I suppose an update is in order. No news is good news when you have CLL, and I’ve had no news for awhile. Now I’m gearing up for treatment again, this time with lenalidomide, better known as Revlimid, also known as "len" for short.
All of last year’s treatments basically bought me stable disease. A CT scan comparison from January to September showed only marginal improvement in abdominal lymph nodes, which is where most of my 11q-deleted disease lives these days. Over time my CLL has become less leukemic, more nodal, and my blood lymphocyte count is practically normal.
I remain at Stage 2, for what it’s worth. When I’m not hemolysing due to autoimmune hemolytic anemia (AIHA), my red blood count, hemoglobin and hematocrit remain well in the normal range for a man. I’ve not seen the slow decline in those counts that follow with progressing disease. Over six years my platelets have gradually dipped, settling now in the 120s. That’s just below what’s considered normal, absolutely high enough for full clotting function, something to note but not to worry over.
My latest FISH test -- I get one every year, and the results have a huge say in how I approach treatment -– still shows the 11q deletion only, on 31 out of 200 chromosomes. This is a monoallele deletion, which means the relevant bit is broken off of the long arm of one of the set of two chromosomes #11. A biallele deletion would mean that both of the chromosomes 11 have lost the ATM gene. So hey, I’ve still got one arm to hang paper with, it seems. (A cautionary note is worth inserting here: As we all should know by now, the FISH test doesn’t probe for all possible chromosomal abnormalities that may eventually prove important in CLL. No news is good news in my case, but it may not be all the news, if you know what I mean.)
So by some measures -– including how I feel on any given day -– I am just sort of trucking along with this thing in neutral. But it ain’t quite so. There are those abdominal nodes remember, none over 5 cm, but a whole, whole lot of them. My B2M is 4.8, a little over the line MD Anderson sets (4.0) to divide between those with better disease and those with worse. For me, the action is taking place in the abdomen.
Plus I’ve got the AIHA, with its hemolysis shoe always waiting to drop, a sign that CLL has gummed up immune function and still continues to do so. I also have squamous cell skin cancer issues. I've had two SCCs removed surgically since 2005, several actinic keratoses frozen off, and I am on far-too-intimate terms with a tube of Efudex. SCCs can be deadly serious in CLLers, whose T cell surveillance function is weakened, because it is T cell surveillance that helps keep those squamous cells in check. CLLer T cells take a hit because of the lowered immunity that accompanies disease progression, and they can further tank due to immunosuppressive therapy, notably fludarabine and Campath.
I haven’t had fludarabine or Campath, which brings us to the menu of choices I now face:
Looking at all the data tells me that my disease is stable-ish but also growing, more or less behaving but capable of getting that much worse if I don’t attend to it. For years I attended to it with single-agent Rituxan, but AIHA changed that game and while Rituxan was clearing the blood the disease found other avenues for growth.
So attending to it for about the past two years has consisted of costlier therapy, RCD, or rituximab, cyclophosphamide and dexamethasone. A recent DEXA scan shows my bones are no worse than they were two years ago, marginally osteopenic here and there. But steroids are not a long-term solution. Cyclophosphamide has done me good so far, nailing hemolysis when it occurs, but it is a potentially mutagenic agent and one to which, if I’m like most other people, I will only develop disease resistance to over time.
So RCD as “maintenance” is not realistic, and “maintenance” to me now means something a lot tougher and potentially more problematic than single-agent Ritxan. I have come to the end of Easy Street and there’s a big sign there that says “Road Closed.”
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So, what to do? Besides lenalidomide, or Revlimid, the FDA has approved ofatumumab, aka Arzerra, aka HuMax-CD20, aka the Monoclonal Antibody Formerly Known as Prince, for use in CLL. This is the bigger, badder, fully humanized anti-CD20 antibody, none of that wussy mouse shit. For someone who has used Rituxan to the max, its presence represents a potential new lease on life, or at least on effectiveness.
And because of that, it is an important drug in my arsenal. I am not treating it the same way I treated Rituxan. Sure, I might get a year or two of stability out of it by using it as a single agent, but then what? I think it is wiser to save Arzerra for combination therapy, the good old FCA, when that becomes front-and-center my only choice.
Which it almost is at this point: FCA, followed by a transplant at relapse, the CLL end game. But enter lenalidomide, an immunomodulator drug that intrigues and mystifies the experts. Some interesting data came out of December’s ASH conference, including a report from MD Anderson, which ran a trial of Revlimid and Rituxan in relapsed patients.
How len seems to help some CLLers is explained succinctly in this online interview with Dr. Asher Chanan-Khan, “Mr. Revlimid” himself, who goes over all the highlights from ASH, including a discussion of len at the end.
When it works -– and it doesn’t work on everyone -– lenalidomide seems to have a way of rebalancing the immune system, weakening the CLL cells themselves and compromising the nurse-like cells that protect them. Len can improve T cell and NK cell function, actually get the immune system to go toe to toe with the CLL. It works on high-risk cytogenetics such as my 11q. And while you have to watch for low neutrophils and low platelets while on the drug -– not to mention tumor flare, rashes, fatigue, nausea, and so on –- it does not appear to have the potentially mutagenic, viral-reactivating, Richtersy transformative potential of immunosuppressive chemo.
And keep in mind, for someone with AIHA, the idea of restoring an equilibrium in the immune system is powerful catnip. I have it on the best authority that two transfusion-dependent, hemolysing AIHA patients were treated with Revlimid; in both cases the hemolysis resolved and one patient is still with us three years later, free of the AIHA curse.
That, plus some added squamous control, plus the prospect of making a dent against that abdominal bulk, makes Dave a potentially very happy man. Which, defined in CLL terms, means someone who is able to control his disease, possibly even weaken it, for a long period of time without really compromising future therapy choices.
So, it’s worth a try. My insurance has rejected it, of course. It costs $60 a day per pill times 365 days and the insurance won’t even give it to patents with multiple myeloma, for which it has FDA approval. But my hem/onc, who now runs her own kick-ass office with a bent on getting patients the care they need come hell or high water, is optimistic that I can qualify for assistance from the maker, Celgene. We’re waiting on that, and on a few other details –- is it better to do with or without Rituxan, for example? –- but I hope to start soon.
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Here's hoping all of you are doing well in your struggles with CLL. Even more, here's hoping you're out there living your lives to the fullest. Nobody gets off this planet alive, whether it is CLL that takes you or something else. Don't die with your regrets intact. Get real and deal and rock and roll. You only go around once, and this is it. Punch cancer in the nose and kiss life on the face.
Over nine years of blogging since transplant for CLL (chronic lymphocytic leukemia) on July 1, 2008 - This picture, painted by son William, launched by blog and was originally painted as a way to remember me after I was gone. Now it just serves to remind...
2 weeks ago