Sunday, April 29, 2007

Friday, bloody Friday

What do you do when your doctor gets fired?

I am about to find out, and it is not something I expected, wanted, or feel like coping with. The past six weeks have been stressful enough without having my horse taken from me in the middle of the CLL-filled, AIHA-ridden, low-immunoglobulin-can-I-get-some-IVIg treatment stream.

What occurred last Friday was a coup, in the best tradition of the Medicis or the Borgias or the Soviets. One minute Alexander Dubcek, president of Czechoslovakia during the 1968 “Prague Spring,” was there in the picture, the next minute he was airbrushed out.

I have written in these pages about my three hematologist/oncologists. Dr
. Lippencot, the first, was rigid and unbending in her insistence that I do single-agent fludarabine, so I went looking elsewhere. Dr. Chopin, the second, was open-minded if a little skeptical, but treated me with single-agent Rituxan for two years. She decided to leave medicine; her replacement was Dr. Belle, who for the past year has been my horse, my Dubcek, and a doctor with whom I was very pleased.

Dr. Belle is a slight, younger woman, short, not a commanding presence. I know that in the professional world women
are often judged on their looks and stature; it is doubly hard for women who are small or a little pudgy or anything other than Thatcheresque to easily gain the respect of colleagues and coworkers -- and this can include other women, as well as men. And I think we all know by now the truism that a man who stands up for his rights is considered to be assertive, while a woman who does the same is often considered to be a bitch. Whether these sorts of things played a role in Dr. Belle’s eventual fate, I can only speculate.

As I grew to know Dr. Belle, I came to like her and respect her more and more. She is not a CLL expert,
but is willing to consult with experts, and to learn. She did not bring a set of unbending judgments to the table, she did not suffer from a God complex, but this did not mean she was “soft.” Behind the sweet Southern exterior was a willingness and a drive to fight for her patients.

I saw this grit last Friday when, unbeknownst to her or to me, I was the last patient she was to see while employed at the oncology group where I have gone for 3 ½ years. My application for IVIg at the neighboring hospital had been rejected because my IGG was 746, just above normal. A new test pegged it at 436, well below normal, and enough to change a “no” to a “yes.” Dr. Belle said she’d have the nurse fax th
e request over that very afternoon, and she wrote at the bottom of the fax that if this request was not approved she would not hesitate to admit me to the hospital, if that’s what it took to get the IVIg into my veins. She was hoping I’d be able to get it on Monday.

When I left at 1:30 p.m. Friday afternoon, I had no idea that a letter, dated two days prior, and mailed the day before, was starting to arrive in the mailboxes of her patients. This letter informed us all
that, effective Friday, the day I saw her, she was no longer associated with the oncology group.

The irony is that, during my appointment with her, I got the impression that she not only liked her job but had definite plans to stay. She talked about “making partner” in another year. This would mean joini
ng the four male doctors in the practice on equal footing. I am certain that she was led to believe one thing would happen when, behind her back, quite the opposite thing was brewing.

And so, perhaps an hour after I left at 1:30 p.m.
, Dr. Belle probably finally got the news, and was left with a few minutes to clean out her desk. Her patients have been left doctorless, and for those of us in the middle of treatment, this is especially nervewracking. I do not know what compelled the partners to make the choice they did, but I have the sense that it involved personality conflicts more than questions of competence. I am obviously biased, because I liked my doctor and was comfortable with her approach and judgment. And I think the way her dismissal was handled was reprehensible.

And so, my treatment, my file, my life, will now be put in the hands of one of those very people whose method of action I regard as dishonorable. How do I look them in the eye with anything less than contempt? How do I trust such a person with my health care, to make the best decisions, to listen to me and give a damn?

And what are the odds that I will find a doctor who is as simpatico with me as Dr. Belle?


Yet I have to go in tomorrow and fight for someone to make sure I get my IVIg, when I don’t even know who my doctor is. It will be chaotic, patients coming to see a doctor who’s no longer there, patients getting chemother
apy on the orders of a doctor who’s been fired.

