Live From LRF (Lymphoma Research Foundation) Educational Forum

View from the Brooklyn Promenade

The weather in Brooklyn is wonderful and the view from the nearby Brooklyn Heights Promenade is iconic.

But I am spending most of the daylight hours indoors at the North American Lymphoma Research Foundation Educational Forum at the Marriott.

And I am happy to be here. LRF does strong work in several areas.

This Forum is an example of the kind of high quality education that it offers on lymphoma. For the approximately 500 patients and caregivers attending, the lectures are clear and comprehensive and certainly not simplistic. All the doctors (Rick Furman and Matthew Davids for CLL) are on top of their game and all volunteer their time.

They have excellent free disease specific publications and online webcasts and more.The website is our start, especially helpful if we are new to the diagnosis.

Another strengths of LRF is funding important research. A blue ribbon scientific advisory boards reviews the grant requests.

They offer support in many ways. One example is the buddy service that links us to someone else with the same diagnosis to share war stories.

The new mobile app is a must download for any with lymphoma.

And finally, they are involved in patient advocacy, from what I see, mostly at the government level, where they work with other advocacy organizations such as LLS (The Leukemia and Lymphoma Society).

The hot advocacy issues today I heard being discussed are research funding being affected by the current budget goings-on in congress, compassionate access, and oral parity.

So what actual educational tidbits have I learned? Please understand that this is not a meeting such as iwCLL or ASH where new research results are revealed, but rather where they are pre-digested and handed back to new and experienced patients in manageable bite size packets.

In the CLL breakout session, Dr. Rick Furman made it clear that the importance of many of the new prognostic factors is becoming more or less moot as we enter an era of small molecules because these new drugs are for the most part oblivious to them. They work well for the vast majority of patients.

However, the groundbreaking work by Dr. Rai on CLL staging published in 1975 still is helpful. One strong warning: you must completely ignore the average life expectancies attached to each stage. Pay no attention to the Kaplan-Meyer curves. Those were retrospective in 1975 and bear no relationship to the present reality with improved management and better therapies. We are all living longer.

And for those who are regular readers of my blog, this last item is hardly news: Dr. Furman sees the end of chemotherapy in CLL. I sure like that.

In the general session, Dr. Sonali Smith admitted to the need to revise the lymphoma staging systems to better reflect what we have learned in the last decades. I learned that in some cases disease burden trumps staging.

Dr. Hsi, a pathologist, said that most labs could perform the bulk of the fancier diagnostic tests on a paraffin specimen. There only a few circumstance where there is a need for the better DNA preservation offered by a frozen section.

Still, before any biopsy for possible lymphoma, I would always ask the surgeon to check with the pathologist to be certain the specimen will be properly handled to give you all the results that you need. A dear friend of mine was moving rapidly towards heavy chemo (and possible transplant) for Richter's Transformation (RT) until she got an outside pathology opinion that showed the biopsy from her enlarged node had a viral infection that was mimicking RT. Whew!

In the end, what is more valuable for me than the lectures at the Forum is the networking with old and new friends with CLL, and to their credit, the meeting planners built in enough time to make sure that happens. That's the upside of having cancer: the amazing people I get to meet and the experience and wisdom and and courage they have to share.

So, if you have never been to North American Lymphoma Research Foundation Educational Forum, plan to come, and if you been before, why aren't you here?

More from tomorrow sessions soon. But first I sleep.

Day 2:

I wish I could say there was much new to report, but what I would say is the take-away message is that the role of chemo-immunotherapy (think BR, FCR, FR, PCR and others) is either dying for all of us or most of us.

I could argue that for the small subgroup of patients (mutated with the appropriate cytogenetics) where it can be predicted in advance of starting therapy that FCR offers a very high chance of a durable remission (10 years or longer) and the hint of a cure (if you are MRD negative 14 years out, are you cured?), that for those of us and only those of us fitting into that tiny cohort, there might be a diminished but important role for chemo-immunotherapy (CIT). I personally would seriously consider the choice of 6 months and done of CIT if it really offered me a 90+% chance at being cured or at a minimum a 10 year remission.

My friend Wayne (WWW) points out there is also an age sweet spot for this therapy: too old and we can't tolerate the suppression of the bone marrow, too young and the risk of secondary cancers, especially MDS (myelodysplastic syndrome) is too high.

Others says just forget the chemo. Use one TKI such as ibrutinib or idelalisib or ABT-199 as long as you can, and if you develop resistance, switch to the next one coming down the pipeline.

Or maybe add a mAb or IMID to the TKI or combine two TKIs and go for the knock out punch.

Hard to argue with that vision of a chemo free future.

The doctors are split on how to proceed, but there are all shifting their stances in response to the  growing data supporting the new meds (TKIs and mAbs)

The world is changing fast. Stay tuned in.

The danger of getting advice from a non CLL expert

My search spiders, primed for anything CLLish, pointed me to a blog by a retired medical oncologist who shares with us his frustration with the limited therapies available for the many CLL patients he treated in the past and his excitement about finding an article reviewing new therapies.


