Dave’s Great Adventure
Book 5, Chapter 1, Verse 3
Irony of Ironies
February 28th was a tough day. We got whipped one way and then the other.
The day before we had gotten the news that my labs indicated the possibility that I had developed the deadly Richters Transformation form of CLL which I've previously mentioned. It happens in about 10% of all folks with chronic lymphocytic leukemia. The transplant folks mentioned that one of my lab tests indicated this possibility (specifically my LDH, lactic dehydrogenase test, which was elevated).
So the next day we went to see my CLL expert doc. You may remember that last August when we found that I had the p53 mutation (which has a much worse prognosis than the form of CLL without this change) he started me on Arzerra to help me hold my own against the disease while they were waiting for some new drugs to be available. He picked the Arzerra because it's an antibody type drug, and as such, does not damage the body's immune system like most chemotherapy regimens. It worked at first but became ineffective after about five months. When I was found to have masses growing in my belly on CT scan a couple of weeks ago, my doc talked to Dr. Keating and was told there was new clinical trial which was just opening up at M. D. Anderson and that I was "Number One" on his list for it. I wasn't told what the trial involved but figured it might include the use of the new Bruton's Tyrosine Kinase drug, PCI 32765, which I've also previously mentioned. More about it later if I actually end up on the drug.
So we saw his nurse practitioner who examined me and went over my labs. She confirmed that the disease was progressing and that my labs indicated the possibility of Richters, though we still haven't confirmed this. She also mentioned that with my new finding of possible Richter’s Transformation, I wouldn't be a candidate for the new PCI 32765 drug. That was an incredible downer to hear. I had been anxiously awaiting this new stuff which seemed much too good to be true; a pill a day without side effects, with a little Rituxan (another antibody type drug) thrown in on monthly basis for a few months. So, after hearing that, Kathy and I sat in the office, glum with disappointment while we waited for Dr. Keating to come in.
But then he came in with a big smile on his face. "Just in time!" he said. The new drug is available and it will be perfect for me, he said. It shrinks tumors, even aggressive ones, and increases antibody levels, reduces infections, is well tolerated, and so on. Folks have been on it for 18 months or more without any serious side effects. He said he'd send in his research nurse to sign me up for the new clinical trial. Wow! After, being so bummed after our discussion with Dr. Keating's nurse, this was a complete turnabout. Kathy and I mentioned how rapidly things seem to change in my disease and that we've been through the CLL roller coaster more than one time. This was yet another up and down and up.
As soon as he left the office for his next appointment his staff started trying to arrange a few things that I would need before starting on the new drug, the PCI 32765. I would need a bone marrow biopsy and an infusion of Rituxan. They were working in getting these set up ASAP, later the same day.
Then Gracie, the research nurse came in. She started to sign me up for the protocol but stopped short, very early on, as we discussed my past treatments. She said she hadn't realized that I'd had Rituxan on three previous occasions (I had had the drug in 2002, 2004 and 2008), thinking instead that I'd only had it twice before. Then she said the new protocol excluded anyone who had had the drug more than three times. "But," I protested, "I have only had it for a total of three times so far!" Yes, she said, but you also had Arzerra earlier this year and that counts as a Rituxan infusion, as it's in the same category of drug.
She then left to try to talk to Dr. Keating, who by now was doing a webcast for the Leukemia and Lymphoma Society, but in between questions and comments, he was texting her back. "WHY!!!" he texted when told I wasn't eligible for the new study. Gracie apparently contacted the folks running the protocol, looking for an exception, but none was forthcoming. After about 45 minutes, she and Dr. Keating's nurse came back to say that it looked final, that I wasn't eligible.
So, here is the incredible irony in all this. The drug that Dr. Keating gave me to try to keep me healthy long enough to get me involved with the new drugs that are just now coming into availability, the Arzerra, is the drug which now makes me ineligible to take part in the study, now that it's finally available. That's just amazing. Depression to elation to depression in 15 minutes. The roller coaster. Again.
Tomorrow I have a PET scan and at some time thereafter (soon I hope) they'll schedule a fine needle aspiration/biopsy of one or more of my tumors. I'm not sure what that'll lead to in the short term, but if I in fact have Richter’s, I think I'll be starting on high dose chemotherapy soon and the stem cell transplant will be expedited. But, that's just conjecture right now. Right now we have no concrete plan, but we'll have to have more details before we leave Houston. I hope to talk to Dr. Keating and his staff again tomorrow to see what they say is the next step, since the step we were left with today fell off a cliff. Stay tuned.
Dave
Tuesday, February 28, 2012
Monday, February 27, 2012
First Update From Houston
Dave’s Great Adventure
Book 5, Chapter 1, Verse 2
First Update From Houston
We had a wonderful trip to Antarctica. We were kept busy with multiple daily landings and cruising out among the wildlife and icebergs in the inflatable zodiacs that we used to go from ship to shore. We were tired from all the activities but it was worth it. Even the 5AM awakenings (which were 2AM Dallas and body time) were ultimately worth it as there was so much to see and because we had to make the most of the precious few days we had available to spend there. It was a special time. This place belongs on everyone’s bucket list.
But as soon as we got home we had to prepare to leave again, as we had to be in Houston for multiple test and evaluations within five days. So, Kathy worked on huge loads of laundry while I caught us up on bills and errands. Then we packed up again and drove to Houston, a drive we have made many, many times in the past five years or so. I was expecting several days’ worth of appointments as we had a lot of ground to cover and many questions to answer about my condition and its possible treatment.
First, as I suspected, they had added on some appointments to the two days' worth that had previously been scheduled. This was mostly because of the many large masses found in my abdomen on the CT scan I had just before we left on our trip a couple weeks previously. So, our originally planned two-day trip turned into a four day “vacation.”
We first met the very nice folks at the transplant clinic and as far as they're concerned, I WAS having a transplant, probably within 3-5 months! There was no question about it! And here I thought we were just going to meet some folks and have some questions answered. My transplant doc, Dr. Khouri, is one of the pioneers of transplant procedures for leukemia. He says, and I've heard this before, that a transplant is the only possible cure for folks like me with the p53 mutation, which I described in some detail a few months ago. So, “full steam ahead,” according to him. He has scheduled a PET scan for a couple of days from now (to check for malignancies) and a lymph node biopsy at some time yet to be determined, but pretty soon, if they can possibly arrange it. They're still actually thinking that I may have the deadly Richter's Transformation lymphoma, based on some of my labs. The PET scan and biopsy will be important to confirm or deny this possibility and will help treatment.
I probably need to stop at this point to explain a couple of things. First I want to tell you why this new mutation I have, the p53 mutation, is so deadly. The p53 gene is called the “tumor suppressor gene.” It tells cells to die when they are damaged. Now, most chemotherapy works by damaging cells so they will die. The alkylating agents and purine analogs that make up most standard chemotherapy regimens, like the Fludara and Cytoxan I’ve had in the past, work on this principle. They damage a cell’s DNA so that they will die. But now that my disease has the p53 mutation (also called the 17p deletion but meaning the same thing), my cells don’t know to die when they’ve been damaged. That’s why my disease is now so resistant to treatment. And that’s why most leukemia experts now strongly urge folks like me to get a stem cell (or bone marrow; same thing) transplant as soon as possible after finding out we have the deadly mutation. But these transplants can have their own risks of death, disability and numerous complications.
But Dr. Khouri quotes “only” a 5-10% mortality from the transplant procedure, better than the 15-25% death rate I've been hearing from most transplant experts. The success rate in curing my disease is said to be 50-70%, depending on my disease and how well might respond to pre-transplant chemotherapy.
We met with the stem cell coordinator also. We already had some cell-typing results showing that my sibs don't match me, from tests done back in 2002 when I first got sick. My cells were also partially tissue-typed during that study. Based on the partial HLA (human leukocyte antigen) tissue typing that was done back then, she searched the marrow banks' data banks and found...get this...70 potential donors! Now, this number will decrease somewhat as they get the final parts of the tissue typing done (I had ten tubes of blood drawn today to get a complete HLA panel done) but as she said, all we need are one or two potential matches. Interesting news. I wonder where all these folks are. Since my dad was full-blooded Swede, I'm half Swede. I wonder if all these folks are in Stockholm or somewhere. Or maybe in the upper Midwest where lots of Swedes settled in the 1800s. Anyway, it will take, she said, 3-5 months to get a donor lined up, which is what limits and sets the time frame for the transplant. We should hear within about ten days about whether a match has been definitely located, though not necessarily if that match is truly available just yet (are they still alive, willing to donate, free of disease, etc.).
If/when I have the transplant, they'll want us to move down to Houston for 3-4 months. Wow! They have given us the name of a social worker who can help us find nearby housing, and my cousin, Amber and her husband, have also offered to put us up at their home west of town if need be. There’s also a huge hotel complex right across the street from M. D. Anderson which is in some way connected to the workings of the medical complex. It even has a skybridge connecting it to the cancer clinics. When I have the transplant I'll be in the hospital for about three weeks and then have to have daily visits for a couple of months! Sounds pretty intensive.
By the way, I had to sign a contract saying that I understood that my kind of transplant would cost anywhere from $560,000 to $1,100,000 or so! “But,” I was told, “that will include today’s consultation.” Man, I’m glad that the consultation wouldn’t be an additional expense on top of the million bucks.
I see my leukemia specialist tomorrow to see about whatever clinical trial he has in mind. The only thing I can see that would interfere with getting the stem cell transplant in the coming months would be if the drugs from this new clinical trial worked much better than anything else ever has. We'll find out his thoughts on this topic tomorrow.
And that's all the news for now. This adventure keeps on getting more exciting.