And I, of course, am one of them. Who will listen to me when I suggest things like low-dose Rituxan, who will read the abstracts and studies I bring in, who will take the time to pore over Dr. Terr
y Hamblin’s three-part series “What is the aim of treatment?,” which I must once again print out and hand to a strange doctor in the hope that some of it might sink in?

I am left to reinvent the wheel at a time when my coping skills have been already been taxed to their limit. I d
o not know what will happen to my treatment program, and I do not know where to turn when it comes to finding another doctor. There are 42 hem/oncs on my health plan, and I am in no mood to go doctor shopping starting with the “A‘s.”

I do have Dr. Belle’s e-mail address. She established a Yahoo account so patients could communicate with her, which was an innovation in an office where giving work e-mail addresses to patients is evidently verboten. I will write to her and tell her how upset I am that this happened, and I will ask her to let me know if she joins another practice, or sets up shop on her own.

And I will tell her that, if letters of recommendation from patients mean anything when doctors apply for work, I will be more than happy to write one. They probably don’t count, but it’s all I can think of to do.

It will be an interesting week, and I am not looking forward to it.


I made contact with Dr. Belle. Turns out she found out about her dismissal from a patient who saw her Friday morning, then went home and read the letter, and then called Dr. Belle that afternoon to ask what was going on. Talk about a chickenshit way to handle a firing!

Dr. Belle will resume practice, somewhere, somehow, in the next few months, so I will be able to see her again. In the meantime she is referring her patients to another office, where I have made an appointment. They've been inundated with Dr. Belle refugees, er patients. While I am not certain I will adopt the new office, I'll at least check it out.

One reason is that it is simply hard, emotionally, to be in the old one. The atmosphere when I went in Monday for my Rituxan was funereal. Most of the staff was shocked and unhappy about what had happened. As much as they felt free to talk, the didn't see it coming, didn't think it was handled right, and didn't think it was a good idea to begin with. When Marilyn told one staffer that we were thinking of switching offices, the employee replied, under her breath, "I don't blame you."

The hardest thing, for me, is imagining myself in an examination room having to be pleasant to one of the underhanded partners. I'll do it if I have to -- ultimately, the head must rule the heart if it is in the best interest of my treatment. But if this new office works out, I may not be put in that position. In the meantime, I wonder how long I can continue getting low-dose Rituxan without actually seeing a doctor.

It's always something. If it's not one thing, it's another -- Roseanne Rosannadanna

Saturday, April 21, 2007

Low-dose Rituxan

As readers of this blog know by now, I am currently being treated with low-dose Rituxan, 20 mg/m2, every Monday, Wednesday, and Friday. The plan calls for this to continue until my white blood count is normalized or until I reach a plateau at which Rituxan no longer appears to be effective.

That “m2,” by the way, stands for per “meter squared,” which means the dosage is calibrated to my body surface area, a calculation involving my weight and height. When they hook the bag up to the IV pole, it actually contains 42 mg of rituximab. The standard dosage would be 375 mg/m2, which I have had often in the past, and which usually translated to about 750 - 780 mg per bag once my body mass was factored in. So, even a math dunce like me can see that it will take somewhere on the order of 18 infusions of low-dose Rituxan -- six weeks’ worth -- to equal one dose of standard-strength mouse juice. I’ve done five weeks so far.

If less can achieve the same or better results as more, there are obvious advantages to using less. These include reducing the possibility of creating disease resistance to the drug, fewer infusion reactions, and reduced chances of unwanted side effects such as delayed-onset neutropenia and potentially dangerous skin problems. Plus, depending upon how much you and your insurance are paying, it costs a lot less. The only loser is the manufacturer, Genentech.

On the other hand, it is important to remember that Rituxan is still Rituxan, and that its use as a single agent is not a panacea for chronic lymphocytic leukemia. Rituxan-induced remissions are not terribly deep nor durable. There is no reason to think that low-dose Rituxan remissions will last any longer than those at standard dose. As one doctor put it to me, “I have used low-dose rituximab a couple of times with no clear evidence of long term effect yet.”