I was pleased to read that an experienced seasoned general oncologist was turning his attention to our rare disease and was anxious to learn his insights.


I was soon disappointed.


He points out the realities when he practiced.


When I was in practice we didn’t have any very effective drugs. We had drugs that could eliminate most of the leukemia cells, but never cure the disease. Eventually, the leukemia would come back in spite of continuing treatment. So when I saw this article, I assumed that there were new treatments and drugs to offer these patients, because I had seen preliminary reports suggesting breakthroughs. Wrong! Yes many new drugs have been developed, but none are particularly effective. The only one that seems to be useful is a drug called Rituximab, which is an antibody directed against a molecule on the CLL surface. But even this drug saved only a few more people when it was added to standard treatment, treatment that is not much different than what I used. And in the key study where this was discovered, most of the patients were much younger than average.


 Later he concludes with this wet blanket for any fire we patients might have for the new therapies.


But for most patients, who are older and have active disease, a disappointment! No breakthroughs like the one for people with chronic myelocytic leukemia (see my article on Kareem and CML) where we have found drugs that are life-saving. Sorry.


What has he been reading? 


This is what happens when you have doctors who are not heavily involved in treating our disease. They may miss when the winds shift.  They are out of touch with the prevailing zeitgeist. 


They have been known to put their faith in gold standard across the board, whether appropriate or not. They too often rely on stale data, and they don't see the coming changes. Their care might be appropriate, compassionate, well meaning and competent, but it is not cutting edge. It is not the best that the present state of knowledge has to offer.


This oncologist blogger to his credit was making an effort, knows about the new prognostic markers, and warns us appropriately that none of the new therapies has yet been proven to extend life. He understands the disease, but doesn't see the import of the coming new therapies because he is not immersed in the research and patient care of CLL patients. He is waiting for the proof for the trials that show the new drugs will add years to our lives. 


That is a long wait, longer than some of have.


Here is what I wrote the doctor:


Contrary to your take, there has never been a more promising time for patients with CLL. Low toxicity  sea change therapies such as Ibrutinib, GS-1101 and other kinase inhibitors are entering phase III trials after extraordinary results in phase I and II trials. Lenilimamide, HDMP, ofatumumab, alemtuzumab, and bendamustine already ofter patients new alternatives for disease control and long symptom free remissions.  While I agree a trial that shows an advantage over the "gold standard" of FCR in survival is what we all want, it is unrealistic and unfair to ask patients to assume that all these game changing therapies will ultimately fail. I for one, like you am waiting for the proof, but I am very encouraged by the early data and like many patients with cancer, must make decisions with imperfect knowledge.


For a nice overview of the research on the new small molecules, please take a look at Blood June 19:
The B-cell receptor signaling pathway as a therapeutic target in CLL
Jennifer A. Woyach, Amy J. Johnson and John C. Byrd


Thanks


Brian Koffman MD -http://bkoffman.blogspot.com/


That is a great article that summarizes much of the recent research.  I recommend it


Truth is that the other blogger and I are both right. 


He is correct when he says that nothing is proven yet. CLL remains incurable for the most part. The best new therapies are just entering Phase III trials and that is a far cry from proving that will keep us alive a minute longer than placebo, let alone FCR.


But I am right too. Patients who were at the end of their therapeutic rope are seeing their lives extended. Patients too old or too sick or too refractory are being routinely salvaged with amazing consistency and minimal toxicity.


This is more than anecdotes. The reported data is getting stronger and stronger. The response rates and progression free survival numbers are to use a most non-medical term,  wonderful.


Could it all crash and burn in the phase III trial? Could every new drug and therapy in trial turn out to a loser? Of course that could happen. But that is not what I and many of my CLL friends and by the way, the smart money on Wall Street is betting. 


I think we got some winners here.


And I am not talking drugs or stocks or careers, but us patients. We are the winners if my vision of the future comes to pass. We will prove my colleague blogger wrong in his disappointment. And I think he will celebrate with us.


One final caveat. This well meaning clearly bright and thoughtful oncologist is out of the CLL loop. Make sure you doctor isn't also. That is why I beg you to get an opinion from a CLL maven. Picking the right team of doctors could save your life.

Four Year Transplant Anniversary: A Request for your Help With CLL Research on Ibrutinib and More to Control and Cure CLL

I received this important email from John Byrd, my doctor at OSU, and one of the most innovative and patient friendly researchers in CLL in general and ibrutinib in particular. He is asking for your support in his fundraising efforts though Pelotonia.


Dr. Byrd is looking for ways to save lives without the risks and miseries of an allogeneic hematopoietic stem cell transplant or maybe even the use of the more toxic old school chemotherapy. 


In another email he said: The new trial that opened with Ibrutinib (Kami Maddocks PI) is being supported entirely by a 100,000 dollar grant from last years Pelotonia.  


