Literature DB >> 15088110

BAX and caspase-5 frameshift mutations and spontaneous apoptosis in colorectal cancer with microsatellite instability.

Joerg Trojan1, Angela Brieger, Jochen Raedle, Nicole Weber, Susanne Kriener, Bernd Kronenberger, Wolfgang F Caspary, Stefan Zeuzem.   

Abstract

BACKGROUND AND AIMS: Hereditary nonpolyposis colorectal cancer (HNPCC) and a subset of sporadic colorectal cancers are characterized by microsatellite instability (MSI) and inactivating frameshift mutations of target genes. Inactivation of BAX, caspase-5 ( cas-5), and other genes coding for pro-apoptotic proteins might contribute to tumor progression by enhancing escape from apoptosis. The aim of this study was to further characterize the role of BAX and cas-5 inactivation for spontaneous apoptosis.
METHODS: Twenty-five colorectal cancers with MSI were analyzed for frameshift mutations in the BAX (G)8 and cas-5 (A)10 tract by fluorescence PCR, cloning, and sequencing. The rate of spontaneous apoptosis was examined by in situ DNA nick end-labeling. The results were compared with 25 stage-matched microsatellite stable (MSS) colorectal cancers.
RESULTS: In colorectal cancer with MSI frameshift mutations in BAX and cas-5 were present in 16 of 25 (64%) and in 12 of 25 (48%) tumors, respectively, whereas neither mutant BAX nor cas-5 alleles were detected in all stage-matched sporadic MSS colorectal cancer. Tumors with MSI showed a higher apoptotic rate than MSS tumors (2.5+/-1.0 vs. 2.1+/-0.7; p <0.05), whereas the presence of BAX or cas-5 frameshift mutations had only minor influence on this finding (2.4+/-1.1% and 2.5+/-0.9%, respectively).
CONCLUSION: Mismatch-repair deficiency itself is associated with increased spontaneous apoptosis, not further accelerated by either inactivating BAX or cas-5 frameshift mutations.

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Year:  2004        PMID: 15088110     DOI: 10.1007/s00384-004-0597-1

Source DB:  PubMed          Journal:  Int J Colorectal Dis        ISSN: 0179-1958            Impact factor:   2.571


  42 in total

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