Bye now,
Dave
Book 5, Chapter 1, Verse 2
First Update From Houston
We had a wonderful trip to Antarctica. We were kept busy with multiple daily landings and cruising out among the wildlife and icebergs in the inflatable zodiacs that we used to go from ship to shore. We were tired from all the activities but it was worth it. Even the 5AM awakenings (which were 2AM Dallas and body time) were ultimately worth it as there was so much to see and because we had to make the most of the precious few days we had available to spend there. It was a special time. This place belongs on everyone’s bucket list.
But as soon as we got home we had to prepare to leave again, as we had to be in Houston for multiple test and evaluations within five days. So, Kathy worked on huge loads of laundry while I caught us up on bills and errands. Then we packed up again and drove to Houston, a drive we have made many, many times in the past five years or so. I was expecting several days’ worth of appointments as we had a lot of ground to cover and many questions to answer about my condition and its possible treatment.
First, as I suspected, they had added on some appointments to the two days' worth that had previously been scheduled. This was mostly because of the many large masses found in my abdomen on the CT scan I had just before we left on our trip a couple weeks previously. So, our originally planned two-day trip turned into a four day “vacation.”
We first met the very nice folks at the transplant clinic and as far as they're concerned, I WAS having a transplant, probably within 3-5 months! There was no question about it! And here I thought we were just going to meet some folks and have some questions answered. My transplant doc, Dr. Khouri, is one of the pioneers of transplant procedures for leukemia. He says, and I've heard this before, that a transplant is the only possible cure for folks like me with the p53 mutation, which I described in some detail a few months ago. So, “full steam ahead,” according to him. He has scheduled a PET scan for a couple of days from now (to check for malignancies) and a lymph node biopsy at some time yet to be determined, but pretty soon, if they can possibly arrange it. They're still actually thinking that I may have the deadly Richter's Transformation lymphoma, based on some of my labs. The PET scan and biopsy will be important to confirm or deny this possibility and will help treatment.
I probably need to stop at this point to explain a couple of things. First I want to tell you why this new mutation I have, the p53 mutation, is so deadly. The p53 gene is called the “tumor suppressor gene.” It tells cells to die when they are damaged. Now, most chemotherapy works by damaging cells so they will die. The alkylating agents and purine analogs that make up most standard chemotherapy regimens, like the Fludara and Cytoxan I’ve had in the past, work on this principle. They damage a cell’s DNA so that they will die. But now that my disease has the p53 mutation (also called the 17p deletion but meaning the same thing), my cells don’t know to die when they’ve been damaged. That’s why my disease is now so resistant to treatment. And that’s why most leukemia experts now strongly urge folks like me to get a stem cell (or bone marrow; same thing) transplant as soon as possible after finding out we have the deadly mutation. But these transplants can have their own risks of death, disability and numerous complications.
But Dr. Khouri quotes “only” a 5-10% mortality from the transplant procedure, better than the 15-25% death rate I've been hearing from most transplant experts. The success rate in curing my disease is said to be 50-70%, depending on my disease and how well might respond to pre-transplant chemotherapy.
We met with the stem cell coordinator also. We already had some cell-typing results showing that my sibs don't match me, from tests done back in 2002 when I first got sick. My cells were also partially tissue-typed during that study. Based on the partial HLA (human leukocyte antigen) tissue typing that was done back then, she searched the marrow banks' data banks and found...get this...70 potential donors! Now, this number will decrease somewhat as they get the final parts of the tissue typing done (I had ten tubes of blood drawn today to get a complete HLA panel done) but as she said, all we need are one or two potential matches. Interesting news. I wonder where all these folks are. Since my dad was full-blooded Swede, I'm half Swede. I wonder if all these folks are in Stockholm or somewhere. Or maybe in the upper Midwest where lots of Swedes settled in the 1800s. Anyway, it will take, she said, 3-5 months to get a donor lined up, which is what limits and sets the time frame for the transplant. We should hear within about ten days about whether a match has been definitely located, though not necessarily if that match is truly available just yet (are they still alive, willing to donate, free of disease, etc.).
If/when I have the transplant, they'll want us to move down to Houston for 3-4 months. Wow! They have given us the name of a social worker who can help us find nearby housing, and my cousin, Amber and her husband, have also offered to put us up at their home west of town if need be. There’s also a huge hotel complex right across the street from M. D. Anderson which is in some way connected to the workings of the medical complex. It even has a skybridge connecting it to the cancer clinics. When I have the transplant I'll be in the hospital for about three weeks and then have to have daily visits for a couple of months! Sounds pretty intensive.
By the way, I had to sign a contract saying that I understood that my kind of transplant would cost anywhere from $560,000 to $1,100,000 or so! “But,” I was told, “that will include today’s consultation.” Man, I’m glad that the consultation wouldn’t be an additional expense on top of the million bucks.
I see my leukemia specialist tomorrow to see about whatever clinical trial he has in mind. The only thing I can see that would interfere with getting the stem cell transplant in the coming months would be if the drugs from this new clinical trial worked much better than anything else ever has. We'll find out his thoughts on this topic tomorrow.
And that's all the news for now. This adventure keeps on getting more exciting.
Bye now,
Dave
Intro to Book Five
Dave’s Great Adventure
Book 5, Intro
April 2, 2012
Astounding…just astounding!
We’ve had an extraordinary spring here in north Texas, with mild temperatures, gentle rains, lots of sun and perfect conditions for new growth. Everywhere one looks the trees are covered with fresh green foliage. And the byways, pastures and meadows are covered with a soft green growth of grass and flowers. Our famous (at least here in Texas) bluebonnets have formed wonderful carpets of blue almost everywhere you look along the roads and they’re interspersed with patches of magenta from the clover flowers and yellows from the daisies and such which are also blooming in profusion in many areas. The breezes have been gentle as well, unlike the typical screaming winds we often have in north Texas in spring. It’s been just about perfect and, I think, it’s the nicest spring we’ve been privileged to experience since our move back to Texas six years ago. It’s a beautiful season of renewal, new life and new hope.
I haven’t written anything in my long-running DGA series in a while, not because nothing has happened, but to the contrary, because we have been so very busy in the last two months. So much has happened that I haven’t been able to keep up. What little I’ve written I haven’t completed and only my family and a few friends have been kept abreast of what has occurred. And some incredible things have happened, both good and bad. I thought now would be a good time to try to catch up. But, since so much has occurred, I’ll break the update into a few shorter stories and send them out a bit at a time.
Some of my family and friends will recognize earlier versions of the chapters as I’ll base them on letters I have shared with them over recent weeks, but many of you will see this stuff for the first time. But the story is just amazing, at least to me and Kathy, in the number things that have occurred in such a short time, and the timing of so many events. I’ll be sending them on shortly. If they become tedious, the “delete” button can be your friend. If you find some of this interesting, I’d love to hear from you as I get the stories out to you.
Dave
Book 5, Intro
April 2, 2012
Astounding…just astounding!
We’ve had an extraordinary spring here in north Texas, with mild temperatures, gentle rains, lots of sun and perfect conditions for new growth. Everywhere one looks the trees are covered with fresh green foliage. And the byways, pastures and meadows are covered with a soft green growth of grass and flowers. Our famous (at least here in Texas) bluebonnets have formed wonderful carpets of blue almost everywhere you look along the roads and they’re interspersed with patches of magenta from the clover flowers and yellows from the daisies and such which are also blooming in profusion in many areas. The breezes have been gentle as well, unlike the typical screaming winds we often have in north Texas in spring. It’s been just about perfect and, I think, it’s the nicest spring we’ve been privileged to experience since our move back to Texas six years ago. It’s a beautiful season of renewal, new life and new hope.
I haven’t written anything in my long-running DGA series in a while, not because nothing has happened, but to the contrary, because we have been so very busy in the last two months. So much has happened that I haven’t been able to keep up. What little I’ve written I haven’t completed and only my family and a few friends have been kept abreast of what has occurred. And some incredible things have happened, both good and bad. I thought now would be a good time to try to catch up. But, since so much has occurred, I’ll break the update into a few shorter stories and send them out a bit at a time.
Some of my family and friends will recognize earlier versions of the chapters as I’ll base them on letters I have shared with them over recent weeks, but many of you will see this stuff for the first time. But the story is just amazing, at least to me and Kathy, in the number things that have occurred in such a short time, and the timing of so many events. I’ll be sending them on shortly. If they become tedious, the “delete” button can be your friend. If you find some of this interesting, I’d love to hear from you as I get the stories out to you.
Dave
Wednesday, February 8, 2012
Bad To Worse
Dave's Great Adventure
Quick Update
February 8, 2012
Just a quick update on what's going on with me. I'd been wanting to do another DGA but not enough info has been available yet.
I have been waiting and waiting to hear something, something, from M. D. Anderson. I've e-mailed repetitively and gotten some hints from Dr. Keating's nurse, but no definitive answer on what's happening next. I'm supposed to be enrolling in some new clinical trial. I'd like to know something about it.
Meanwhile, last Friday, I got a call from my local doc's nurse. He was ordering a kidney ultrasound because my creatinine had gone up a bit. I thought that was weird as I was wondering what they could possible see on a sono that might be causing it to go up a bit. Normal is about 1.0; mine had been about 1.2 to 1.4 recently, but now was 1.6. So I had the US done. It showed slight enlargement of the left kidney and "soft tissue masses" impinging on the bladder. As soon as that report hit my doc's desk, he ordered an immediate CT scan of my abdomen and pelvis...actually dragged me out of the tub the next morning to get back down to the hospital. He had to hurry as we're supposed to be leaving for Antarctica (a long way from any medical care) tomorrow!
