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Biotech / Medical : VD's Model Portfolio & Discussion Thread
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To: squetch who wrote (2167)8/26/1997 12:04:00 AM
From: Miljenko Zuanic   of 9719
 
Stan:

Regards the p53 and telomerase activation:

ncbi.nlm.nih.gov

>>Genomic instability due to germline p53 mutations drives preneoplastic
progression toward cancer in human cells.

Tainsky MA, Bischoff FZ, Strong LC

Department of Tumor Biology, University of Texas, M.D. Anderson Cancer Center, Houston, USA.

Cells heterozygous for mutations in p53 demonstrate extreme genomic instability and develop mutations detectable at the
chromosome level as well as the molecular level. This genomic instability causes initially nontumorigenic ras-expressing
immortal LFS cells to progress to a tumorigenic state presumably due to additional mutational events. It is not surprising that
LFS families with these p53 mutations develop the additional mutations necessary for cancer to occur at such high frequencies.
This observation is consistent with increased cancer rates in these families being due to abrogation of a rate limiting step rather
than a rate expected for one less step in a multistep carcinogenic process. Although p53 has been shown to be able to function
as a transcription factor, mutations in p53 appear to affect genomic stability in LFS fibroblasts with double minutes and
telomeric associations being prominent early events. One possibility is that p53 controls the expression of genes required for
fidelity of replication or telomerase activity. Alternatively p53 may itself be a replication factor like the transcription factor CTF.
In the future, we plan to investigate whether p53 plays a direct role in replication.

mz
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