Apoptosis and tumor regression in locally advanced non-small cell lung cancer with neoadjuvant therapy

被引:0
作者
Junker, K
Müller, KM
Bosse, U
Klinke, F
Heinecke, A
Thomas, M
机构
[1] Ruhr Univ Bochum, Klin Bergmannsheil, Inst Pathol, D-4630 Bochum, Germany
[2] Inst Pathol, Osnabruck, Germany
[3] St Raphael Hosp, Ostercappeln, Germany
[4] Univ Munster, Inst Med Informat & Biomath, D-4400 Munster, Germany
[5] Univ Munster, Med Klin A, D-4400 Munster, Germany
来源
PATHOLOGE | 2003年 / 24卷 / 03期
关键词
apoptosis; therapy-induced tumour regression; non-small cell lung cancer; neoadjuvant therapy;
D O I
10.1007/s00292-002-0607-4
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Dysregulation of apoptosis is closely associated with malignant cell transformation. On the other hand, apoptosis is induced by chemotherapy or irradiation. Therefore, in 54 patients with locally advanced non-small cell lung cancer (NSCLC, 36 squamous cell carcinomas, 18 adenocarcinomas, stage IIIA/IIIB), apoptotic indices were comparatively analysed before onset and after termination of neoadjuvant therapy. The results were compared with the response to neoadjuvant therapy (extent of therapy-induced tumour regression) as well as the survival times. A statistically significant difference could not be established between pre-therapeutically and post-surgically established apoptotic indices (mean values: 0.93% vs. 1.1%). Neither before therapy nor after surgery did the apoptotic indices show a significant predictive value concerning different overall survival times. These results suggest that neoadjuvant therapy does not modify the extent of apoptosis in lung cancer in the long term. Only a few weeks after the completion of the neoadjuvant chemoradiotherapy this contributes to a net proliferation of the residual tumour tissue which is largely equivalent to that of the untreated tumour.
引用
收藏
页码:214 / 219
页数:6
相关论文
共 26 条
[1]   DEMONSTRATION OF DNA-DAMAGE REPAIR IN INDIVIDUAL CELLS USING IN-SITU END LABELING - ASSOCIATION OF P53 WITH SITES OF DNA-DAMAGE [J].
COATES, PJ ;
SAVE, V ;
ANSARI, B ;
HALL, PA .
JOURNAL OF PATHOLOGY, 1995, 176 (01) :19-26
[2]   INDUCTION OF A RETINOBLASTOMA PHOSPHATASE-ACTIVITY BY ANTICANCER DRUGS ACCOMPANIES P53-INDEPENDENT G(1) ARREST AND APOPTOSIS [J].
DOU, QP ;
AN, B ;
WILL, PL .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (20) :9019-9023
[3]  
EASTMAN A, 1990, CANCER CELL-MON REV, V2, P275
[4]   APOPTOSIS IN CANCER-THERAPY - CROSSING THE THRESHOLD [J].
FISHER, DE .
CELL, 1994, 78 (04) :539-542
[5]   IDENTIFICATION OF PROGRAMMED CELL-DEATH INSITU VIA SPECIFIC LABELING OF NUCLEAR-DNA FRAGMENTATION [J].
GAVRIELI, Y ;
SHERMAN, Y ;
BENSASSON, SA .
JOURNAL OF CELL BIOLOGY, 1992, 119 (03) :493-501
[6]  
GOTZ C, 1995, INT J ONCOL, V6, P1129
[7]   APOPTOSIS AND CANCER-CHEMOTHERAPY [J].
HICKMAN, JA ;
POTTEN, CS ;
MERRITT, AJ ;
FISHER, TC .
PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY OF LONDON SERIES B-BIOLOGICAL SCIENCES, 1994, 345 (1313) :319-325
[8]  
Joseph B, 2000, ANN NY ACAD SCI, V926, P204
[9]   p53 tumour-suppressor gene in non-small-cell lung cancer with neoadjuvant therapy [J].
Junker, K ;
Wiethege, T ;
Müller, KM ;
Thomas, M .
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY, 2000, 126 (04) :238-245
[10]  
Junker K, 1997, PATHOLOGE, V18, P131, DOI 10.1007/s002920050201