Silicon Investor (SI) -- The First Internet Community

STOCKTALK

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor. We ask that you disable ad blocking while on Silicon Investor in the best interests of our community. If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.

Biotech / Medical : Introgen Therapeutics -- Ignore unavailable to you. Want to Upgrade?

To: zeta1961 who wrote (505)	3/10/2006 11:07:06 AM
From: Jibacoa	Read Replies (1) \| Respond to of 802

O.T. Author Block: Marta M. Alonso, Ramon Alemany, Candelaria Gomez-Manzao, Manel Cascallo, Frederick F. Lang, Jing Xu, Verlene Henry, Alfred W.K. Yung, Alfred W.K. Yung, Juan Fueyo. MD Anderson Cancer Center, Houston, TX, Instituto Catala d'Oncologia, Barcelona, Spain Is that where you are planning on doing some work when you move there or will be fully retired ? <g>

To: zeta1961 who wrote (505)	3/10/2006 11:44:12 AM
From: Jibacoa	Read Replies (3) \| Respond to of 802

O.T. and Dr. Alemany[now in Birmingham, Alabama University] I thought he was still in Barcelona, as he was Academic Vice-Rector of the Universitat Oberta de Catalunya.<g> For the last couple of years, the research on oncolytic adenoviruses has been interesting, but I don't thing that INGN's patents on p53 include that area.<g> " Oncolytic or tumor-selective adenoviruses are constructed as novel antiglioma therapies. After infection, the invading genetic adenoviral material is activated within the host cell. E1A and E1B adenoviral proteins are expressed immediately. E1A protein interacts with cell cycle regulatory proteins, such as retinoblastoma (Rb), driving the cell into the S phase and ensuing viral replication. The action of E1A stimulates the cellular p53 tumor suppressor system, which results in growth arrest or apoptosis, and halts adenovirus replication. However, adenoviral E1B interacts with p53 protein, preventing the DNA replication process from being abrogated by the induction of p53-mediated apoptosis. It was subsequently hypothesized that mutant adenoviruses that were unable to express wild-type E1A or E1B proteins could not replicate in normal cells with functional Rb or p53 pathways but instead would replicate and kill glioma cells that had defects in the regulation of these tumor suppressor pathways." Snip neurology.org