Early word on low-dose Rituxan’s effectiveness

Still, if Rituxan is your poison, low-dose -- hereafter referred to as LDR -- may be worth considering. Here is the early data, some anecdotal, some from pilot studies:

One patient has posted her experience online, pointing out that her absolute lymphocyte count (ALC) dropped from 137k to 4.6k after eight weeks of LDR at 30 mg, given intravenously three times a week. She had used standard-dose Rituxan in the past.

A pilot study conducted by Dr. Ron Taylor (photo below) and other researchers at the University of Virginia, during which patients were given LDR by IV three times a week over four weeks, showed results ranging from stable disease to complete response (link at end of post, along with lots of other links). Not surprisingly, the complete responses were achieved in patients with the highest levels of CD20, and both were, it is interesting to note, 17p-deleted cases.

Another patient experience, detailed in a CLL Topics Alert, shows the more middling, “stable disease” end of LDR response -- the patient’s counts had been rising, almost doubled in the month before LDR began, and were stalled by LDR, but not reduced. After four weeks of subcutaneous injection of LDR, 20 mg three times a week, his ALC went from 44.7 to 46.0. Are his results a matter of his state of disease, his CD20 expression, or could the sub-Q method of administration be less effective than IV?

There is now a clinical trial underway, using a flat 20 mg of LDR, to help answer the question of LDR’s effectiveness in a larger cohort of patients than Dr. Taylor’s original pilot study. After all, the proof of any theory is in the patient pudding. The bottom line is not how elegant the theory, but how concrete the result. Your donations to CLL Topics are helping fund Dr. Taylor’s laboratory analysis of the trial data.

It should be noted that LDR can also be accompanied by nasty infusion reactions, so adequate premedication (usually Benadryl, Tagamet, Tylenol, and a steroid such as Solu-Cortef to reduce the inflammatory response) is a must. I know of one patient whose first infusion of 20 mg/m2 was a near-disaster, exacerbated by her doctor’s refusal to adequately premedicate her, which borders on malpractice. I do my LDR infusions with no premeds, but I have had standard-dose Rituxan 25 times in the past, so I know my limits and my tolerance. Even then, when the nurse ran the bag through a little too quickly one time, I got a chill and broke out in a sweat. LDR is not a license to forget about precautionary measures, and this also includes pre-treatment allopurinol and drinking lots of water, both of which help protect the kidneys from tumor lysis, which can happen when millions of cells die at once.

My experience with LDR

In my case, so far, LDR is bringing down the white count. As you may recall, I also had 72 mg of methylprednisolone daily for a week, which did an excellent job of debulking me, and which has been gradually tapered and is now at 4 mg a day. The importance of the steroid in my particular treatment cannot be overemphasized. Its addition to the protocol was triggered by the onset of autoimmune hemolytic anemia (AIHA). The hemolysis soon stopped, and my red counts have since been recovering, slowly but steadily.

One effect the steroid had was pushing CLL cells out of the spleen, nodes, and marrow, doubling my WBC to 364k at one point. Then, almost as quickly as it doubled, it dropped: to 271k after another week, and to 95k after another. LDR was only one factor here, I think. Another is the steroid itself, which has lympholytic (lymphocyte-killing) properties and very likely some synergy with Rituxan. Another significant factor was probably the ramping down and end of an infection that likely had precipitated the AIHA, and which had been driving my white count upward even before the AIHA set in. As any CLL patient who has gotten a cold knows, your count will go up and then down again when the cold is over. My supportive meds -- Bactrim, diflucan, augmentin, and acyclovir -- no doubt had something to do with the end of the infection.

Since my white count fell below 100k, the LDR has been dropping it steadily, from 95k to 81k three weeks ago, from 81k to 67k two weeks ago, and from 67k to 49k last week. At this rate, my count should be normalized in about three weeks. I say “should,” because as we go lower, we encounter a greater chance of reaching a plateau point, where the effectiveness of Rituxan ends and cells shorn of CD 20 begin. (Back in October, when I did standard-dose Rituxan three days a week, that plateau point was 22k, achieved after just five infusions.)

The bottom line today is that the steroid and LDR combination has worked better than I had hoped -- so far. That is the operative phrase: “so far.” The bulk is largely staying off and the count is going down. If I can get a normalized WBC and have reduced the bulk by a substantial amount, it will have been a successful treatment experience.