So, we got down there, drank the lovely 24 oz. drink of "contrast, waited 90 minutes and had the CT. It took all of maybe 5 minutes.
The CT shows widespread adenopathy (either swollen lymph nodes [hopefully!] or a new tumor, a lymphoma) in my belly, along my aorta, around my bowel, and some up to 6-8cms in size (tennis ball to orange size) near the bladder. That's not good news.
Many calls went between me an my local doc and my local doc and Dr. Keating. They say nothing is going to change in the next 12 days so I'm free to go to Antarctica, but some stuff is gonna happen when I get back. I'm not yet sure what all is going to happen, but I did get a clue about the clinical trial.
I was thinking that the CT findings might represent what's called Richter's Transformation, a deadly form of lymphoma that can CLL morph into about 10% of the time. That would leave a predicted longevity of 6-8 months. But I guess my docs don't think so, as they're letting me go ahead, and they're still planning on enrolling me in the new clinical trial. If I had RT, I would probably need intense chemotherapy ASAP followed almost immediately by a bone marrow transplant.
But Dr. Keating says he still plans on enrolling me in the clinical trial when I get back, and I will be the very first on the list. He believes it will be approved by the end of this week. Great, but I still don't know what the trial involves. But...I'm Number One!
After we leave town tomorrow we will be out of telephone and, for the most part, e-mail contact until we get back on the 21st. So, I won't know any more until we get back to town, and may not know any more until we get back to Houston in late February. We have appointments on the 27th and 28th.
And that's all for now. More later.
Dave
Quick Update
February 8, 2012
Just a quick update on what's going on with me. I'd been wanting to do another DGA but not enough info has been available yet.
I have been waiting and waiting to hear something, something, from M. D. Anderson. I've e-mailed repetitively and gotten some hints from Dr. Keating's nurse, but no definitive answer on what's happening next. I'm supposed to be enrolling in some new clinical trial. I'd like to know something about it.
Meanwhile, last Friday, I got a call from my local doc's nurse. He was ordering a kidney ultrasound because my creatinine had gone up a bit. I thought that was weird as I was wondering what they could possible see on a sono that might be causing it to go up a bit. Normal is about 1.0; mine had been about 1.2 to 1.4 recently, but now was 1.6. So I had the US done. It showed slight enlargement of the left kidney and "soft tissue masses" impinging on the bladder. As soon as that report hit my doc's desk, he ordered an immediate CT scan of my abdomen and pelvis...actually dragged me out of the tub the next morning to get back down to the hospital. He had to hurry as we're supposed to be leaving for Antarctica (a long way from any medical care) tomorrow!
So, we got down there, drank the lovely 24 oz. drink of "contrast, waited 90 minutes and had the CT. It took all of maybe 5 minutes.
The CT shows widespread adenopathy (either swollen lymph nodes [hopefully!] or a new tumor, a lymphoma) in my belly, along my aorta, around my bowel, and some up to 6-8cms in size (tennis ball to orange size) near the bladder. That's not good news.
Many calls went between me an my local doc and my local doc and Dr. Keating. They say nothing is going to change in the next 12 days so I'm free to go to Antarctica, but some stuff is gonna happen when I get back. I'm not yet sure what all is going to happen, but I did get a clue about the clinical trial.
I was thinking that the CT findings might represent what's called Richter's Transformation, a deadly form of lymphoma that can CLL morph into about 10% of the time. That would leave a predicted longevity of 6-8 months. But I guess my docs don't think so, as they're letting me go ahead, and they're still planning on enrolling me in the new clinical trial. If I had RT, I would probably need intense chemotherapy ASAP followed almost immediately by a bone marrow transplant.
But Dr. Keating says he still plans on enrolling me in the clinical trial when I get back, and I will be the very first on the list. He believes it will be approved by the end of this week. Great, but I still don't know what the trial involves. But...I'm Number One!
After we leave town tomorrow we will be out of telephone and, for the most part, e-mail contact until we get back on the 21st. So, I won't know any more until we get back to town, and may not know any more until we get back to Houston in late February. We have appointments on the 27th and 28th.
And that's all for now. More later.
Dave
Wednesday, January 18, 2012
Arzerra and Beyond...But To Where?
Dave’s Great Adventure
Book 4, Chapter 1, Verse 6
January 13, 2012
[[[ “If you want to make God laugh, tell Him your plans.” --Anonymous
I’ve used this quote a couple of times over the years but it’s again appropriate. We only “think” we have our lives planned out. The following message was started in mid-November, but then I didn’t get back to it for quite a while. Meanwhile, things have changed again. Read on. ]]]
---November 14, 2011---
I think there are real signs of hope with this new stuff. I believe it’s working better than I thought it might.
When I last wrote about what was going on I had just finished Phase One of my Arzerra (ofatumumab) treatments. The treatments had begun rather abruptly in August. In mid-August, after waiting five weeks to hear the results of the cytogenetic tests which I described in excruciating detail in my last letter, my local doc got the details about the development of my worrisome p53 mutation and the plan for treatment, from my doc in Houston. With that information, we began the Arzerra almost immediately, within a week. In fact, we started the first dose of the Arzerra on August 23rd, our 42nd wedding anniversary. I try to make our anniversaries memorable for Kathy.
The Arzerra infusions have gone very well. The first phase of the treatment was eight weekly infusions. The side effects have been relatively minimal, all things considered, and that’s because I haven’t been getting any poisons this time. With all my previous treatments I had combinations of drugs which included poisons, as most chemotherapy targets fast growing cells, like cancer cells. The problem is, of course, that all fast-growing cells in one’s body are not cancer cells, so normal cells get affected as well. And that leads to side effects; the nausea, hair loss, mouth sores, etc. One of the drugs which I had in all three previous chemotherapy regimens is some stuff called cyclophosphamide, which advertises its role in chemotherapy by its trade name, Cytoxan. That’s a play on its activity within the body. “Cyto-” means cell; “toxin” means poison. Therefore, its trade name, Cytoxan, or “cyto-toxin” literally means “cell poison.”
But the Arzerra I’m now getting is not a poison, per se. It is pure antibody, an antibody directed against white blood cells with a protein called CD20, which is on the cell membrane of all CLL cells (CLL cells are actually abnormal B-lymphocytes, which are the kind that make your antibodies). It attaches to the CD20 protein and allows the body’s immune system to bore a hole in the leukemia cell’s membrane, popping it rather like a microscopic balloon. That’s the good or even great part about the antibody treatments. They target only a specific population of cells, ignoring the rest. But when they simultaneously pop billions of leukemia cells, all those dying cells spill their cell contents into your blood stream, and all those proteins, histamines, DNA and such, can clog your kidneys, cause severe allergic reactions, breathing problems, low blood pressure, and the like. Because of this possibility, before each treatment we are given antihistamines and steroids, to suppress the allergy-like reactions, and we are given the drug very, very slowly. The first treatment I got took us from 8:30 in the morning until 6:30 in the evening to complete. As I got used to the drug and as my white blood cell counts dropped (giving the Arzerra ever fewer “targets” to seek out), we were able to start giving the drug faster and faster and by the end of my eight consecutive weeks of treatments, we were able to complete the infusions by 3:00PM.
By the way, my clinic billed about $25,000 for each weekly treatment. These newer chemotherapy drugs are wonderful but they are also fantastically expensive.
But the Arzerra has worked extremely well, dropping my white blood cell counts from a pre-treatment level of just under 80,000 (normal is about 3,000 to about 9,000) to about 4,000 after the eight weeks of treatment. Now, that count is in the normal range, but the count still is not “normal,” as another test that looks for abnormal white cells in my blood, determined that 35% of my remaining white blood cells were still leukemia cells. But that’s not really a surprise. The Arzerra really wasn’t expected to put me into a complete remission anyway.
Despite that minor point, things are going very well, better than I’d hoped. When I started the Arzerra I was told that there was only about a 50% chance I would have a response to the drug because I now have the more aggressive leukemia mutation. Well, I’m obviously in the 50% of the population on whom the new drug works. Then, after we finished the eight consecutive weeks of infusions, and waited a full four weeks for the start of my monthly treatments, my white counts continued to drift down. In other words, despite stopping the drug for a month, my disease didn’t come charging back. I hope this trend continues. So far it has. I’ve had one of the monthly infusions and my white counts have remained around 3,000 or so. My next treatment will be in early December and will continue monthly through next February.
But just about any treatment will have side effects, and the major side effect that one gets with the Arzerra stems from its ability to seek out and kill only white blood cells with the CD20 marker on its cell wall. Unfortunately, all NORMAL B-lymphocytes (the ones we depend on to make our antibodies) ALSO have the CD20 antigen. So, that means that while the Arzerra is wiping out billions of leukemia cells, it’s also taking out a large number of my normal lymphocytes, too. That puts me at risk for infections as well as other tumors and so forth. But, that’s the chance I have to take to be able to hold my disease at bay long enough to try to find another, better, long term treatment and possibly a cure. In any case, the plan all along with the Arzerra has been to give me this drug over about six months, then wait perhaps six more months until it stopped working and then do…something. What, exactly, has been unclear.
