Expression of tumour necrosis factor-related apoptosis-inducing ligand death receptors in sporadic and hereditary colorectal tumours: Potential targets for apoptosis induction

被引:41
作者
Koornstra, JJ
Jalving, M
Rijcken, FEM
Westra, J
Zwart, N
Hollema, H
de Vries, EGE
Hofstra, RWM
Plukker, JTM
de Jong, S
Kleibeuker, JH
机构
[1] Univ Groningen, Dept Gastroenterol, Med Ctr, NL-9700 RB Groningen, Netherlands
[2] Univ Groningen, Med Ctr, Dept Med Oncol, NL-9700 AB Groningen, Netherlands
[3] Univ Groningen, Med Ctr, Dept Med Genet, Groningen, Netherlands
[4] Univ Groningen, Med Ctr, Dept Pathol, Groningen, Netherlands
[5] Univ Groningen, Med Ctr, Dept Surg, Groningen, Netherlands
关键词
TRAIL; apoptosis; HNPCC; FAP; colorectal cancer; BAX;
D O I
10.1016/j.ejca.2005.02.018
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) and antibodies against TRAIL receptors death receptor 4 (DR4) and death receptor 5 (DR5) are under investigation for cancer therapy. To study the potential application of these agents, the expression of DR4 and DR5 were studied immunohistochemically in colorectal adenomas and carcinomas from patients with sporadic disease (n = 74 and 56, respectively), familial adenomatous polyposis (FAP, n = 41 and 4, respectively) and hereditary non-polyposis colorectal cancer (HNPCC, n = 50 and 21, respectively). BAX, which is frequently mutated in tumours with high-frequency microsatellite instability (MSI-H) may play a role in sensitivity to TRAIL. Therefore, MSI-H carcinomas (n = 42, of which 27 sporadic and 15 HNPCC) were analysed for apoptotic activity, assessed by M30 immunoreactivity, and BAX mutations. Most adenomas from all three patient groups expressed DR4 and DR5. Most carcinomas expressed DR4, except for six cases, all with mucinous histology. All carcinomas, including mucinous carcinomas, showed DR5 expression. BAX mutations were found in 6/ 42 MSI-H cancers with similar apoptotic indices and expression of DR4, DR5 and TRAIL in BAX mutant and wild-type cases. Since most sporadic and hereditary colorectal neoplasms express DR4 and DR5, targeting of these receptors may be a potential prevention or treatment strategy. (c) 2005 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1195 / 1202
页数:8
相关论文
共 39 条
[1]
Safety and antitumor activity of recombinant soluble Apo2 ligand [J].
Ashkenazi, A ;
Pai, RC ;
Fong, S ;
Leung, S ;
Lawrence, DA ;
Masters, SA ;
Blackie, C ;
Chang, L ;
McMurtrey, AE ;
Hebert, A ;
DeForge, L ;
Koumenis, IL ;
Lewis, D ;
Harris, L ;
Bussiere, J ;
Koeppen, H ;
Shahrokh, Z ;
Schwall, RH .
JOURNAL OF CLINICAL INVESTIGATION, 1999, 104 (02) :155-162
[2]
The addition of low-dose leucovorin to the combination of 5-fluorouracil-levamisole does not improve survival in the adjuvant treatment of Dukes' C colon cancer [J].
Bleeker, WA ;
Mulder, NH ;
Hermans, J ;
Otter, R ;
Plukker, JT .
ANNALS OF ONCOLOGY, 2000, 11 (05) :547-552
[3]
Boland CR, 1998, CANCER RES, V58, P5248
[4]
Isotype-dependent inhibition of tumor growth in vivo by monoclonal antibodies to death receptor 4 [J].
Chuntharapai, A ;
Dodge, K ;
Grimmer, K ;
Schroeder, K ;
Marsters, SA ;
Koeppen, H ;
Ashkenazi, A ;
Kim, KJ .
JOURNAL OF IMMUNOLOGY, 2001, 166 (08) :4891-4898
[5]
Increased susceptibility to tumor initiation and metastasis in TNF-related apoptosis-inducing ligand-deficient mice [J].
Cretney, E ;
Takeda, K ;
Yagita, H ;
Glaccum, M ;
Peschon, JJ ;
Smyth, MJ .
JOURNAL OF IMMUNOLOGY, 2002, 168 (03) :1356-1361
[6]
Long-term treatment with sulindac in familial adenomatous polyposis: A prospective cohort study [J].
Cruz-Correa, M ;
Hylind, LM ;
Romans, KE ;
Booker, SV ;
Giardiello, FM .
GASTROENTEROLOGY, 2002, 122 (03) :641-645
[7]
Death receptor ligands, in particular TRAIL, to overcome drug resistance [J].
de Jong, S ;
Timmer, T ;
Heijenbrok, FJ ;
de Vries, EGE .
CANCER AND METASTASIS REVIEWS, 2001, 20 (1-2) :51-56
[8]
Microsatellite instability [J].
de la Chapelle, A .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 349 (03) :209-210
[9]
TRAIL-induced apoptosis requires Bax-dependent mitochondria release of Smac/DIABLO [J].
Deng, YB ;
Lin, YH ;
Wu, XW .
GENES & DEVELOPMENT, 2002, 16 (01) :33-45
[10]
Gliniak B, 1999, CANCER RES, V59, P6153