Whatever the end result -- whether I get as good as I’m hoping, or whether the counts plateau at a higher level -- the question comes up of how durable the result will be. The count is not everything; indeed, in a patient prone to bulkiness like me, it is less important than the nodes. Many patients who have used steroids to debulk report that the nodes come back within a month or so. It will be interesting to see if that happens in my case. The steroid dosage is now so low that it is doing little to hold back activity in the nodes. I have noticed a very minor uptick in one node on the side of my neck, and I get the impression that even as my counts continue to drop with LDR, the nodes will gradually begin their return.

So, I am left to wonder: Where will I be a month after treatment ends? Will the nodes be back to where they were before I started? Will they be a shadow of their former selves, indicating that the treatment has ramped the disease down to a good degree? How long might they be held in check before retreatment is needed?

As we all know in CLL, there are no easy answers, and different patients get different results with the same protocol. As the Romans used to say, experientia docet -- experience teaches.

Planning my encore

So, what do I do for an encore? It depends, to a great extent, on how my treatment plays out. But doing nothing until the disease gets as bad as it was before I started would not be wise. Those days are over. In my case, the “just let it go until you hit the wall” approach brings with it infections and AIHA, which are not worth the risk. Getting mashed against the wall like a bug on a windshield is messy and unpleasant, to say the least.

One option is to do another cycle, as it were, perhaps giving my body a month’s rest and then using a four-day course of steroids to debulk again, followed by more LDR. Chemotherapy often runs in cycles of up to six go-arounds of treatment. Would more cycles benefit me? Would I be able to gradually erode the disease through this method?

If it works, then I might be able to adopt a new “low-tox” route of disease maintenance: Repeat this process every so often -- say every four months -- to keep the disease in check. Add periodic IVIG to boost my immunity against infections. Take maintenance acyclovir, one 400 mg pill a day, to control the herpes virus (my titer for this was high recently). Acyclovir may also help against the Epstein-Barr virus, which I know I have floating around in my system, as I had infectious mononucleosis as a child. An EBV titer test has been taken, and the results are pending.

Another option, depending upon how deep a remission I get, is to consider following this treatment with Campath consolidation. Having unmutated, 11q-deleted CLL means the disease will return faster than it would in many other patients. Would using Campath at this point in my CLL career be worth the risks that accompany this important, highly immunosuppressive monoclonal antibody? I will be studying the ins and outs of Campath over the next month or two. Stay tuned.

What about other chemo drugs?

My thought on FCR is that it is still best saved for transplant conditioning, by which time it will probably be FCH (as in HuMax CD20) and likely a more effective regimen than FCR. While I have accepted the likelihood of having a transplant at some point, I see no survival advantage to doing it now, as opposed to putting it off for as long as reasonably possible. I am only 50 and have a ten-year window to accomplish the task. And so far, by the way, I have no signs of marrow failure.

Chlorambucil is another option, as is cyclophosphamide, which is considered to level the playing field for 11q patients. But I would have to investigate how much one of these drugs would meaningfully add to what I am already doing.

Meanwhile, back at low-dose Rituxan Ranch

The whole theory behind low-dose Rituxan has to do with CD20 shaving and complement, a subject that Dr. Taylor has been studying for several years. We all know that Rituxan is a man-made antibody that affixes itself to the CD20 “fingers” on B cells. In cancers such as non-Hodgkins lymphoma, where there is a lot of CD20 per B cell, Rituxan works pretty well. In CLL, there are fewer fingers, and therefore it is less effective. (HuMax CD20, Genmab’s new anti-CD20 monoclonal that will probably be on the market in a year or two, requires fewer finger to work well, and may be able to do in CLL what Rituxan does in NHL.)