I’ve been trying to re-evaluate my expected longevity based on the results of the Arzerra so far. When I first found out I had the p53 mutation, which I already knew was bad, I went back to my sources, one of which is an excellent CLL web based resource called “CLL Topics,” a well researched, critical review of all things related to CLL and its treatment. Here I found the article which noted that average longevity was just 13 to 15 months! Just over a year. But, it’s now been six months since I started the Arzerra and things seem to be going well. Since the CLL hasn’t stormed back between my monthly infusions so far, I’m guessing I may have more than a year left after all. Other sources I’ve checked suggest average longevity is perhaps 1 to 2 years and another source says 2 to 3 years. In any case, if these are accurate, those are AVERAGE numbers meaning half the patients will live longer, the other half less than that. And all of us cancer patients just KNOW we’re going to be in the longer-lived half. It’s unclear also, if these numbers are for treated or untreated patients, and if treated, what the treatment was. We shall see. In any case, I’m feeling much too normal to think that I’ll be dead within the year.
---January 11, 2012---
Things have changed. I wrote all the above about eight weeks ago but then couldn’t get back to it to finish the report. I had been very encouraged by the results of the Arzerra treatments since they seemed to be holding off the advancement of the disease. But, in the last several weeks, though my lab tests still show improvement, my lymph nodes are again enlarging in my armpits and some are now growing in my neck as well. Not good. My local oncologist here in Denton recently reported this to Dr. Keating, my doc in Houston at M. D. Anderson, and we got an unexpected phone call a few days ago.
Dr. Keating called back with some surprising and potentially very exciting news. He has cancelled the last of my four monthly infusions of Arzerra, since it hasn’t worked all that well in the last couple of months anyway and, after I’ve been off the drug for a month, which will be at the end of January, I am to get in contact with him again to talk about enrolling in a clinical study of some kind. What kind of clinical trial? I don’t yet know. When will it start? I don’t know. How long will it be? I don’t know. What are the risks involved? I don’t know.
He had been talking about possibly going to a stem cell transplant in the very near future. In fact, I have several appointments set up in late February to speak to the transplant team in Houston. That seems to be the new approach to treating folks with the p53 mutation. Rather than try multiple treatments of chemotherapy which will likely not work, they’re going to transplantion sooner in the course of treatment, as the transplant works better when done in patients who are not critically ill. Of course, with a 15 to 25% mortality rate associated with transplant, it’s a hard sell to folks who don’t feel or look critically ill, but that’s the current trend and I have been rather expecting to be going that direction in the near future.
But, now Dr. Keating is talking about enrolling me in a clinical trial which is just now opening. Unfortunately for me, the message I received did not mention what the trial would be, so I’m a bit in the dark. We have talked about the new, rather unfortunately named “btk inhibitors” like CAL 101 and PCI 32765 (this would be a good time to use Google!) which is what I am hoping he’s going to get me into. These seem to have great promise in destroying the disease and seem to have minimal side effects. The treatment consists of simply taking a pill daily, with most patients having minimal side effects. That sounds too good to be true. I mentioned the unfortunate naming…. The drugs are called “Bruton’s tyrosine kinase inhibitors,” hence the “btk” designation. But not too many years ago there was a serial killer in Wichita, Kansas who went by the name of the “BTK killer,” for “Bind, Torture, Kill.” Well, this stuff kills CLL cells, I suppose. Maybe it tortures them too!
Other possibilities for the clinical trial include a combination of drugs using lenolidamide, a derivative of the notorious birth defect causing drug Thalidomide. It is also a pill form of anti-CLL drug, but is frequently used in combination with other drugs such as Arzerra. And then there are the new CARs treatments. This stands for “Chimeric Antigen Receptors” and is the basis for the treatment that made a big splash in the press last summer, as having cured a few patients. It involves treating one’s own T-lymphocytes and training them to attack the leukemia cells. This has worked well in a very few patients, but thus far there is no long term follow-up, just a year or so. It may take the place of stem cell transplants some day, but is extremely labor intensive and expensive, since it involves taking a patient’s T-lymphocytes out, treating then, and reinjecting them into the same patient. Every patient will have to have a personalized treatment with his/her own T-lymphocytes. My cells wouldn’t work for someone else, and vice versa. More about T-lymphocytes later, if I end up in that kind of program.
Or, the clinical trial could be something else entirely. The message I got was third hand, having gone from Dr. Keating to my local doc’s message machine and then passed to my doc’s nurse, who called me. If there were more details in the message, I didn’t get them. I’ve sent a message to my team in Houston asking for more information but have yet to hear back from them. Wish me luck.
And so, that’s the latest. My disease is getting aggressive again, the Arzerra isn’t working as well, and now I’m off it entirely. And, some experimental medicine looms in my future, probably within a month or so.
But despite all this, I’m still doing pretty well. I don’t feel ill, I get to do most of the things I want to do if I don’t do too much of it and, really, the only consequence of my disease that I can discern is that I feel more tired than I‘d like and my muscles ache some. But hey, I’m 65 years old now. Maybe I should feel more tired that I used to.
And that’s all for now. I’ll be back when I learn more about what’s coming my way in the next few months or so.
Dave
***As I start yet another chapter in my battle against leukemia, I am reminded of this quote:
--“It is never too late to start. It is always too soon to quit.”—Norma R. Lineberger--
Norma worked for the Legal Defense and Education Foundation, and died of leukemia in September 2009.
www.adventureswithleukemia.blogspot.com
Book 4, Chapter 1, Verse 6
January 13, 2012
[[[ “If you want to make God laugh, tell Him your plans.” --Anonymous
I’ve used this quote a couple of times over the years but it’s again appropriate. We only “think” we have our lives planned out. The following message was started in mid-November, but then I didn’t get back to it for quite a while. Meanwhile, things have changed again. Read on. ]]]
---November 14, 2011---
I think there are real signs of hope with this new stuff. I believe it’s working better than I thought it might.
When I last wrote about what was going on I had just finished Phase One of my Arzerra (ofatumumab) treatments. The treatments had begun rather abruptly in August. In mid-August, after waiting five weeks to hear the results of the cytogenetic tests which I described in excruciating detail in my last letter, my local doc got the details about the development of my worrisome p53 mutation and the plan for treatment, from my doc in Houston. With that information, we began the Arzerra almost immediately, within a week. In fact, we started the first dose of the Arzerra on August 23rd, our 42nd wedding anniversary. I try to make our anniversaries memorable for Kathy.
The Arzerra infusions have gone very well. The first phase of the treatment was eight weekly infusions. The side effects have been relatively minimal, all things considered, and that’s because I haven’t been getting any poisons this time. With all my previous treatments I had combinations of drugs which included poisons, as most chemotherapy targets fast growing cells, like cancer cells. The problem is, of course, that all fast-growing cells in one’s body are not cancer cells, so normal cells get affected as well. And that leads to side effects; the nausea, hair loss, mouth sores, etc. One of the drugs which I had in all three previous chemotherapy regimens is some stuff called cyclophosphamide, which advertises its role in chemotherapy by its trade name, Cytoxan. That’s a play on its activity within the body. “Cyto-” means cell; “toxin” means poison. Therefore, its trade name, Cytoxan, or “cyto-toxin” literally means “cell poison.”
But the Arzerra I’m now getting is not a poison, per se. It is pure antibody, an antibody directed against white blood cells with a protein called CD20, which is on the cell membrane of all CLL cells (CLL cells are actually abnormal B-lymphocytes, which are the kind that make your antibodies). It attaches to the CD20 protein and allows the body’s immune system to bore a hole in the leukemia cell’s membrane, popping it rather like a microscopic balloon. That’s the good or even great part about the antibody treatments. They target only a specific population of cells, ignoring the rest. But when they simultaneously pop billions of leukemia cells, all those dying cells spill their cell contents into your blood stream, and all those proteins, histamines, DNA and such, can clog your kidneys, cause severe allergic reactions, breathing problems, low blood pressure, and the like. Because of this possibility, before each treatment we are given antihistamines and steroids, to suppress the allergy-like reactions, and we are given the drug very, very slowly. The first treatment I got took us from 8:30 in the morning until 6:30 in the evening to complete. As I got used to the drug and as my white blood cell counts dropped (giving the Arzerra ever fewer “targets” to seek out), we were able to start giving the drug faster and faster and by the end of my eight consecutive weeks of treatments, we were able to complete the infusions by 3:00PM.
By the way, my clinic billed about $25,000 for each weekly treatment. These newer chemotherapy drugs are wonderful but they are also fantastically expensive.
But the Arzerra has worked extremely well, dropping my white blood cell counts from a pre-treatment level of just under 80,000 (normal is about 3,000 to about 9,000) to about 4,000 after the eight weeks of treatment. Now, that count is in the normal range, but the count still is not “normal,” as another test that looks for abnormal white cells in my blood, determined that 35% of my remaining white blood cells were still leukemia cells. But that’s not really a surprise. The Arzerra really wasn’t expected to put me into a complete remission anyway.
Despite that minor point, things are going very well, better than I’d hoped. When I started the Arzerra I was told that there was only about a 50% chance I would have a response to the drug because I now have the more aggressive leukemia mutation. Well, I’m obviously in the 50% of the population on whom the new drug works. Then, after we finished the eight consecutive weeks of infusions, and waited a full four weeks for the start of my monthly treatments, my white counts continued to drift down. In other words, despite stopping the drug for a month, my disease didn’t come charging back. I hope this trend continues. So far it has. I’ve had one of the monthly infusions and my white counts have remained around 3,000 or so. My next treatment will be in early December and will continue monthly through next February.
But just about any treatment will have side effects, and the major side effect that one gets with the Arzerra stems from its ability to seek out and kill only white blood cells with the CD20 marker on its cell wall. Unfortunately, all NORMAL B-lymphocytes (the ones we depend on to make our antibodies) ALSO have the CD20 antigen. So, that means that while the Arzerra is wiping out billions of leukemia cells, it’s also taking out a large number of my normal lymphocytes, too. That puts me at risk for infections as well as other tumors and so forth. But, that’s the chance I have to take to be able to hold my disease at bay long enough to try to find another, better, long term treatment and possibly a cure. In any case, the plan all along with the Arzerra has been to give me this drug over about six months, then wait perhaps six more months until it stopped working and then do…something. What, exactly, has been unclear.
