Patients need to be patient (pun intended!)
Late last year I published a positively rosy article titled “CAL-101: Dawn of a new era“. Fortunately the subtitle “At last, a “Gleevec” of our own?” had a question mark at the end of it, giving me a little bit of cover. ASCO 2011 has an important abstract on how CAL-101 performed in an early Phase-I trial with previously treated CLL patients. I thought you would want to see it. The abstract is below, followed by my two cents. And an editorial on the importance of patients being patient in their assessment of new drugs.
2011 ASCO Annual Meeting
J Clin Oncol 29: 2011 (suppl; abstract no. 6631)
Phase I study of CAL-101, an isoform-selective inhibitor of phosphatidylinositol 3‑kinase P110d, in patients with previously treated chronic lymphocytic leukemia.
Author(s): S. E. Coutre, J. C. Byrd, R. R. Furman, J. R. Brown, D. M. Benson, N. D. Wagner-Johnston, I. W. Flinn, B. S. Kahl, S. E. F. Spurgeon, B. J. Lannutti, H. K. W. Hsu, R. Ulrich, S. Peterman, L. Holes, L. L. Miller, A. S. Yu; Stanford Cancer Center, Stanford, CA; The Ohio State University Comprehensive Cancer Center and Arthur G. James Cancer Hospital and Solove Research Institute, Columbus, OH; Weill Cornell Medical College, New York, NY; Dana-Farber Cancer Institute, Boston, MA; The Ohio State University, Columbus, OH; Washington University School of Medicine, St. Louis, MO; Sarah Cannon Research Institute and Tennessee Oncology, Nashville, TN; University of Wisconsin, Madison, WI; Oregon Health & Science University, Portland, OR; Calistoga Pharmaceuticals, Seattle, WA
Background: The class I phosphatidylinositol 3-kinases (PI3Ks) regulate cellular functions relevant to oncogenesis. Expression of the PI3K p110δ isoform (PI3Kδ) is restricted to cells of hematopoietic origin. CAL-101 is an isoform-selective inhibitor of PI3Kδ that induces apoptosis of chronic lymphocytic leukemia (CLL) cells. Methods: This phase I study evaluated CAL-101 in patients with previously treated hematologic cancers. CAL-101 was administered orally 1 or 2 times per day (QD or BID) continuously in 28-day cycles, until disease progression or unacceptable toxicity. Efficacy analyses were based on standard criteria. Results: At data cutoff, the study had enrolled 54 patients with CLL. Patient characteristics included: median [range] age of 62 [37‑82] years; 82% males; 72% with refractory disease, 81% with bulky disease, 36% with del(17p), and a median [range] of prior therapies of 5 [2‑15]. CAL-101 dose levels were 50 mg, 100 mg, 150 mg, 200 mg, and 350 mg BID; and 300 mg QD. The median [range] of CAL‑101 treatment cycles was 8 [1-19]. Grade ≥3 adverse events included pneumonia (24%), neutropenia (24%), thrombocytopenia (7%), neutropenic fever (7%), anemia (6%) and ALT/AST increase (6%). CAL‑101 reduced lymphadenopathy by ≥50% in 80% of patients. A transient increase of >50% from baseline in peripheral absolute lymphocyte counts occurred in 58% of patients. The overall intention-to-treat response rate by IWCLL 2008 criteria was 26%. Medians for duration of response and progression-free survival had not been reached (>11 months), with 46% of patients continuing on treatment. CAL-101 reduced constitutive overexpression of phospho‑AKT in patient CLL cells and normalized plasma concentrations of CCL3, CCL4, and CXCL13. PK analyses showed minimal increases in plasma Cmax and AUC at doses >150 mg BID. Accrual is ongoing and updated data will be presented. Conclusions: CAL-101, an oral PI3Kδ-selective inhibitor, shows acceptable safety and promising clinical activity in heavily pretreated patients with CLL. Dose‑response assessments support the 150 mg BID dose for future single-agent and combination chemo/immunotherapy studies.