Briefly, the idea behind CD20 shaving is this: One of the ways in which cell-kill is achieved when Rituxan is used is by complement-dependent cytotoxicity, or CDC. The body’s complement system provides a fundamental level of immunity, and includes those mighty cell-chomping macrophages, which look like something out of a science fiction movie (photo below). In a process called phagocytosis, those macrophages, along with granulocytes, kill “invaders” such as Rituxan-tagged B cells (and innocent little red cells, when things go haywire in AIHA). But they become overwhelmed by the sheer number of Rituxan-B cell complexes when a lot of Rituxan is used (Taylor et al are still trying to define “a lot,” but is appears to be somewhere above 30 mg, definitely above 60 mg, and therefore includes standard-dose Rituxan). At a certain point, rather than killing the cells, the cells are sent to the liver, where they are shorn of their Rituxan-B cell complexes but not killed. In other words, the body has taken a shortcut to solving the problem. Et voila -- what returns to the bloodstream is a B CLL cell, minus its CD20 and any Rituxan that was attached to it. You have now officially shot yourself in the foot, or somewhere worse. Yes, CD20 may grown back over time, but there is no doubt that this process is a setback in treatment that is better off avoided. You don’t want to end up feeling like the cat in the photo at the end of this post.

Complementary medicine

Beyond this, there is evidence that the massive cell-kill process initiated when Rituxan is used also depletes complement. It recovers, but not immediately, rendering diminishing results in the interim. Early in his research, Taylor looked at this end of the problem and asked: What if we give the patient more complement? In a 2002 abstract, Taylor and colleagues concluded: “We suggest that if an anti-tumor mAb such as Rituxan requires robust Complement (C) activation for therapeutic efficacy, then insuring an adequate level of C activity in a patient, by supplementation with either fresh plasma or a purified C component such as C2, may provide an important approach for improving the therapeutic efficacy of a C-fixing mAb.”

This sounds logical, and an abstract presented at ASH in 2005 by Israeli doctors showed that this worked in one patient: a woman who had been through the chemo mill, including fludarabine and cyclophosphamide as well as Rituxan, and who was barely responsive to therapy anymore. Her doctors gave her two units of fresh-frozen plasma followed by 400 mg/m2 of Rituxan on day one, and the same amount of plasma followed by 275 mg/m2 of Rituxan on day two. They described her response as “dramatic,” and this included “marked reduction of lymphadenopathy” and resolution of other symptoms.

“To the best of our knowledge,” the doctors concluded, “this is the first description of a case where successful induction of dramatic and rapid improvement of both clinical and laboratory parameters in a patient with advanced CLL previously resistant to Rituxan-containing chemo-immunotherapy was achieved by combining Rituxan therapy with fresh frozen plasma as a source for complement. This observation has to be verified in additional patients in order to confirm the approach of potentiation of Rituxan effect by providing increased amount of complement in order to augment CDC.”

So, why not go this route? Well, I tried to get my second hem/onc, Dr. Chopin, interested in it back in 2005, and she looked at me like a deer caught in the headlights. The fact is that it is impractical and experimental. Using lower-doses of Rituxan, so that complement does not become overwhelmed in the first place, is far more practical, as well as more cost effective.

Non-standard standards

How did 375 mg/m2 get to be the standard dose for Rituxan in CLL? There appears to be some question about this. One suggestion is that this was an arbitrary dose, determined by how much was on hand in an early study and how many patients needed to be treated. Another explanation is that it is based on a pivotal trial of Rituxan in patients with relapsed indolent lymphomas such as low-grade NHL. In this trial, the results published in 1998 by McLaughlin et al of MD Anderson, dosages of 375 mg/m2 once weekly for four weeks were used. This formed the basis for the use of 375 mg/m2 in the 2001 CLL study by Byrd et al -- it is directly cited -- in which patients were given Rituxan three times a week. This was in an effort to make up for the difference in effectiveness, as it were, between CD20 expression in indolent lymphomas and CLL. (Dr. Byrd still uses this protocol, and this is the one I tried last October until a plateau was reached, so the results in my case were rather disappointing.)

The larger point is this: There may not always be a truly logical reason behind the dose-selection of drugs. If the story about arbitrary dosage of Rituxan is true, that certainly raises a red flag. Even if the 375 mg/m2 is based on results in NHL, that may not hold water as a logical step in CLL. Low-dose Rituxan is no less logical than any of the above, and may be supported by better theory. So if it seems “weird,” it is certainly no less “weird” than the “standard.”

