A MMA list member recently posted an item from the CancerCare bulletin titled “the latest in multiple myeloma research,” which lists a series of different conventional drugs and their anti-myeloma activity. I went down the list, did a wee bit of research and made a discovery…not a very startling one, come to think of it…but anyway, here goes:
- Monoclonal antibodies. Often compared to guided missiles, monoclonal antibodies zero in on cancer cells whose surfaces have a “target molecule.” For example, the combination of lenalidomide with a monoclonal antibody called elotuzumab holds promise in treating multiple myeloma that comes back after traditional treatments.
- Growth blockers. These drugs are designed to block the growth of myeloma cells by depriving them of substances they need, such as vascular endothelial growth factor (VEGF). When tumor cells spread through the body, they release VEGF to create new blood vessels. These blood vessels supply oxygen, minerals, and other nutrients to feed the tumor.
- Proteasome inhibitors. Bortezomib was the first in its class of proteasome inhibitors. Another promising drug, called carfilzomib, appears to work the same way as bortezomib.
- Immunomodulators. A new form of the drug thalidomide is showing promise in people whose multiple myeloma has returned after previous treatment. Called pomalidomide (Actimid), this medication stops the growth of blood vessels that feed tumors. It also boosts the immune system and may kill cancer cells directly.
- Histone deacetylase (HDAC) inhibitors. This class of drugs works by killing cancer cells or stopping their growth. Two HDAC inhibitors, vorinostat (Zolinza) and panobinostat, have been combined with bortezomib. This combination has been shown to be effective in many people whose tumors resist treatment with bortezomib alone.
- Akt inhibitors. These drugs aim to disrupt cancer cell membranes and block the actions of proteins involved in cancer growth. An Akt inhibitor called perifosine holds promise as a treatment for multiple myeloma, when combined with bortezomib.
- Heat shock protein-90 (Hsp90) inhibitors. Heat shock proteins are key players in a number of processes that cancer cells use to survive and grow. Multiple myeloma cells contain more of a heat shock protein, called Hsp90, than normal cells. Two drugs—alvespimycin and tanespimycin—block the actions of Hsp90. Research suggests that combining these drugs with bortezomib may be more effective than treatment with bortezomib alone.
- mTOR inhibitors. This class of drugs blocks a mechanism called the mammalian target of rapamycin (mTOR) pathway, which promotes tumor growth. Preliminary research suggests that combining lenalidomide with an mTOR inhibitor called everolimus (Afinitor) may stall the growth of multiple myeloma.
- Cyclin-dependent kinase (CDK) inhibitors. CDK inhibitors, such as the drug flavopiridol, block proteins that promote the growth of multiple myeloma cells.
- Telomerase inhibitors. One drug, known as imetelstat, blocks an important enzyme found to be active in myeloma cells. This enzyme allows cancer cells to resist chemotherapy.
- RANK ligand inhibitors. This new class of drugs works differently from other types of drugs that treat bone complications. They are designed to block a factor in bone development known as RANK ligand. RANK ligand stimulates cells that break bone down. By blocking RANK ligand, RANK ligand inhibitors may increase bone density and strength. Denosumab (Xgeva) is being tested in people with multiple myeloma for the treatment of bone complications. The FDA has recently approved denosumab to help prevent bone fractures and bone pain in non-myeloma patients whose cancer has spread (metastasized) and damaged the bone.
Now, with the exception of item #1 (=monoclonal antibodies), the myeloma targets mentioned in the remaining 10 items on this list are inhibited, all of them!!!!!, by something that many of us already take….a non-toxic something that inhibits VEGF, HDAC, mTOR, Akt, blablabla…all the way down to RANKL, the final item. Can you guess what the “something” might be? 🙂
And there is more.
Just this morning I read a newly published “Blood” abstract (yes, I am finally able to read an abstract without falling asleep… 😉 ): http://goo.gl/MMFMp It mentions a new myeloma target (I think I’ve seen this one before, but I don’t have the energy to check right now…) called “glycogen synthetase kinase-3 beta” (GSK3beta).
Well, the above-mentioned, not-so-mysterious-after-all substance happens to inhibit GSK3beta, too. Have you guessed yet? 😉
This is bloody ridiculous. And frustrating. I mean, how much more proof will we need to provide before our official myeloma organizations begin taking notice of non-toxic, anti-myeloma substances…substances that can target myeloma via multiple pathways, which is the only way a cure for myeloma will ever be found???
Let me give you this image: if you hit a tumor with only one missile, its chances of surviving the strike are high, very high indeed. But if you hit the tumor in different areas and with many different types of missiles, you stand a good chance of annihilating it…
It all boils down to plain common sense…
So I ask my question once again: how much more proof do we need in order for some money to be poured into non-toxic research? I am sick and tired of hearing about denosumab (see my posts on this topic) and conventional treatments that are really, or potentially, toxic…really sick and tired…
Basta, I say!!!