The author list is very impressive, as is also the list of high pedigree research institutions that participated in this study. While you are about it, you should also click on the link to the financial disclosures , it makes for interesting background. Along the same lines, I hereby disclose I received no money or any other favors from Calistoga Pharmaceuticals and neither I nor my family own a single stock in the company :)
Since this abstract is the only document to go by, we have access to only this limited amount of information. Down the road, I hope we will have more detailed journal articles describing this study and its results.
- 54 previously treated CLL patients were enrolled in this Phase-I study. Patients took CAL-101 (orally taken pill) 1 or 2 times a day for 28 day cycles. Treatment continued until the patient’s disease progressed or there was unacceptable toxicity.
- No question, this was a tough crowd of patients. Median age was 62 (OK, that is not too far gone). But 72% had refractory disease (remember, “refractory” is far worse than merely “relapsed”). 81% had bulky lymph nodes, which makes it harder for many drugs to work (Campath is ruled out in such cases, for example). 36% of the patients had the high risk 17p deletion (FISH test). On average, patients had been around the block more than a couple of times. As a matter of fact, they had been in therapy 5 times before.
- Since this was a Phase-I trial, one of the most important objectives was finding the right dose for the drug. In the patients that took the pill only one time per day, the dosage was 300mg. Patients who took the pill twice daily ranged over the dosage of 50mg – 350mg.
- Once again, we are given the adverse effects only in terms of “greater than or equal to grade 3”. In other words, pretty heavy duty stuff. You need to know these grade levels. Grade 1 is sissy stuff. Grade 2 will get you a little sympathy from your friends and family. Grade 3 and 4 will require medical advice / intervention most likely. Grade 5 means you won’t be needing your doctors any more since you would no longer be living.
- Just about a quarter of the folks had pneumonia, same number had neutropenia. So, if you thought CAL-101 is without infection risk, you (and me) were a little off the mark.
- Continuing the list, risk of decreased platelets was ‘only’ 7%; neutropenic fever and anemia were also in the same ballpark. I was pleased to see liver toxicity (measured by ALT/AST) was only 6%. I would have expected higher level of liver toxicity.
- Now for the results: Bulky nodes were reduced by 50% or more in 80% of the patients. This is actually pretty impressive stuff, especially since these were pretty heavily pre-treated patients and bulky nodes are a lot harder to treat than simply reducing white blood counts. (I wonder how they measured amount of reduction – was it merely by feel or did they do CT scans? Hand measurement is notoriously prone to observer / researcher bias).
- There was the expected rise in WBC increase in about half the patients. Expected, since it is now well understood all of those CLL cells getting flushed out of the lymph nodes have to go some where, and the likely place is out into open blood circulation.
- The overall response rate was 26%. Remember, this include complete and partial responses. I must confess I was hoping this would be higher.
- This abstract made no mention about bone marrow status. That really bugs me. There is some information floating out there that CAL-101 does not do a good job of clearing CLL infiltrated bone marrow. Reassurances to the contrary, I continue to think this is an important issue. A heavily infiltrated bone marrow cannot do its job of producing all the different blood cell lines. Infiltrative Rai stage – IV is pretty heavy duty stuff.
- The study has not been going on long enough to get a good fix on remission length. But 46% of the patients are still taking the drug (remember, they were taken off the drug only if their disease progressed or there was too many adverse effects). So, if I am reading the tea leaves right, 54 % of the patients went off the study because they progressed, had too many adverse effects – within an average of 11 months since start of the study?
- They sorted out the drug dosage bit. In future we are going to be seeing 150mg twice daily as the standard dosing.