I’ve been trying to re-evaluate my expected longevity based on the results of the Arzerra so far. When I first found out I had the p53 mutation, which I already knew was bad, I went back to my sources, one of which is an excellent CLL web based resource called “CLL Topics,” a well researched, critical review of all things related to CLL and its treatment. Here I found the article which noted that average longevity was just 13 to 15 months! Just over a year. But, it’s now been six months since I started the Arzerra and things seem to be going well. Since the CLL hasn’t stormed back between my monthly infusions so far, I’m guessing I may have more than a year left after all. Other sources I’ve checked suggest average longevity is perhaps 1 to 2 years and another source says 2 to 3 years. In any case, if these are accurate, those are AVERAGE numbers meaning half the patients will live longer, the other half less than that. And all of us cancer patients just KNOW we’re going to be in the longer-lived half. It’s unclear also, if these numbers are for treated or untreated patients, and if treated, what the treatment was. We shall see. In any case, I’m feeling much too normal to think that I’ll be dead within the year.
---January 11, 2012---
Things have changed. I wrote all the above about eight weeks ago but then couldn’t get back to it to finish the report. I had been very encouraged by the results of the Arzerra treatments since they seemed to be holding off the advancement of the disease. But, in the last several weeks, though my lab tests still show improvement, my lymph nodes are again enlarging in my armpits and some are now growing in my neck as well. Not good. My local oncologist here in Denton recently reported this to Dr. Keating, my doc in Houston at M. D. Anderson, and we got an unexpected phone call a few days ago.
Dr. Keating called back with some surprising and potentially very exciting news. He has cancelled the last of my four monthly infusions of Arzerra, since it hasn’t worked all that well in the last couple of months anyway and, after I’ve been off the drug for a month, which will be at the end of January, I am to get in contact with him again to talk about enrolling in a clinical study of some kind. What kind of clinical trial? I don’t yet know. When will it start? I don’t know. How long will it be? I don’t know. What are the risks involved? I don’t know.
He had been talking about possibly going to a stem cell transplant in the very near future. In fact, I have several appointments set up in late February to speak to the transplant team in Houston. That seems to be the new approach to treating folks with the p53 mutation. Rather than try multiple treatments of chemotherapy which will likely not work, they’re going to transplantion sooner in the course of treatment, as the transplant works better when done in patients who are not critically ill. Of course, with a 15 to 25% mortality rate associated with transplant, it’s a hard sell to folks who don’t feel or look critically ill, but that’s the current trend and I have been rather expecting to be going that direction in the near future.
But, now Dr. Keating is talking about enrolling me in a clinical trial which is just now opening. Unfortunately for me, the message I received did not mention what the trial would be, so I’m a bit in the dark. We have talked about the new, rather unfortunately named “btk inhibitors” like CAL 101 and PCI 32765 (this would be a good time to use Google!) which is what I am hoping he’s going to get me into. These seem to have great promise in destroying the disease and seem to have minimal side effects. The treatment consists of simply taking a pill daily, with most patients having minimal side effects. That sounds too good to be true. I mentioned the unfortunate naming…. The drugs are called “Bruton’s tyrosine kinase inhibitors,” hence the “btk” designation. But not too many years ago there was a serial killer in Wichita, Kansas who went by the name of the “BTK killer,” for “Bind, Torture, Kill.” Well, this stuff kills CLL cells, I suppose. Maybe it tortures them too!
Other possibilities for the clinical trial include a combination of drugs using lenolidamide, a derivative of the notorious birth defect causing drug Thalidomide. It is also a pill form of anti-CLL drug, but is frequently used in combination with other drugs such as Arzerra. And then there are the new CARs treatments. This stands for “Chimeric Antigen Receptors” and is the basis for the treatment that made a big splash in the press last summer, as having cured a few patients. It involves treating one’s own T-lymphocytes and training them to attack the leukemia cells. This has worked well in a very few patients, but thus far there is no long term follow-up, just a year or so. It may take the place of stem cell transplants some day, but is extremely labor intensive and expensive, since it involves taking a patient’s T-lymphocytes out, treating then, and reinjecting them into the same patient. Every patient will have to have a personalized treatment with his/her own T-lymphocytes. My cells wouldn’t work for someone else, and vice versa. More about T-lymphocytes later, if I end up in that kind of program.
Or, the clinical trial could be something else entirely. The message I got was third hand, having gone from Dr. Keating to my local doc’s message machine and then passed to my doc’s nurse, who called me. If there were more details in the message, I didn’t get them. I’ve sent a message to my team in Houston asking for more information but have yet to hear back from them. Wish me luck.
And so, that’s the latest. My disease is getting aggressive again, the Arzerra isn’t working as well, and now I’m off it entirely. And, some experimental medicine looms in my future, probably within a month or so.
But despite all this, I’m still doing pretty well. I don’t feel ill, I get to do most of the things I want to do if I don’t do too much of it and, really, the only consequence of my disease that I can discern is that I feel more tired than I‘d like and my muscles ache some. But hey, I’m 65 years old now. Maybe I should feel more tired that I used to.
And that’s all for now. I’ll be back when I learn more about what’s coming my way in the next few months or so.
Dave
***As I start yet another chapter in my battle against leukemia, I am reminded of this quote:
--“It is never too late to start. It is always too soon to quit.”—Norma R. Lineberger--
Norma worked for the Legal Defense and Education Foundation, and died of leukemia in September 2009.
www.adventureswithleukemia.blogspot.com
Wednesday, November 2, 2011
...but the news was just horrible.
Dave’s Great Adventure
Book 4, Chapter 1, Verse 5
November 2, 2011
I didn’t expect this. I was doing so well. I felt good and was getting along just fine. I mean, I had done all those half-marathons, right? How could I be this sick?
We had a busy spring and early summer. My disease, which had relapsed the previous year, had been advancing faster with my white counts doubling every couple of months or so. I was expecting to have to do more chemotherapy by about mid-summer, so we packed our travel plans into the early part of the summer. We went to Oklahoma City for a marathon (in the rain and cold) in May, went to San Diego for one there in June. We went to a reunion of my Vietnam vet buddies in Tampa in late June, to a family reunion in North Carolina in July, and more. In the midst of all these trips we went to Houston in early July to see my doc there, who is one of the world’s foremost gurus in the management of chronic lymphocytic leukemia.
I was still feeling well; maybe a little more tired than I’d care to admit, but over all, I was doing okay except that my lab tests told another story. My disease was advancing rapidly. I talked things over with my doc, Dr. Michael Keating, and we went over some possible treatments. I say “possible,” because after you’ve been treated for this disease once or twice, there are no standard “best” treatments anymore, just lots of possibilities.
But he wanted to do a few more cytogenetic (chromosome) tests before we started anything, to help guide us to, hopefully, the best of our options. He said I’d hear something about the test results “in a couple of weeks.”
Now, to me, “a couple of weeks” mean exactly fourteen days. When I didn’t hear anything in those fourteen days, I made a series of calls to M. D. Anderson and played phone-tag for a few weeks, never getting any information about my lab tests. I was getting worried.
Meanwhile, a long-scheduled appointment with my local oncologist came up so I saw him and explained how things were going. We also talked over some possible options for treating my disease and then he said he’d call Houston and get the information for me. I was grateful, as I really wanted to hear the results of the cytogenetics.
Later that day I got a call from my local doc. He had heard from Houston. He had news, but the news was just horrible. He talked for a while but all I remember was something like “…blah, blah, blah…p53 mutation…blah, blah…Arzerra…blah, blah…50% chance of it working.”
What this means
When I got sick with this disease, chronic lymphocytic leukemia, almost ten years ago, it was only “one” disease. The doctors and researchers working with it knew that some folks with this disease died in two or three years while some folks lived, without needing treatment, for maybe twenty years or more. They knew that some patients responded well to treatments while others didn’t. They just didn’t know why. But about eight years ago they found that CLL is actually a group of diseases, differentiated by the chromosomes in the leukemia cells and several other protein “markers” exhibited by the disease. There are at least seven or eight major sub-groups of CLL and perhaps more, and survival and resistance to treatment varies greatly among the groups. By looking at the mutations of the chromosomes in your cells physicians can tell how long you’ll likely survive and what treatments might work best for you, and also how aggressive they should be with trying to treat your disease.
A couple of years after I got sick, they tested my chromosomes. They were 46XY, normal male chromosomes, as you’ll no doubt remember from your high school biology course. That was very good, as normal chromosomes were a marker of easier to treat disease and generally longer survival. Curiously, however, there is one mutation called 13q- (13q deletion) which is even better than normal chromosomes in terms of survival. But there are also several possible mutations of the disease that indicate a more aggressive and harder to treat disease. These can be ranked in order of increasing resistance to treatment and subsequently, shorter survival. And since patients with CLL tend to mutate to harder to treat forms of the disease over time, my doc in Houston was retesting my disease to see if I had mutated. And the tests in July at M. D. Anderson now showed that I had the p53 mutation, also called the 17p deletion (17p-), one of the very worst of the several variations.
Details
I’ll include a short description of what this genetic shorthand means for my friend Steve who lives in either Englewood, Colorado, or Centennial, Colorado, or maybe unincorporated Arapahoe County (I don’t remember which for sure), in the Denver suburbs. He likes details. Anyway, normally we all have 46 chromosomes per cell, 22 pairs of “somatic” chromosomes plus our sex chromosomes, the XX for females and XY for the guys. The other 22 pairs are numbered 1 though 22. Also, if you remember looking at pictures of chromosomes in textbooks, they look rather like stretched out X shaped figures, usually arranged with shorter arms at the top and longer arms at the bottom.
