与子宫内膜癌分化程度、组织学分级、临床分期、肌层浸润和淋巴结转移有关 (P <0 .0 5 )。结论 PCNA和Ki -67LI的检测可作为判断子宫内膜癌生物学行为的较好指标。

PCNA和Ki-67在脑膜瘤组织中的表达及其意义

目的 探讨增殖细胞核抗原 (PCNA )和Ki-6 7核抗原在脑膜瘤中的表达及其与肿瘤良、恶性及复发的关系。方法 采用LSAB法检测 80例脑膜瘤组织中PCNA和Ki-6 7的表达。结果 恶性脑膜瘤PCNA标记指数 (PCNALI)和Ki -6 7标记指数 (Ki -6 7LI)明显高于良性脑膜瘤 (P <0 .0 1)和非典型性脑膜瘤 (P <0 .0 5 ) ,复发脑膜瘤PCNALI显著高于未复发脑膜瘤 (P<0 .0 1) ,复发脑膜瘤Ki -6 7LI也显著高于未复发脑膜瘤 (P <0 .0 1)。Ki -6 7表达与PCNA表达呈正相关。结论 脑膜瘤细胞标记指数可作为判断脑膜瘤良、恶性的客观指标之一 ,标记指数对预测脑膜瘤的复发有一定意义。