Editorial
It is hard to be patient when you are facing life or death issues. It is all too easy to wish for rapid turnround in drug approval process, cut a few corners in scientific or ethical considerations, if it means we will have access to the latest sexy drug candidate. Wishful thinking gets to all of us. Me included, my last article on the subject of CAL-101 had the very rosy title of “Dawn of a new era”. But clinical trial process takes a long time. Especially when we are dealing with long fuse cancers such as CLL. How can we tell whether or not a new drug is safe, whether it will actually do any good, prolong remissions and overall life, unless we do the hard work of clinical testing in well conducted clinical trials? How can we judge the validity of results until they have been subjected to the scrutiny of peer review? Statistically valid results do not guarantee that an individual patient will get exactly the same result – but they sure as hell give him a fighting chance of not buying a pig in the poke!
It is all too easy to look for scapegoats (the FDA is a popular target). Be very careful what you wish for folks. Next time you are tempted to lynch the FDA drug approval committees, be sure you understand they stand between you and careless research – if not downright self-serving and / or fraudulent results. Before you get suckered into rabble rousing on internet chat rooms, be sure you take a second look at the potential conflicts of interest. Everyone has agendas. I will be the first one to point out, patient advocates are no exception either – all of which means you need to be your own best advocate!
My initial response to this early phase clinical trial results was dismay. I hoped for much better results. A second and third careful reading took away some of the initial angst. This glass is definitely not full, but in my layperson opinion it is not completely empty either. As the title of this article indicates, I call this a half-full glass. And it is important not to throw the baby out with the bathwater.
These were extremely advanced cases, most of the patients had very poor prognosis going into the trial. CAL-101 did not perform a miracle, but it did get a fair amount of responses. Will it work better in a less tough crowd, patients with less advanced disease? Obviously. Most drugs work better when they are not fighting an uphill battle. Will CAL-101 do better if coupled with other drugs that work well in tandem with it? I hope so – and I think there is good reason to hope for that. When results are published from more late stage trials, I will be sure to review them for you. You can then judge for yourself whether the glass is half full or half empty.
Postscript
Dr. Susan O’Brien of M. D. Anderson is a well known CLL expert. She gave a recent interview on the subject of kinase inhibitors such as CAL-101 and PCI-32765. You can read her comment by clicking on this link.
28 comments on "CAL-101 Update: half full glass"
Chaya,
I recall Dr. Furman of Cornell Weill explaining the low 26% response rate in terms of the criteria for an overall response. Since lymphocytosis occurred in many cases, they did not qualify as responses, though in fact, their disease burden is shifting out to the blood.
That does not explain where the 54% went, or the adverse effects, and I’d like more details to be forthcoming on those.
Thanks for following this one closely.
Heléne
I wonder if the PCI 32765 results will be any rosier, or maybe ABT263. Hope springs eternal.
On the glass is half full side, I think it’s really important to remember that these were refractory patients, and from reading message boards, it seems that some of them are still doing well on CAL 101.
As always, a million thanks for all that you do.
Jenn
Elmer:
You got it just right. My concern too is why 54% of the patients were off study after a median follow up of 11 months. Surely the initial spurt in WBC counts (as CLL cells migrated from the lymph nodes to open blood circulation) would have had a chance to get resolved by then?
Rather than lymphcytosis lingering on for so long as the logical explanation for the low response rate, I think this 26% number is a reasonable reflection of the heavily pre-treated nature of the patients, as well as their high risk prognostics.
50% reduction in bulky lymph nodes is good, but that still leaves quite a lot of CLL cells that can grow back and fill the newly vacated eco-niches. This would be particularly true in cases where the cancer has reached an aggressive and proliferative stage. Perhaps future studies will show that the right time to use this and other kinase inhibitors is in early stage disease, especially when the bone marrow is not yet heavily infiltrated.
Thank you for the information. Always nice to have someone like you translate and assess the latest research for us.
Thanks for the financial disclosure link.
Who would want to go to a doctor for treatment when the doctor is gambling his money in the stock market on the outcome of your life?
A faculty position at a major institution in a 6 figure job.
