Wednesday, May 22, 2013


The advent of T-DM1 and its success in delivering chemotherapy specifically to cells that are engaged in neoplastic transformation while posting relevant receptor (in this case the receptor is to Herceptin), open the door to possibility of doing the same for therapy that will target genes!  And this will minimize the impact on normal cells!
T-DM1, a conjugate of Herceptin and Emtansine, a powerful chemotherapy that cannot be infused theoritically in living human because it is so potent (theoritically), is now being delivered to cell that express the Herceptin receptor (wait to see this drug used in those 10% of Gastric cancer that have Herceptin receptors).  If we conjugate this with PSA, we could theoritically deliver Emtansine to prostate cancers!  To CEA may be to colon cancer, well it does not need to be Emtansine, how about the delivery of some more powerful Doxorubicin related compounds!

Beyond this "game" with more powerful chemotherapy drugs, let' replace the powerful drug by a driver gene.  We know some leukemia are characterized by immortality, and TIAF1 may be the gene driving this.  Leukemia is known to have some typical CD, cluster of differentiation, why not combine Anti-TIAF1 and that particular CD to ensure delivery of the anti-gene to specifically that cell.  Where we have a Wnt activated in triple negative breast cancer, we send in anti-CREB attached to TGF beta  or other positive receptor.  You know that cancer with c-MET amplification you got to go to the Hepatic Growth factor because it is the only known ligand to this receptor.  A cancer with over-expression of RNA polymerase that we discussed earlier, we will send in an anti-TAF 15 or anti-POLR2C of some sort!  Commanding this conjugate technology is a must and is the future in Oncology!  Game is on!  Increasing effect of Taxotere, try anti ARHGEF2. In all disease where cyclins play a major role, targeting the JAKs will be the answer!  NF-kB know the answer!
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