Another example is FCR therapy. It appears from reading CLL Topics that the FCR “lite” protocol currently in trial at the University of Pittsburgh may be every bit as effective as the regular-strength FCR protocol pioneered at MD Anderson. One would like to be a fly on the wall at meetings where dosages are determined. Is there a dartboard in the room? Do our famed researchers use “paper, scissors, rock” to decide how much fludarabine to give?

I’d like to think, of course, that the soundest of science is backing these choices, but I have a feeling that educated guesswork is every bit as common. However dosages are determined, the bottom line for us patients could not be more important. Thousands of us CLLers may have been unnecessarily overusing Rituxan for years, until a light bulb went off in Ron Taylor’s head. We shall see, of course, how brightly it shines and where it leads us.

Reading up on LDR

For those who want to examine LDR in more detail, here are some useful links that I have assembled.

Dr. Taylor does a nice job of explaining CD20 shaving in layman’s terms in a short piece he wrote for the UK CLL Support Association entitled Shaving and Rituximab: Targeting the Sharks. Chaya Venkat of CLL Topics does her usual excellent job of translating medicalese into English in the article CD 20 Shaving with Rituxan. An earlier article of Chaya’s, Role of Complement in Rituxan Therapy, is also worth reading and contains the complete abstract of Dr. Taylor’s early work suggesting that the addition of complement to Rituxan may be useful.

Dr. Taylor and colleagues have published three abstracts you might want to read. They are:

Pilot Study of Thrice-Weekly Low-Dose Rituximab (RTX) in Chronic Lymphocytic Leukemia (CLL): Decreased CD20 Loss Via "Shaving" and a Novel Strategy for Enhanced Therapeutic Targeting

A Pilot Study of Thrice-Weekly Low Dose Rituximab (RTX) in the Treatment of Chronic Lymphocytic Leukemia (CLL) Suggests Enhanced Therapeutic Targeting Compared to Standard Dose Regimens

Thrice-Weekly Low-Dose Rituximab Decreases CD20 Loss via Shaving and Promotes Enhanced Targeting in Chronic Lymphocytic Leukemia

Here is the clinical trial now underway at the NIH, which is apparently still recruiting patients, so those of you with a hankering to visit Bethesda, MD may wish to consider it:

Lower But More Frequent Dose Rituximab to Treat Chronic Lymphocytic Leukemia

The Israeli abstract -- Successful Induction of a Rapid Improvement of Both Clinical and Laboratory Parameters in a Patient with Advanced CLL by Combining Rituximab with Fresh Frozen Plasma as a Source for Complement. A Novel Therapeutic Approach? -- is only available online by logging into ASH and looking up their 2005 conference. Registration is free and it is abstract #5030.

Sunday, April 15, 2007

A lymphomaniac in the White House?

You may have heard by now that former Sen. Fred Thompson, who is considering a run for the Republican nomination for president, has Marginal Zone Lymphoma, for which he has been treated with my favorite mouse cocktail, Rituxan. MZL is described as an “indolent lymphoma,” and here is a report last week from, in blue print:

Thompson, 64, said in a statement that his cancer was initially detected during a routine physical two and a half years ago, and he initially received chemotherapy to treat it.

This means, that for the time being, Thompson has no signs or symptoms of the cancer. Thompson's cancer is also a case of "indolent" lymphoma -- a type of cancer that, while rarely cured, is slow-growing and associated with a much more favorable prognosis.

"I have had no illness from it, or even any symptoms," Thompson said in a statement issued Wednesday. "My life expectancy should not be affected. I am in remission, and it is very treatable with drugs if treatment is needed in the future -- and with no debilitating side effects."

Dr. Bruce Cheson, professor of medicine and head of hematology at Georgetown University Hospital, treated Thompson. He says the senator's prognosis is favorable. "Some lymphoma are very aggressive, but people with slow-growing types, like Sen. Thompson's, often die from natural causes associated with old age, rather than from the disease," Cheson said in a statement, also issued Wednesday.

What Indolent Lymphoma Means

The word "lymphoma" is actually a general term used to describe more than 30 different types of cancer that affect the lymphatic system, all with varying degrees of aggressiveness.

