I'm tempted to say that this is an exciting time to be diagnosed with MM, but that's not exactly true. I wouldn't call having MM really exciting in any way. However, the landscape has changed dramatically in the last 5 to 10 years, and there is now a lot more reason to be hopeful for extended remission and even possibly a cure coming down the road.
The recent ASCO conference in Chicago unveiled a number of promising new therapies that have been successful against a number of cancers. While there were no dramatic breakthroughs for MM, there is a lot of cross fertilization, where an an agent successful against one cancer might be useful in another. Basically, current research efforts are focusing on more individualized and targeted therapies, based on more detailed diagnoses using sophisticated tests, as well as genetic profiles.
This past weekend, an old high school friend of mine, Ken, sent me an article that ran in Sunday's New York Times. (Ken's not that old, but he's a bit older than I am, which I am fond of reminding him.) Here is the link: Genetic attack on cancer shows promise. This is a case where a cancer lab researcher contracted acute lymphoblastic leukemia and was dying. His lab colleagues went to work sequencing his genome and RNA and found a rogue gene that was spurring the growth of his cancer. Fortunately, there was a drug available that was approved for kidney cancer that worked on that particular gene. He was the first person to take it for leukemia and his cancer is now in remission.
Last week I came across an interesting paper referenced in the Myeloma Beacon regarding a culprit behind the t(4;14) high risk MM. Of course this is of particular interest to me. Here is a link to a discussion about this paper: Culprit behind chemo resistance to t(4;14). What they found is that there is a particular genetic RNA component in t(4;14) patients, called ACA11. This RNA gene allows the cancer cells to grow better and be resistant to chemotherapy.
This is great news! While there may not yet be a drug available that can specifically attack this ACA11 genetic RNA aberration, this is an important clue telling researchers where to look. As the summary to this article explains, “Now we have an angle for just focusing on the drugs that we know work
better, as well as on experimental approaches for these patients,” he
says. “It gives us a new way to study how we can improve their care.”
Fortunately, Velcade and Revlimid both seem to be chemo drugs that work effectively on t(4;14) patients, such as myself. However, if researchers can find a mechanism to shut down the ACA11 effect, it can only be to the benefit of all of us t(4;14) patients.
I think the future of cancer research in general and MM research in particular will be to isolate specific genetic sources of the cancer, and then find targeted drugs to specifically attack these rogue genetic aberrations. There have already been some successes, but to really push the envelope here, genetic sequencing will have to become less expensive and more available as a routine diagnostic procedure. Then, it will become easier to identify specific genetic cancer markers and concentrate on finding drugs to neutralize their effects.
I am very hopeful that all these research efforts will prove to be successful during my lifetime.