Fragile histidine triad protein expression in nonsmall cell lung cancer and correlation with Ki-67 and with p53
Fragile histidine triad protein expression in nonsmall cell lung cancer and correlation with Ki-67 and with p53
复制标题
非小细胞肺癌中脆性组氨酸三联体蛋白的表达及其与 Ki-67 和 p53 的相关性
DOI：
--
复制
发表时间：
2003
影响因子：
24.3
通讯作者：
J. Sculier
中科院分区：
文献类型：
--
作者：
C. Mascaux;B. Martin;J. Verdebout;A. Meert;V. Ninane;J. Sculier
脆性组氨酸三联体（FHIT）是一种肿瘤抑制基因，在包括肺癌在内的多种上皮性肿瘤中发生改变。其致瘤性的生物化学和功能途径尚不清楚。它在肿瘤增殖中的作用特别有争议。本研究的目的是将FHIT蛋白在非小细胞肺癌（NSCLC）中的表达与肿瘤增殖（用Ki-67抗原和抑癌基因p53估计）相关联。采用免疫组化法检测119例NSCLC中FHIT、Ki-67和p53的表达。总的来说，58个肿瘤对FHIT呈阴性（表达<10%）。肿瘤中的中位表达为15%阳性细胞，而正常匹配肺组织中为100%。仅19例表达与正常组织一样强。FHIT在鳞状细胞癌（SCC）中的表达（5%）显著低于腺癌（ADC）（64%）。Ki-67的中位表达为20%，69%的肿瘤为阳性（表达>10%）。Ki-67在SCC中的表达（33.3%）明显高于ADC（10%）。FHIT蛋白的丢失与p53（中位数：7.5%，阳性肿瘤的58%，阳性细胞的截止值为10%）或Ki-67的表达无关。而p53和Ki-67的标记细胞百分比显著相关。结果表明，对于脆性组氨酸三联体，肿瘤发生的途径是独立的p53和肿瘤增殖，如先前在体外报道的。
Fragile histidine triad (FHIT) is a tumour suppressor gene, which is altered in a variety of epithelial tumours, including lung cancer. Biochemical and functional pathways of its tumourigenicity are not yet understood. Its role in tumour proliferation is particularly controversial. The purpose of this study was to correlate the expression of FHIT protein in nonsmall cell lung cancer (NSCLC) with tumour proliferation as estimated by Ki-67 antigen and with p53, a suppressor gene. FHIT, Ki-67 and p53 expression were evaluated by immunohistochemistry in 119 resected NSCLC. Altogether, 58 tumours were negative (expression <10%) for FHIT. The median expression in tumours was 15% positive cells, in comparison with 100% in normal matched lung tissue. The expression was as strong as in normal tissue in only 19 cases. FHIT expression was significantly lower in squamous cell carcinoma (SCC) (5%) than in adenocarcinoma (ADC) (64%). The median expression of Ki-67 was 20% and 69% of tumours were positives (expression >10%). Ki-67 expression was significantly higher in SCC (33.3%) than in ADC (10%). The loss of FHIT protein was not correlated with the expression of p53 (median: 7.5%, 58% of positive tumours for a cut-off of 10% of positive cells) or Ki-67. But percentage of labelled cells for p53 and Ki-67 were significantly correlated. The results suggest that for fragile histidine triad, the pathway of tumourigenesis is independent of p53 and of tumoural proliferation, as reported previously in vitro.
登录
查看更多内容
Fhit 丢失在 I 期非小细胞肺癌和慢性吸烟者的肺部中很常见。
DOI：
--
发表时间：
1999
期刊：
Cancer research.
影响因子：
--
作者：
Tseng,JE;Kemp,BL;Khuri,FR;Kurie,JM;Lee,JS;Zhou,X;Liu,D;Hong,WK;Mao,L
通讯作者：
Mao,L
影响因子：
11.2
作者：
D. Greenspan;D. Connolly;R. Wu;R. Y. Lei;Joshua T C Vogeistein;Young-Tak Kim;J. Mok;Nubia Mufloz;F. Bosch;K. Shah;Kathleen R. Cho;Spain
通讯作者：
D. Greenspan;D. Connolly;R. Wu;R. Y. Lei;Joshua T C Vogeistein;Young-Tak Kim;J. Mok;Nubia Mufloz;F. Bosch;K. Shah;Kathleen R. Cho;Spain
影响因子：
11.2
作者：
T. Druck;P. Hadaczek;Tie-bo Fu;M. Ohta;Z. Siprashvili;R. Baffa;M. Negrini;K. Kastury;M. L. Veronese;D. Rosen;J. Rothstein;P. Mccue;M. Cotticelli;H. Inoue;C. Croce;K. Huebner
通讯作者：
T. Druck;P. Hadaczek;Tie-bo Fu;M. Ohta;Z. Siprashvili;R. Baffa;M. Negrini;K. Kastury;M. L. Veronese;D. Rosen;J. Rothstein;P. Mccue;M. Cotticelli;H. Inoue;C. Croce;K. Huebner
影响因子：
11.2
作者：
Bao-Zhu Yuan;C. Keck-Waggoner;D. Zimonjic;S. Thorgeirsson;N. Popescu
通讯作者：
Bao-Zhu Yuan;C. Keck-Waggoner;D. Zimonjic;S. Thorgeirsson;N. Popescu
肾肿瘤中 Fhit 表达的丢失或减少：与组织发生类别的相关性。
影响因子：
3.3
作者：
Hadaczek,P;Kovatich,A;Gronwald,J;Lubinski,J;Huebner,K;McCue,PA
通讯作者：
McCue,PA