"It really depends on the type of lymphoma you have as to your outlook," said ABC News Medical Editor Dr. Timothy Johnson on ABC News Radio Wednesday morning. In Thompson's case, Johnson said, the fact that he is still in remission after his initial treatment is a positive sign.

"With a very slow-growing, or indolent, as we sometimes call it, form of lymphoma, sometimes in those people you just watch and wait and monitor the situation," said Johnson.

"It sounds like he's got one of those forms of lymphoma that is very slow-growing. Many people with this kind live a normal life span."

Indeed, current figures suggest that patients with indolent lymphoma can generally expect to survive for another seven to 10 years.

However, it is unlikely that Thompson's cancer is completely curable using current treatments. Since most cancer treatments today target fast-growing cells, it's hard for doctors to completely wipe out slow-growing ones.

Chance of Recurrence Remains

Even though Thompson is currently in remission, given the nature of the disease it is possible that the cancer could recur in the years to come. After initial treatment, most patients with this type of cancer have a remission period of between 1.5 and 4 years, after which they will relapse. Doctors will then treat the cancer again, usually with a stronger course of treatment.

Subsequent periods of remission are often shorter than the first. But since these periods are measured on the scale of years, many patients can expect to live for many years after diagnosis -- perhaps eventually dying of old age rather than from the cancer.

This likely means that if Thompson is considering a serious presidential bid, it is unlikely that his cancer will hold him back.

"There's always a chance of recurrence with this, and any kind of lymphoma, at which point it usually can be treated again," Johnson said. "So I think at least for the next few years, he should be physically able to run for president."

Sounds a lot like some cases of chronic lymphocytic leukemia, right? After all, CLL is medically considered to be a low-grade lymphoma.

There was a budding discussion on the ACOR CLL list about the ramifications of having someone with this condition -- our condition -- in the White House. It was posited by a couple of members that disease-related fatigue would be debilitating, and that chemotherapy might lead to “chemo brain.”

I replied thusly:

"I think it is pretty evident that some presidents can have 'chemo brain' without ever having had chemotherapy. There are those who are physically fit and yet who are unfit for office. I would have no problem voting for a candidate with indolent lymphoma, or CLL, whose prognosis indicated that serious complications would be unlikely for at least four years, and who appeared to be mentally sound and had the wisdom and ability to do a good job."

Alas, this discussion has been cut short by the on-duty moderator, who thinks it is about politics, a list no-no, when it really is about the question of whether CLL and its cousins render its victims potentially incompetent to do demanding work. (This rather short-sighted approach is why I do most of my posting at CLL Forum, where there is currently a civil discussion of this very same issue.)

But I think the discussion that began on ACOR deserves to continue, and so I will post about it here, and elaborate a little bit more.

There are indeed people with CLL-related fatigue, and those who need rest during chemotherapy. Not everyone with CLL, or indolent lymphoma, has the energy to run errands, let alone run the country. But an enormous number of patients, probably the vast majority, do have the energy. They have jobs. They raise families. Many have positions of responsibility in all walks of life. The case of the late 60 Minutes newsman Ed Bradley is the most prominent example of someone who maintained a high-powered career with CLL. There are likely other rather well-known CLLers, who keep their disease a secret, fearing it would color perceptions of their competence and ability, leading to diminished opportunities.

This is already the case with Joe and Jane Average, patients who really do face the prospect of employment discrimination if they are honest about their condition. I personally know of people who have been eased out, let go, even fired, following disclosure at work of their CLL diagnosis. Not only is an income at stake for these folks, so, often, is health insurance. (Beyond these practical matters, of course, are issues of vocational fulfillment and self-image.)

In the same way that the American people have come to realize that you can be a woman and hold high office; or be an ethnic minority and hold high office; or be gay and hold high office; or be of a religious minority, such as a Jew or a Mormon, and hold high office; or be in a wheelchair and hold high office; has not the time come for us to realize that you can also have a chronic disease like CLL or indolent lymphoma and do the same? Indeed, having a disease like CLL can broaden one's horizons in a way that might actually serve the country well.

I am not rooting for Fred Thompson to win, since I think we desperately need a break from Republicans. But I am rooting for him to enter the race, which will raise the profile of people like me, as well as the consciousness of the public at large.