Bax expression in benign and malignant thyroid tumours: Dysregulation of wild-type P53 is associated with a high Bax and P21 expression in thyroid carcinoma
Authors:
Open Access
- 4 April 2001
- journal article
- research article
- Published by Wiley in International Journal of Cancer
- Vol. 92 (6) , 805-811
Abstract
The purpose of our study was to determine the expression of the pro‐apoptotic BAX protein in relation to the mutational status of BAX and p53 (as transcriptional activator of the BAX gene) in benign and malignant thyroid tissue. In 47 patients with thyroid tumours (14 follicular and 3 papillary carcinomas, 14 adenomas and 16 goitres), the DNA was screened for mutations of BAX (exon 1–6) and p53 (exon 5–8) by single‐strand conformation polymorphism polymerase chain reaction (SSCP‐PCR). Furthermore, the protein expression of BAX, p53 and p21 (which is also increased transcriptionally by p53) was investigated by immunohistochemistry. Surprisingly, we observed elevated BAX levels in patients with thyroid carcinomas compared with patients with adenomas (unpaired t‐test: pppp<0.05 in the carcinomas compared with the non‐malignant lesions). Consequently, the overexpressed p53 might be a correlate for dysregulation without loss of function. This, in turn, might be a reason for the good outcome of some patients with thyroid cancer.Keywords
This publication has 43 references indexed in Scilit:
- BCL-2 family members and the mitochondria in apoptosisGenes & Development, 1999
- Analysis of the p53/BAX Pathway in Colorectal Cancer: Low BAX Is a Negative Prognostic Factor in Patients With Resected Liver MetastasesJournal of Clinical Oncology, 1999
- Ordering the Cytochrome c–initiated Caspase Cascade: Hierarchical Activation of Caspases-2, -3, -6, -7, -8, and -10 in a Caspase-9–dependent MannerJournal of Cell Biology, 1999
- p21/p53, Cellular Growth Control and Genomic Integrity1998
- Cytochrome c and dATP-Dependent Formation of Apaf-1/Caspase-9 Complex Initiates an Apoptotic Protease CascadeCell, 1997
- APOPTOSIS AND DISEASE: Regulation and Clinical Relevance of Programmed Cell DeathAnnual Review of Medicine, 1997
- Overexpression of the death-promoting gene bax-alpha which is downregulated in breast cancer restores sensitivity to different apoptotic stimuli and reduces tumor growth in SCID mice.Journal of Clinical Investigation, 1996
- Bax-Deficient Mice with Lymphoid Hyperplasia and Male Germ Cell DeathScience, 1995
- A novel form of Epstein-Barr virus latency in normal B cells in vivoCell, 1995
- Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programed cell deathCell, 1993