作者: Hans-Stefan Hofmann , Andreas Simm , Andreas Hammer , Rolf-Edgar Silber , Babett Bartling
DOI: 10.1007/S00432-002-0364-Z
关键词: Pathology 、 Gene expression 、 Cancer research 、 Survivin 、 Apoptosis 、 Gene product 、 Adenocarcinoma 、 Carcinoma 、 Biology 、 XIAP 、 Carcinogenesis 、 Oncology 、 General Medicine
摘要: Abstract Purpose. Apoptotic cell death contributes to the regulation of tumour regression but can be prevented by proteins IAP family. Although survivin identified as tumour-specific gene product, role other members family is mainly unclear in non-small lung cancer (NSCLC). Therefore, we hypothesise that hIAP-1, hIAP-2, and XIAP are associated with carcinogenesis, too. Methods. To define expression levels, samples from 34 NSCLC patients adenocarcinoma (16) squamous carcinoma (18) were included. Analyses performed standardised RT-PCR immunoblotting. Paired non-tumour tissues served controls. All showed a strong mRNA up-regulation compared Results. Investigations revealed an overall increase (median: 1,083 vs 605 rel. U; P =0.02). In contrast, hIAP-2 was nearly identical all control samples. Furthermore, elevated hIAP-1 especially 8.58 3.44 <0.01). Using median 50% determined tumours cut-off point, 11/16 only 6/18 elevation mRNA. This could observed low TMN adenocarcinomas (7/9 I, increase: +289% 2/5 III–IV, +44.6%). An enhanced respective confirmed on protein level immunoblot analyses. Conclusions. Our results indicate involvement anti-apoptotic pathogenesis NSCLC, while preferentially seems play important low-stage adenocarcinoma.