(By the way, our chromosomes don’t just stretch out and pose for the pictures that we see in books and magazines; they have to be manipulated with various chemicals to make them look this way. Normally they’re all balled up in a tangled mass in our cells’ nuclei.)
The short arms at the top of the chromosomes are called the “p” arms; the longer ones at the bottom are the “q” arms. If you took a part of the “q” arm off a 21 chromosome, it would be called a deletion and written as 21q-. Sometimes extraneous genetic material gets added onto chromosomes. These are additions, written as 21p+, for example.
The p53 mutation
So, now I have the dreaded p53 mutation, also called the 17p- mutation, the 17p deletion. Over the last few years my disease had changed, which is what it typically does for most patients with CLL. p53 is a gene, the “tumor suppressor gene,” which normally resides on the short, “p” arm of the 17 chromosome. Now it’s not there; in my case; it’s been “deleted” somehow. This is a very important gene which, as its name suggests, suppresses tumor growth and malignancy formation. Now I don’t have it anymore. When you read about the p53 mutation in CLL you see things like, “much more difficult to treat,” and “more aggressive disease” and “average survival of about 13-15 months.” Our friend Larry Love recently died here in Denton. Larry had an extremely rare case of metastatic basal cell skin cancer. Basal cell cancers are generally among most easily treated of all skin cancers yet in Larry’s case, this usually innocuous skin cancer spread throughout his body and despite three years of treatments, he died because the disease could not be controlled. Larry’s skin cancer had the p53 mutation. The p53 mutation is not good news.
Arzerra
This is the drug my doc picked to treat my disease this time around. Now, if you’ve been reading my stuff for any length of time at all, you’ve read about Rituxan, which has been a part of my three different previous chemotherapy regimens. Rituxan (rituximab) is a mouse-based antibody against leukemia cells. It targets a specific protein (called the CD20 receptor) that all CLL cells have. It works extremely well at doing this. The only problem is that being mouse-based (or “murine”), it itself is a foreign protein and humans can form antibodies against these murine antibodies, inactivating them.
Arzerra (ofatumumab) is similar to Rituxan in that it is also an antibody which attacks the CD20 protein receptor. It has been around in Europe for a few years but has only been approved for use in the US for about 18 months. In Europe it is called HuMax, which reflects the interesting fact that it is a humanized antibody against the CD20 site. In theory at least, it should be better for attacking the leukemia cells since humans shouldn’t create antibodies against it. In addition, it binds more tightly and for a longer time to the leukemic cells than does Rituxan, if you believe the manufacturer.
Interestingly, when reading the prescribing information that comes with this drug, the manufacturer states that it will not cure, put into remission or reduce the symptoms of any patient with CLL. This is an amazing thing to put in writing. It must either be something required by the FDA or perhaps it’s just their lawyers lowering expectations. Otherwise, it would be no more than a placebo drug!
I was very disappointed, at first, to be prescribed single-agent therapy with the Arzerra. My disease is now much more aggressive, yet I was being given a drug that would be very unlikely to put me back into remission. Studies of the drug in patients with my mutation showed only about a 50% rate of successful treatment. From the very beginning of my adventure I have wanted to be as aggressive as possible in treating the disease. Here it looked to me as if we weren’t doing as much as we could. I had found, on-line, several studies of Arzerra being used in combination with other drugs with apparent good success in short term studies. I wanted to use lots of drugs. I wanted to kill the leukemia. I want to rid my body of it. That’s always been my goal.
But in the larger picture, moderation may be better in treating my disease. Yes, it’s much more aggressive now. Yes, my survival seems to have been shortened by the mutation. Yes, it’s harder to treat. But, there are several, and I mean several as in four to six or so new therapies which are just over the horizon and at least some of these depend on a patient’s functioning immune system to be effective. In the past my chemotherapy regimens have included the use of several toxic medications which have vigorously attacked my disease with a “chemical machete,” clear-cutting my marrow, taking away good cells as well as bad, severely damaging my immunity. The use of these drugs now could jeopardize my ability to use some of the newer therapies which are still in the study phase and just on the verge of being more widely available. Three of these are in pill form and are taken daily, at home, much like the vaunted drug Gleevac, which has shown such remarkable success in treating (but not curing) another form of leukemia known as chronic myelogenous leukemia (CML). And there are studies using gene therapy to train one’s own T-lymphocytes (a topic for another day) to attack and kill the leukemia cells. This therapy has reportedly “cured” two people in a study recently released by the Abramson Cancer Center in Philadelphia, though the follow-up was a short ten months. And if nothing else works, there is a stem cell transplant, which is the ultimate treatment for my form of CLL with the p53 mutation. With the p53 mutation, some docs reportedly give you one course of chemotherapy and if you fail go directly to transplant. The problem is that there is somewhere between a 10% and 25% mortality (death) rate with stem cell transplants. You don’t go into them lightly. But, they are said to give “durable remissions” in patients with the p53 mutation. Notice that the word “cure” wasn’t used. It rarely is.
Anyway, I’ve been through “Phase One” of the Arzerra treatments and the short story is that it has worked well, dropping my white count from 80,000 to about 4,000 (normal) in just eight weekly treatments, with minimal side effects. “Phase Two” starts later this month. I’ll leave the details of all this for the next update, since this has gotten long enough. And I hope to have it to you before another six months goes by.
Dave
I read these words in a USA Today recently, while sitting in a chair in the waiting room of the Leukemia Clinic at M. D. Anderson.
“Have you come to the Red Sea place in life,
Where, in spite of all you can do,
There is no way out, there is no way back,
There is no other way but through?”
---Annie Johnson Flint
www.adventureswithleukemia.blogspot.com
Book 4, Chapter 1, Verse 5
November 2, 2011
I didn’t expect this. I was doing so well. I felt good and was getting along just fine. I mean, I had done all those half-marathons, right? How could I be this sick?
We had a busy spring and early summer. My disease, which had relapsed the previous year, had been advancing faster with my white counts doubling every couple of months or so. I was expecting to have to do more chemotherapy by about mid-summer, so we packed our travel plans into the early part of the summer. We went to Oklahoma City for a marathon (in the rain and cold) in May, went to San Diego for one there in June. We went to a reunion of my Vietnam vet buddies in Tampa in late June, to a family reunion in North Carolina in July, and more. In the midst of all these trips we went to Houston in early July to see my doc there, who is one of the world’s foremost gurus in the management of chronic lymphocytic leukemia.
I was still feeling well; maybe a little more tired than I’d care to admit, but over all, I was doing okay except that my lab tests told another story. My disease was advancing rapidly. I talked things over with my doc, Dr. Michael Keating, and we went over some possible treatments. I say “possible,” because after you’ve been treated for this disease once or twice, there are no standard “best” treatments anymore, just lots of possibilities.
But he wanted to do a few more cytogenetic (chromosome) tests before we started anything, to help guide us to, hopefully, the best of our options. He said I’d hear something about the test results “in a couple of weeks.”
Now, to me, “a couple of weeks” mean exactly fourteen days. When I didn’t hear anything in those fourteen days, I made a series of calls to M. D. Anderson and played phone-tag for a few weeks, never getting any information about my lab tests. I was getting worried.
Meanwhile, a long-scheduled appointment with my local oncologist came up so I saw him and explained how things were going. We also talked over some possible options for treating my disease and then he said he’d call Houston and get the information for me. I was grateful, as I really wanted to hear the results of the cytogenetics.
Later that day I got a call from my local doc. He had heard from Houston. He had news, but the news was just horrible. He talked for a while but all I remember was something like “…blah, blah, blah…p53 mutation…blah, blah…Arzerra…blah, blah…50% chance of it working.”
What this means
When I got sick with this disease, chronic lymphocytic leukemia, almost ten years ago, it was only “one” disease. The doctors and researchers working with it knew that some folks with this disease died in two or three years while some folks lived, without needing treatment, for maybe twenty years or more. They knew that some patients responded well to treatments while others didn’t. They just didn’t know why. But about eight years ago they found that CLL is actually a group of diseases, differentiated by the chromosomes in the leukemia cells and several other protein “markers” exhibited by the disease. There are at least seven or eight major sub-groups of CLL and perhaps more, and survival and resistance to treatment varies greatly among the groups. By looking at the mutations of the chromosomes in your cells physicians can tell how long you’ll likely survive and what treatments might work best for you, and also how aggressive they should be with trying to treat your disease.
A couple of years after I got sick, they tested my chromosomes. They were 46XY, normal male chromosomes, as you’ll no doubt remember from your high school biology course. That was very good, as normal chromosomes were a marker of easier to treat disease and generally longer survival. Curiously, however, there is one mutation called 13q- (13q deletion) which is even better than normal chromosomes in terms of survival. But there are also several possible mutations of the disease that indicate a more aggressive and harder to treat disease. These can be ranked in order of increasing resistance to treatment and subsequently, shorter survival. And since patients with CLL tend to mutate to harder to treat forms of the disease over time, my doc in Houston was retesting my disease to see if I had mutated. And the tests in July at M. D. Anderson now showed that I had the p53 mutation, also called the 17p deletion (17p-), one of the very worst of the several variations.