There was a document released about a school in Texas which released everyone’s salary and 200-350,000 was not unusual for tenured professors with experience. A doctor has to make more than the average history professor. Do they really need the money that badly?
No matter how much integrity someone has, how can this factor not be in the back of their mind when decided what drug treatment to put someone on?
I think they have cracked down on doctors owning pharmacies but this practice of speculating on drugs directly in someone’s practice also needs to go, imo.
CLL is a progressive, non curable, and highly individualistic disease. These researchers decided to take on a very tough crowd (72% refractory from many rounds of treatment and over a third with the 17p deletion). I would think that patients who had been through 4 or 5 rounds of treatments with the likes of FCR and were refractory would probably have high incidents of pneumonia unrelated to Cal-101. I would have liked to seen two groupings with a second group of previously untreated patients in need of starting treatment. There is nothing in these results that should dim the high hopes of those in W&W that we may have a much better alternative than FCR in the pipeline. The jury is still out on the marrow effects. I am still very optimistic about Cal-101 and PCI-23765- another valuable arrow in the quiver. As usual- time will tell.
The folks in this trial are being given Cal-101 only or in combo with other stuff?
Chaya
Very interesting update. Thank you for continuing to follow-up on the progress of this new trial.
It’s greatly appreciated!
Azzy said–A faculty position at a major institution in a 6 figure job.
There was a document released about a school in Texas which released everyone’s salary and 200-350,000 was not unusual for tenured professors with experience. A doctor has to make more than the average history professor. Do they really need the money that badly?
I am best friend’s with two “Super” Docs in Texas. One is a highly qualified surgeon and still—the tenured professor’s salary is way higher than these doctors salaries. Most clinics like MD Anderson have a cap on salary for their physicians.
I am disappointed in the fact that the pharma companies backing Cal-101 and PCI-23765 are not requiring any bone marrow biopsies. When Tom was a trial rat for FCR, a bone marrow biopsy was taken every three months for at least a year. Now that he is on PCI-23765, he only has a CTScan every three months. NO BMB IS ASKED FOR! I wonder if it is because “they” know it is not clearing the marrow of CLL.
Thank you Chaya for your input on both these trials. I think they would both work better when the next trials synergize Rituximab or Revlimid or another drug with the inhibitors. I have heard rumors that Revlimid will be used with the PCI-23765 trial.
Jenny Lou
tsvieps:
This was a single agent study – clearly identified as such in both the abstract and my analysis.
Mschwalm:
Yes, these were heavily pre-treated and high risk patients. Nevertheless, 24% grade 3 or higher risk of neutropenia and 24% pneumonia is daunting. As also the fact that “only” 46% are still on study after a median follow-up of just 11 months. This is not quite a home run.
Azzy:
I thought it was important to note the financial disclosures. But once again, please remember not to throw the baby out with the bathwater. Let us not paint everyone with ulterior motives, that does none of our patients any good.
Jenny Lou:
I have no doubt there are going to be many more clinical trials with combinations of these kinase inhibitors with other drugs. This is early stage stuff, something that needs to get done so we understand the lay of the land. I too am disappointed that they are not doing before and after bone marrow biopsies. I hate to think it is because something “fishy” is going on.
I am in one of the follow-up trials to the Phase 1 study you reviewed: CAL-101 and Rituxan. I’m currently in the middle of the sixth 28-day cycle and I can tell you that CT scans are used to assess the nodes. In fact, the schedule is one screening scan and five more over 12 cycles. I assume the single-arm study also used CT scans. I also had a BMB before the trial and have another scheduled for next month. If anything, the study has too many CT scans.
About these kinase inhibitors being the Gleevec for CLL, that would be great, of course. But we shouldn’t expect that we’ll be able to take this drug for years and that will be the end of it. An article about Gleevec in Smithsonian magazine opened my eyes to the reality that patients taking Gleevec, although it extended their lives and is truly a miracle drug, typically became resistant and had to change to different drugs as each of those new drugs stopped working. The first patient to take Gleevec, who was literally on her deathbed, is now on her fifth medication in ten years.
