Cell lines:
- In several breast cancer cell (BCC) lines, TPA-induced apoptosis appears to be mediated through a p53-independent pathway, and the up-regulation of p21WAF1 and Bax may be the molecular mechanisms by which TPA induces apoptosis (Li Y. et al., 1998).
- The somatostatin analog octreotide was shown to elicit cytotoxic response in MCF-7 BCC, leading to apoptosis, which is associated with a rapid, time-dependent induction of wild-type p53 and an increase in Bax (Sharma K. and Skrikant C.B., 1998).
- In tamoxifen-treated MDA-MB-231 BCC, an increase in levels of Bax, TGF-beta1, and c-Myc was observed (Fattman C.L. et al., 1998).
- The up-regulation of Bax and p21WAF1 could be the molecular mechanism by which the isoflavonoid genistein (present in soy products) induces apoptosis in MDA-MB-231 BCC (Li Y. et al., 1999).
Tumors:
- Bax and
Bcl2 expression were determined in 239 breast carcinomas. Bax immunostaining was cytoplasmic and heterogenous. High Bax expression was associated with positive nodal status and high
Bcl2 expression and was more frequent in high-grade tumours. No association was seen with tumour size, histologic type,
ER status or p53 status. In the node-negative subgroup, Bax expression was associated with small tumour size (Veronese S. et al., 1998).
- In a group of 142 T1 (<2 cm) ductal breast carcinomas, expression of anti-apoptotic proteins Bcl-2 and Bcl-x was found in 57.0% and 62.75% of tumors, respectively. Bcl-2 expression, but not Bcl-x expression, was related to loss of apoptosis. Expression of the apoptotic proteins Bax and Bak was present in 58% of Bcl-2-negative tumors and associated significantly with an increase in apoptosis (Sierra A. et al., 1998).
- In a study of 23 cases of ductal carcinoma in situ, alterations at microsatellite repeat motifs in the coding regions of four cancer-associated genes (TGF beta RII, IGFIIR, BAX, and E2F-4) were not observed (Walsh T. et al., 1998).
- In some tumors, defects in mismatch repair enzymes lead to errors in the replication of simple nucleotide repeat segments. This condition is commonly known as microsatellite instability (MSI) because of the frequent mutations of microsatellite sequences. Simple nucleotide repeats were evaluated in the transforming growth factor type II receptor, insulin-like growth factor type II receptor, BAX, and E2F-4 genes, which are frequently mutated in tumors with microsatellite instability. No mutations of these genes were found in any of the 30 breast cancer cell lines and 61 primary breast cancer samples examined. These results indicate that mismatch repair errors characteristic of the MSI phenotype are uncommon in human breast cancer (Anbazhagan R. et al., 1999).