Details
I’ll include a short description of what this genetic shorthand means for my friend Steve who lives in either Englewood, Colorado, or Centennial, Colorado, or maybe unincorporated Arapahoe County (I don’t remember which for sure), in the Denver suburbs. He likes details. Anyway, normally we all have 46 chromosomes per cell, 22 pairs of “somatic” chromosomes plus our sex chromosomes, the XX for females and XY for the guys. The other 22 pairs are numbered 1 though 22. Also, if you remember looking at pictures of chromosomes in textbooks, they look rather like stretched out X shaped figures, usually arranged with shorter arms at the top and longer arms at the bottom.
(By the way, our chromosomes don’t just stretch out and pose for the pictures that we see in books and magazines; they have to be manipulated with various chemicals to make them look this way. Normally they’re all balled up in a tangled mass in our cells’ nuclei.)
The short arms at the top of the chromosomes are called the “p” arms; the longer ones at the bottom are the “q” arms. If you took a part of the “q” arm off a 21 chromosome, it would be called a deletion and written as 21q-. Sometimes extraneous genetic material gets added onto chromosomes. These are additions, written as 21p+, for example.
The p53 mutation
So, now I have the dreaded p53 mutation, also called the 17p- mutation, the 17p deletion. Over the last few years my disease had changed, which is what it typically does for most patients with CLL. p53 is a gene, the “tumor suppressor gene,” which normally resides on the short, “p” arm of the 17 chromosome. Now it’s not there; in my case; it’s been “deleted” somehow. This is a very important gene which, as its name suggests, suppresses tumor growth and malignancy formation. Now I don’t have it anymore. When you read about the p53 mutation in CLL you see things like, “much more difficult to treat,” and “more aggressive disease” and “average survival of about 13-15 months.” Our friend Larry Love recently died here in Denton. Larry had an extremely rare case of metastatic basal cell skin cancer. Basal cell cancers are generally among most easily treated of all skin cancers yet in Larry’s case, this usually innocuous skin cancer spread throughout his body and despite three years of treatments, he died because the disease could not be controlled. Larry’s skin cancer had the p53 mutation. The p53 mutation is not good news.
Arzerra
This is the drug my doc picked to treat my disease this time around. Now, if you’ve been reading my stuff for any length of time at all, you’ve read about Rituxan, which has been a part of my three different previous chemotherapy regimens. Rituxan (rituximab) is a mouse-based antibody against leukemia cells. It targets a specific protein (called the CD20 receptor) that all CLL cells have. It works extremely well at doing this. The only problem is that being mouse-based (or “murine”), it itself is a foreign protein and humans can form antibodies against these murine antibodies, inactivating them.
Arzerra (ofatumumab) is similar to Rituxan in that it is also an antibody which attacks the CD20 protein receptor. It has been around in Europe for a few years but has only been approved for use in the US for about 18 months. In Europe it is called HuMax, which reflects the interesting fact that it is a humanized antibody against the CD20 site. In theory at least, it should be better for attacking the leukemia cells since humans shouldn’t create antibodies against it. In addition, it binds more tightly and for a longer time to the leukemic cells than does Rituxan, if you believe the manufacturer.
Interestingly, when reading the prescribing information that comes with this drug, the manufacturer states that it will not cure, put into remission or reduce the symptoms of any patient with CLL. This is an amazing thing to put in writing. It must either be something required by the FDA or perhaps it’s just their lawyers lowering expectations. Otherwise, it would be no more than a placebo drug!
I was very disappointed, at first, to be prescribed single-agent therapy with the Arzerra. My disease is now much more aggressive, yet I was being given a drug that would be very unlikely to put me back into remission. Studies of the drug in patients with my mutation showed only about a 50% rate of successful treatment. From the very beginning of my adventure I have wanted to be as aggressive as possible in treating the disease. Here it looked to me as if we weren’t doing as much as we could. I had found, on-line, several studies of Arzerra being used in combination with other drugs with apparent good success in short term studies. I wanted to use lots of drugs. I wanted to kill the leukemia. I want to rid my body of it. That’s always been my goal.
But in the larger picture, moderation may be better in treating my disease. Yes, it’s much more aggressive now. Yes, my survival seems to have been shortened by the mutation. Yes, it’s harder to treat. But, there are several, and I mean several as in four to six or so new therapies which are just over the horizon and at least some of these depend on a patient’s functioning immune system to be effective. In the past my chemotherapy regimens have included the use of several toxic medications which have vigorously attacked my disease with a “chemical machete,” clear-cutting my marrow, taking away good cells as well as bad, severely damaging my immunity. The use of these drugs now could jeopardize my ability to use some of the newer therapies which are still in the study phase and just on the verge of being more widely available. Three of these are in pill form and are taken daily, at home, much like the vaunted drug Gleevac, which has shown such remarkable success in treating (but not curing) another form of leukemia known as chronic myelogenous leukemia (CML). And there are studies using gene therapy to train one’s own T-lymphocytes (a topic for another day) to attack and kill the leukemia cells. This therapy has reportedly “cured” two people in a study recently released by the Abramson Cancer Center in Philadelphia, though the follow-up was a short ten months. And if nothing else works, there is a stem cell transplant, which is the ultimate treatment for my form of CLL with the p53 mutation. With the p53 mutation, some docs reportedly give you one course of chemotherapy and if you fail go directly to transplant. The problem is that there is somewhere between a 10% and 25% mortality (death) rate with stem cell transplants. You don’t go into them lightly. But, they are said to give “durable remissions” in patients with the p53 mutation. Notice that the word “cure” wasn’t used. It rarely is.
Anyway, I’ve been through “Phase One” of the Arzerra treatments and the short story is that it has worked well, dropping my white count from 80,000 to about 4,000 (normal) in just eight weekly treatments, with minimal side effects. “Phase Two” starts later this month. I’ll leave the details of all this for the next update, since this has gotten long enough. And I hope to have it to you before another six months goes by.
Dave
I read these words in a USA Today recently, while sitting in a chair in the waiting room of the Leukemia Clinic at M. D. Anderson.
“Have you come to the Red Sea place in life,
Where, in spite of all you can do,
There is no way out, there is no way back,
There is no other way but through?”
---Annie Johnson Flint
www.adventureswithleukemia.blogspot.com
Sunday, May 29, 2011
It's Back!
Dave’s Great Adventure
Book 4, Chapter 1, Verse 4
May 29, 2011
“It’s back.”
When you have a malignancy of any kind, breast, colon, prostate, or whatever, and you’ve gone through a bunch of treatments with chemotherapy and surgery or radiation and all the other things that go along with these kinds of treatments, it’s a wonderful thing to be told you’re in remission. It makes all the torture and misery of the treatments worthwhile. You start to feel like things are back to normal, that you don’t need to worry about dying too soon or having to go through more treatments. But then, at some point, perhaps quite unexpectedly, you’re told, “It’s back.”
That’s probably one of the most economical ways to give really bad news. A couple of words, eight letters, that tell you the thing you’ve been fearing, that unseen disease in your body, wants to take over again. And wants to take you from everything and everyone you know.
I’ve known from the very beginning, from when I was first diagnosed with leukemia, that it was, and is, incurable. Yet, like every other person with any kind of cancer, I want to believe that I’m going to be the exception to that “incurable” rule and that I’m going to survive, I’m going to outlive this disease. After each of my courses of chemotherapy I’ve been told that I was in complete remission. I focus on the word “complete” and try to translate that into “cured.” I know, intellectually, that I’m not cured, but I want to believe that I am.
After each round of chemotherapy, after I get over the side effects and regain my strength, I start living a fairly normal life. It’s easy to forget that I have an incurable disease lurking in my body. I actually sort of forget about it, or think that it’s just been a bad dream, and that it’s not real. But at some point I get the news…
“It’s back.”
…and Kathy and I look at each other and are fairly roughly thrust back into the reality that I have an incurable, lethal disease. And we know that my future holds more treatments and that with each treatment I undergo, I have fewer and fewer options left for the “next time.”
I’ve had three different courses of chemotherapy in the last nine years. I’m very lucky, actually, that there have been these options for me as this wasn’t the case in the past. And with each course of chemotherapy, each of which was experimental, I’ve been put into a complete remission. And each time I’ve been thrilled with the news. But each time I’ve eventually heard the words, “It’s back.” It took a year the first time, eighteen months the second time.
My third course of chemotherapy was my longest and most intense, at six months long and including four different drugs. A year out from the completion of my chemotherapy I still was in complete remission. I had a bone marrow biopsy done about that time and they couldn’t any trace of the disease even with a “molecular probe.” Now, that was particularly good news as I’ve heard of folks like me who have gone through similar courses of chemotherapy and then been found to have a negative molecular probe, and some of them have been alive and free of disease many years, even a decade later. I thought that would be me, too. Later, my doc even told me that with this finding there were three chances out of four that I’d be in remission for up to ten years!
“It’s back.”
I heard those words again just days after I had been told I might be in remission for up to ten years, in a particularly cruel sequence of events. I suppose I was just that one person in four to whom the statistics were unkind. It has to happen to somebody or there wouldn’t be any odds to try to beat.
My disease actually reappeared over a year ago but I’ve felt so relatively normal during that time that I’ve continued to train with the wonderful folks from The Leukemia and Lymphoma Society’s Team In Training and, since I recovered from my last course of chemotherapy, I’ve completed eight half marathons, even as my disease slowly grew within my body. And soon, within a week, I’ll do my ninth. And then I’ll leave my training schedule behind and start another task and schedule, the schedule that our lives revolve around when I’m undergoing chemotherapy. And that schedule does, in fact, rule our lives.
I don’t know yet what that schedule will be. I have some appointments coming up in June to see my local oncologist and to get some more blood tests, but I won’t know with any certainty what the future holds until we see my doc at M. D. Anderson in Houston. I’ve gotten my appointment with him moved up to early July and that’s when we’ll hear what he thinks we should do. As one of the nation’s preeminent specialists, specifically in my form of leukemia, I have great respect for his opinions.