Thanks for the info Jlou, was not aware of any salary caps. I don’t think I was inferring anyone made decisions based on their stock portfolio, only that it would he hard to get out of the back of their mind. A needless temptation to resist as it were. I think having doctors who have gone out of their way to make sure the appearance is that there are no doubts that they have the best interest of their patient at heart would do the mmost for patients. Many professions now go by the rule that there should be no appearance of conflict of interest, regardless of the actual conflict of interest. This does not seem like an unreasonable thing for medicine.
I’ve spent a lot of search time trying to assess the importance of bone marrow status for CLL, From what I can determine on PubMed, there hasn’t been a single study that looked at bone marrow status as an independent predictor of CLL health status in the last ten years. Staging has come to be relied on as a far more reliable indicator of one’s well-being and future prospects,
Perhaps it’s time to listen to Rick Furman, who puts far more faith in hemoglobin and platelets as a comprehensive and unbiased metric of bone marrow status. He notes that BM biopsies are subject to significant sampling error based on the conditions of the exact locale chosen for the biopsy,
I know this kicks a favored hobbyhorse in the tush, but my best efforts to find any contemporary studies talking about the independent value of bone marrow infiltration have come up completely empty handed,
mschaeffer:
You are welcome to believe what ever you want, and I certainly do not want to get into an argument with you. But here is some information that might be useful to our members.
Bone marrow biopsy as a way of diagnosing CLL is certainly not necessary and has rightly fallen out of favor in the last 5-10 years. That was not the point here, initial diagnosis of people.
But if you read the very definitive and latest guidelines, bone marrow biopsy is still needed for defining remission status – especially if it looks like the patient is likely to get a full CR.
Here is the title of the “Blood” 2008 article; this is the latest word on how to diagnose, treat and assess response in CLL patients:
“Guidelines for the diagnosis and treatment of chronic lymphocytic leukemia: a report from the International Workshop on Chronic Lymphocytic Leukemia updating the National Cancer Institute–Working Group 1996 guidelines”.
And you can read the full text of the article for free, here is the link:
http://bloodjournal.hematologylibrary.org/content/111/12/5446.long
You might want to look up this section:
“5.1.6. For patients in clinical trials (Table 3), a marrow aspirate and biopsy should be performed at least 2 months after the last treatment and if clinical and laboratory results listed in sections 5.1.1 through 5.1.5 demonstrate that a CR has been achieved.”
With these clearly spelled out guidelines, I am at a loss why end-of-therapy BMBs are not being done – unless the researchers feel there are no candidates with a likely full CR? That seems unlikely, especially in the trials where the patients are chemo naive and therefore the responses are likely to be more robust.
There is a new movement afoot to use less invasive four color flow cytometry to detect residual disease, rather than do BMBs. Frankly, I would be in full support of such a position and we reviewed the technology in an earlier article “How much chemo is too much?” Jenny Lou, perhaps you can tell us. Are the CAL-101 clinical trials using four color flow cytometry to stage patients at the end of a certain number of cycles?
As for hobby horses, I do not have too many of them and in any case quite willing to sacrifice them when facts prove me wrong. Here is a case where I would love to be proved wrong, that normalized blood counts also mean good bone marrow clearance, low tumor burden overall and therefore long duration remissions when patients go off the drug.
My first reaction to reading this abstract was also mild disappointment. I’m not in the habit of reading abstracts and, after reflecting a bit, it seemed to me that all they provide are the bare statistics—-without the opportunity for editorial comment by the authors. I suspect that ASCO limits both the length and content.
Some of the explanations that make me feel better about these trial results have already been offered in this discussion thread. I’m sure that we will learn a great deal more during and after the ASCO meeting in June.
In the meantime, let me offer these two unscientific observations.
I am treated at Cornell Weill. The clinic staff, both doctors and nurses who are closest to the patients in the trials, are uniformly enthusiastic in their praise for both CAL-101 and PCI-32765 (my stuff).