In the last year or so he has dropped hints about what we might consider doing if/when I relapsed. I believe he’s going to want to treat me with a combination of two new drugs, Revlimid and Hu-Max. (I won’t go into too much detail about these drugs until I know for sure that we’ll actually be using them, even though our friend Steve out in Englewood, Colorado loves technical details) but I will mention that if we use this particular combination, I’ll be taking a pill form of chemotherapy 21 days a month (the Revlimid) in combination with intermittent IV infusions of the Hu-Max, which is an artificial antibody against the leukemia cells. The course of therapy lasts up to forty weeks. Using a pill form of a drug will certainly be convenient, if we end up doing this particular protocol.
But I have to tell you, I’m as worried about the course of my disease and the side effects of the drugs as I have been in a long time. These drugs, and particularly the Revlimid, can induce some particularly nasty side effects. And the incidence of inducing complete remission really isn’t all that high. I’ve seen 9% reported in some early studies after forty weeks of treatment. And the logical question that comes to my mind is, “Well, if I’m not in complete remission after those forty weeks…well…, then what?”
But I’m getting way ahead of this. I tend to be a planner and a worrier and should learn to wait and see what actually happens, but that’s hard for me.
Since I don’t have any more details to pass on at this time I want to begin closing by thanking all of you for being so generous in helping me with my San Diego fund raising drive. I’m not looking for donations any more, as I’m well over my goal, but please take a moment to look again at my fund drive page and see what you guys did. You are all awesome. Thanks so much.
http://pages.teamintraining.org/ntxok/rnr11/deckberg
I have failed to thank each of you individually so far, but each of you WILL hear from me.
I’ll close by passing on a bit of good news. About a year and a half ago, or so, I had an echocardiogram which seemed to show that my heart was failing and that I would soon need open heart surgery to repair my mitral valve. I wondered how that could be, as I was feeling well and, in fact, had recently completed a couple of half marathons. Well, after having follow-up echocardiograms in three months, six months and then again in another six months, well…, everything is described as “stable” and there is no longer any talk of needing surgery any time soon. At least that part is doing well.
I’ll be back if there are any significant changes or after I go to Houston and find that we have a plan. Until then, thank you again for all your help with my fund drive and thanks for helping the researchers who are looking for better treatments for me and so very many people like me. As I’ve told many folks at many different meetings, my only hope of outliving this disease is for some researcher, somewhere, to find a cure in my lifetime.
Bye now,
Dave
www.adventureswithleukemia.blogspot.com
PS: After our armed forces recently “removed” the person responsible for the mass murder of 3,000 of our fellow citizens, I am reminded of the quote, usually attributed to George Orwell, which goes:
“We sleep soundly in our beds because rough men stand ready in the night to visit violence on those who would do us harm."
Please take a moment this Memorial Day to remember our fellow countrymen, these “rough men” (and women, too), the many, many thousands of them, who have died in the service of our country.
Book 4, Chapter 1, Verse 4
May 29, 2011
“It’s back.”
When you have a malignancy of any kind, breast, colon, prostate, or whatever, and you’ve gone through a bunch of treatments with chemotherapy and surgery or radiation and all the other things that go along with these kinds of treatments, it’s a wonderful thing to be told you’re in remission. It makes all the torture and misery of the treatments worthwhile. You start to feel like things are back to normal, that you don’t need to worry about dying too soon or having to go through more treatments. But then, at some point, perhaps quite unexpectedly, you’re told, “It’s back.”
That’s probably one of the most economical ways to give really bad news. A couple of words, eight letters, that tell you the thing you’ve been fearing, that unseen disease in your body, wants to take over again. And wants to take you from everything and everyone you know.
I’ve known from the very beginning, from when I was first diagnosed with leukemia, that it was, and is, incurable. Yet, like every other person with any kind of cancer, I want to believe that I’m going to be the exception to that “incurable” rule and that I’m going to survive, I’m going to outlive this disease. After each of my courses of chemotherapy I’ve been told that I was in complete remission. I focus on the word “complete” and try to translate that into “cured.” I know, intellectually, that I’m not cured, but I want to believe that I am.
After each round of chemotherapy, after I get over the side effects and regain my strength, I start living a fairly normal life. It’s easy to forget that I have an incurable disease lurking in my body. I actually sort of forget about it, or think that it’s just been a bad dream, and that it’s not real. But at some point I get the news…
“It’s back.”
…and Kathy and I look at each other and are fairly roughly thrust back into the reality that I have an incurable, lethal disease. And we know that my future holds more treatments and that with each treatment I undergo, I have fewer and fewer options left for the “next time.”
I’ve had three different courses of chemotherapy in the last nine years. I’m very lucky, actually, that there have been these options for me as this wasn’t the case in the past. And with each course of chemotherapy, each of which was experimental, I’ve been put into a complete remission. And each time I’ve been thrilled with the news. But each time I’ve eventually heard the words, “It’s back.” It took a year the first time, eighteen months the second time.
My third course of chemotherapy was my longest and most intense, at six months long and including four different drugs. A year out from the completion of my chemotherapy I still was in complete remission. I had a bone marrow biopsy done about that time and they couldn’t any trace of the disease even with a “molecular probe.” Now, that was particularly good news as I’ve heard of folks like me who have gone through similar courses of chemotherapy and then been found to have a negative molecular probe, and some of them have been alive and free of disease many years, even a decade later. I thought that would be me, too. Later, my doc even told me that with this finding there were three chances out of four that I’d be in remission for up to ten years!
“It’s back.”
I heard those words again just days after I had been told I might be in remission for up to ten years, in a particularly cruel sequence of events. I suppose I was just that one person in four to whom the statistics were unkind. It has to happen to somebody or there wouldn’t be any odds to try to beat.
My disease actually reappeared over a year ago but I’ve felt so relatively normal during that time that I’ve continued to train with the wonderful folks from The Leukemia and Lymphoma Society’s Team In Training and, since I recovered from my last course of chemotherapy, I’ve completed eight half marathons, even as my disease slowly grew within my body. And soon, within a week, I’ll do my ninth. And then I’ll leave my training schedule behind and start another task and schedule, the schedule that our lives revolve around when I’m undergoing chemotherapy. And that schedule does, in fact, rule our lives.
I don’t know yet what that schedule will be. I have some appointments coming up in June to see my local oncologist and to get some more blood tests, but I won’t know with any certainty what the future holds until we see my doc at M. D. Anderson in Houston. I’ve gotten my appointment with him moved up to early July and that’s when we’ll hear what he thinks we should do. As one of the nation’s preeminent specialists, specifically in my form of leukemia, I have great respect for his opinions.
In the last year or so he has dropped hints about what we might consider doing if/when I relapsed. I believe he’s going to want to treat me with a combination of two new drugs, Revlimid and Hu-Max. (I won’t go into too much detail about these drugs until I know for sure that we’ll actually be using them, even though our friend Steve out in Englewood, Colorado loves technical details) but I will mention that if we use this particular combination, I’ll be taking a pill form of chemotherapy 21 days a month (the Revlimid) in combination with intermittent IV infusions of the Hu-Max, which is an artificial antibody against the leukemia cells. The course of therapy lasts up to forty weeks. Using a pill form of a drug will certainly be convenient, if we end up doing this particular protocol.
But I have to tell you, I’m as worried about the course of my disease and the side effects of the drugs as I have been in a long time. These drugs, and particularly the Revlimid, can induce some particularly nasty side effects. And the incidence of inducing complete remission really isn’t all that high. I’ve seen 9% reported in some early studies after forty weeks of treatment. And the logical question that comes to my mind is, “Well, if I’m not in complete remission after those forty weeks…well…, then what?”
But I’m getting way ahead of this. I tend to be a planner and a worrier and should learn to wait and see what actually happens, but that’s hard for me.
Since I don’t have any more details to pass on at this time I want to begin closing by thanking all of you for being so generous in helping me with my San Diego fund raising drive. I’m not looking for donations any more, as I’m well over my goal, but please take a moment to look again at my fund drive page and see what you guys did. You are all awesome. Thanks so much.
http://pages.teamintraining.org/ntxok/rnr11/deckberg
I have failed to thank each of you individually so far, but each of you WILL hear from me.
I’ll close by passing on a bit of good news. About a year and a half ago, or so, I had an echocardiogram which seemed to show that my heart was failing and that I would soon need open heart surgery to repair my mitral valve. I wondered how that could be, as I was feeling well and, in fact, had recently completed a couple of half marathons. Well, after having follow-up echocardiograms in three months, six months and then again in another six months, well…, everything is described as “stable” and there is no longer any talk of needing surgery any time soon. At least that part is doing well.
I’ll be back if there are any significant changes or after I go to Houston and find that we have a plan. Until then, thank you again for all your help with my fund drive and thanks for helping the researchers who are looking for better treatments for me and so very many people like me. As I’ve told many folks at many different meetings, my only hope of outliving this disease is for some researcher, somewhere, to find a cure in my lifetime.
Bye now,
Dave
www.adventureswithleukemia.blogspot.com
PS: After our armed forces recently “removed” the person responsible for the mass murder of 3,000 of our fellow citizens, I am reminded of the quote, usually attributed to George Orwell, which goes:
“We sleep soundly in our beds because rough men stand ready in the night to visit violence on those who would do us harm."
Please take a moment this Memorial Day to remember our fellow countrymen, these “rough men” (and women, too), the many, many thousands of them, who have died in the service of our country.
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