In addition, Gilead must have known about these trial results before buying Calistoga recently for $600 million.
(my hand slipped and I posted my comments before finishing these final thoughts)
It seems obvious that Gilead liked what they saw before shelling out for the right to continue to develop and eventually market CAL-101.
I’m looking forward to ASCO. I expect that many of the questions raised by the abstract will then be answered and the previous excitement about CAL-101 will continue to be justified.
Best wishes to us all—–David
once again chaya – you follow up for us……thank you –I too was hoping for so much more…….but baby steps are in order.
thanks for keeping us in the loop!!
Darlene
re BMB,
We had a similar discussion before when someone asked about them, but I am not sure about the link.
I think there is also some confusion about the terms.
http://www.mayoclinic.com/health/bone-marrow-biopsy/MY00305
If you are looking for residual CLL cells, that is usually done by PCR and would require only the aspirate of the liquid. If you are looking for packed marrow, or lack of it, you need a bone chip, both biopsy and aspirate are called bone marrow exam, a term I have never heard used in CLL, although I have seen slides of the bone chips. Of course they are very subjective. What I have seen called a packed marrow for CLL looks nothing like a packed marrow for other cancers where the entire marrow is jammed with cells. As I noted earlier, there is a large amount of skill for this procedure and many people in CLL draw a large amount of blood in what should be a bloodless sample. Obviously a contaminated bm aspirate with blood will throw off the conclusion and any prognostic value.
To turn this into a prognostic marker has practical difficulties since it is assumed no one has extensive marrow involvement at first. It could be used to diagnose time from relapse but again strict criteria for what is a person with packed marrow would be needed.
It would be nice to know the genes differences involved in the people who wound up with packed marrow, since they could be given targeted strategy but that would mean a long prospective study.
Well Chaya, I still think your Xmas present about the ‘Cal 101 and the dawn of a new era’ was one of the best I’ve ever had.It gave me hope, something in very short supply when you’re incurable. These new KID drugs seem miraculous compared to the dark ages of chemo blasting out our already depleted bodies. We do seem to be making good progress with leukemia, firstly with FCR and now the new KIDs on the block. Twenty five years ago when my sister had myloid type, she had twenty times the dosage of chemo that we give now and it nearly killed her; it seems we are getting there slowly but surely.
MLMG-Mollie
Thanks Chaya, So much to learn and you make it learnable to me.
Bone marrow biopsy: Hmmm! I have had two, one in Dec. 2010 and one in April 2011. My second one followed the procedure outlined by Chaya…two months after the cessation of FCR. Result: blood, lymphs, & spleen are completely clear including my lungs which have been a source of controversey between my SCCA (Hutch to you who do not live in Seattle area)hematologist, my hematologist at MDA, and my pulmonologist. Guess what, the lungs cleared after HDM+R in 2008 and cleared again after two rounds of FCR. I was pulled off FCR by the guy in MDA because my neuts (nearly disappeared–0.08) and platelets dropped “unexpectedly” four weeks after round two. Go figure, right? Wrong!!! The bone marrow infusion at SCCA showed that depending on which test you examined, I still have 44 to 50% of my marrow clogged with CLL. Of course that is better than 95% as it was in December 2010 when it was 5% and I didn’t have enough sense know I was on the edge of falling off this world.
Anyone who criticizes BMB needs to look at the continual contradictory information available on all segments of CLL whether is peripheral blood, spleen, lymph nodes, or bone marrow. Until something better comes along, I vote for BMB both before and after treatment drug(s). By the way wasn’t BMB a source of discussion after Chaya’s first piece on CAL-101?
For what it is worth, you can get a BMB that is painless. I found two great nurses at SCCA who do painless biopsies and that is without the secondary drug used to knock you partially out as I travel alone to Seattle.
Barry
How exactly do you get a painless BMB? I’d really like to know because the one I had nearly made me pass out it was so painful and subsequently I refused to have one post FC chemo treatment.
I’m with Jenny Lou. I hope we are both wrong, but it does not compute for me that they “pass” on the best proof of marrow clearing (a BMB). I’m slated for CAL-101 next … probably in the Fall. I’m in the “too much chemo” club, including a transplant in ’05. Believe it or not, I have had a dozen (maybe even 13) BMBs. They ranged from excruciating to “not so bad”, but never the painless good fortune Barry has had. Mind you, I am not complaining. My feet are still on the ground, and CAL-101 is on the horizon.
For the umpteenth time, thankyou Chaya for the amazing way you help us.
Chaya,
Have you gotten any sense that AVs (Adverse Events) or AV severity could be linked to the percent of signal blocking achieved by any given kinase inhibitor? Is too much of a good thing being considered in the goal of early trials to determine Maximum Tolerated Dosage?
It would seem that the treatment objectives using Chemo, where it is argued that the maximum dose tolerated by the patient is the proper way to achieve best result, should be giving way to a more nuanced approach, representing kinase inhibitors, that could include a more measured and patient specific dosing to achieve a goal of disease management.
Because of the signaling pathway and kinase placement within that context, would the maximum inhibition of signaling be less effective or even counter productive to the maintenance of the proper balance of signaling, given that kinase signaling is needed?
Regarding Barry’s claim of painless BMB: Please enlighten us! My sole experience was at OSU where I was caught off guard by a painless ASPIRATION (colorless fluid) withdrawl followed by a MARROW sampling that elicited an involuntary scream. Depending on what is being looked for can an aspiration be sufficient?
My understanding of the procedure is that the pain is due to the nerve being hit by the needle and since the location of the nerve cannot be seen the pain is less due to technician competency than luck of draw.
WWW
Re ~ “My understanding of the procedure is that the pain is due to the nerve being hit by the needle and since the location of the nerve cannot be seen the pain is less due to technician competency than luck of draw.”
Although Chaya has noted previously that discussion of BMB reactions is not a fruitful topic, I wanted to reference my experience at NIH relevant to this nerve hit. As soon as I experienced the running flame of a nerve prick, Janet immediately made an adjustment and continued with a pain free process.
I’d be happy to be lucky but training and experience are more reliable.
I have had bone marrow aspiration and bone biopsy on three different occasions at MD Anderson as part of a clinical trial and was favorably impressed by the competency of two of the technicians because they knew exactly where to insert the needles to avoid pain (the two needles were of different sizes) but I was less pleased by another technician who managed to locate the most painful spot. Because I believed that some technicians were more skilled than others I tried to get the technician I knew from previous experience was good even if it meant having to wait a longer time for my turn. Dr Keating found the results of the procedures to be very useful.
Makoto, what was the technician’s name who performed the more agreeable BMB on you? A first name along with his surname initial would be okay.
I’m probably going to start on the CAL-101 + Rituxan trial at MD Anderson after seeing Keating on 6-29-11.
But as to the published trial on the heavily refractory group with single CAL-101, what was the point of that? I suppose they wanted to see if the TKI would work wonders on it’s own. But my understanding is that the TKI is useful mainly to draw the CLL cells out of the nodes, spleen, and hopefully the bone marrow into the blood circulation. Then the Rituxan kills them. Using the single agent by itself seems to me comparable to giving soldiers rubber bullets to fight a war…
Art
I found out I have CLL some 15 years ago. I have had chemo five times and was at the end of the road. About a year ago my doctor said “I have done all I can do”! My sisters had flunked the blood match test and our regional center had done five stem cell transplant on CLL, one is still alive. My wife, a FNP found a cal- 101 study in Nashville, TN and they took me on. It is now a year later, counts are all “normal” play nine holes of golf about everyday. (also walk) Glass half full, no glass is really full! I don’t know what the future will bring but so far sooooooo good!
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