He also wrote that the money raised is supporting the following studies that would not be happening without Pelotonia


1.  Post-doctoral fellow working on understanding role of autophagy in drug resistance in CLL
2.  PhD student working on an entirely new kinase inhibitor target for CLL 
3.  An idea grant from another lab (with us) looking at ATF3 as an immunosuppressive stromal factor in CLL


Four years ago today I had my transplant on Canada Day. It failed but I am still here.  Maybe it was a good thing that I never engrafted? I was spared the potential horrors of GVHD, but on the other hand maybe I would have been "cured" by now if it had taken. I will never know, but I do wonder.


Would I have made the same choice today with all the new options opening up?  The answer is probably not, but the data to help with that decision is far from being conclusive. We need to know more. It is so early in the research.


I am in the process of composing a post on the role of transplant in this nascent era of the new small molecules for CLL. It is an increasingly common question posed by patients and doctors alike.


If you can, please help Dr. Byrd and others in their research to get the answer to this and so many other cancer questions. Please consider clicking on the link to donate.


Thanks.


Please see Dr. Byrd's email below.


Dear Brian,

I am wrting to you because your help is needed.  I have decided to ride in Pelotonia and would greatly appreciate you to consider supporting me.  

Pelotonia is a grassroots bike tour with one goal: to end cancer. More than 10,000 supporters are expected to be a part of Pelotonia 12 on August 10-12, 2012. The ride will span two days and will cover as many as 180 miles. In its first three years, Pelotonia has attracted over 8,300 riders from 38 states, over 2,800 volunteers, hundreds of thousands of donors and raised $25.4 million for cancer research. In 2011 alone, a record $13.1 million was raised. Because operational expenses are covered by Pelotonia funding partners, 100% of every dollar raised is donated directly to life-saving cancer research at The Ohio State University Comprehensive Cancer Center-James Cancer Hospital and Solove Research Institute. I am writing to ask you to help me raise funds for this incredible event. Large or small, every donation makes a difference.

What will your donation be used for?  The money derived from this race supports research to identify new drugs and also to perform clinical trials in cancer.  I am a leukemia doctor focused on curing a disease called chronic lymphocytic leukemia (CLL).  In the laboratory, Pelotonia is supporting idea grants to bring novel ideas that might translate into new therapies some day.  Additionally, it is supporting students and post-doctoral fellows to work on new antibodies (different from rituximab) and small molecules that could some day be therapies.  Addtionally, one of the trials that Pelotonia is supporting with money rasied from last year is with ibrutinib, a highly active bruton tyrosine kinase inhibitor that is very active in CLL.   We have seen this agent help many CLL patients and are delighted to have the support of Pelotonia to allow us how to use this medication better and along the way help patients with this disease.  Without Pelotonia, the trial with ibrutinib coul
d not happen.  I see Pelotonia as a way for us to move quicker to converting cancer to a chronic disease or one that is cured.   This is something I am passionate about supporting.  I hope you will contribute and remember no amount is too small.

When you follow the link below, you will find my personal rider profile and a simple and secure way to make any size donation you wish.

Think of this as a donation not to me, or Pelotonia, but directly to The OSUCCC-James to fund cancer research. Please consider supporting my effort and this great cause. My rider profile can be found at the following link: http://www.mypelotonia.org/riders_profile.jsp?MemberID=1227

Thanks for the support!

John

A Personal Note: My Good News on Ibrutinib

Let me get personal here.

While I believe with all my soul that we are all in this together and I celebrate every move forward as exemplified by the amazing 100% overall response rate of the first cohort in my clinical trials presented in the interim reports on ibrutinib (PCI-32765) at the annual 2012 ASCO (American Society of Clinical Oncology), let me now share my personal good news.

My "n" is one, not statistically significant, but personally critical.

After only one cycle of four weeks of ibrutinib, my CT scan of my thorax, abdomen and pelvis showed that all my lymph nodes had significantly shrunk.

Yahoo.

Some details: Here is what happened to my biggest honkin' mesenteric node left in my belly. It is now measuring 2.5 x 5.8 cm compared to 3.2 x 8.9 cm when I rolled into Ohio to start the trial, a dramatic reduction of about 50% in area and certainly more in volume.

Other nodes have shrunk even more, and they have shrunk everywhere - the pelvis, the gut, near the liver and the blood vessels, and in the axillae (armpits).

Now it is possible that ofatumumab may have played some small role in reducing my tumor burden as my baseline CT scan was done before I started my infusions of that antibody, but if I make the logical but unproven assumption that what was happening to my palpable nodes was being mimicked by what was happening inside, then ibrutinib did the lion's share of the clearing out the cancer. My neck and axillary nodes changed little on the OFA.

But add the ibrutinib, and one formerly huge internal nodes that was 10.1 cm is now a petite 3.3 cm.

And all this in only four weeks, with almost no side effects and nearly normal labs and improved energy.

I harbor no illusions. A persistent 5.8 cm lymph node is still a nasty thing, but I also have no reason to doubt that it and its buddies will soon to be shadows of their former bulky selves. My palpable nodes are certainly continuing to get smaller and smaller.

What I know now for sure is that I have had a profound and deep response, despite my two evil complex clones, despite my failed transplant, despite my new small batch of 17p deleted cancer cells, despite the immaturity of my clone being unmutated and the chattiness of it being CD38 and ZAP 70 positive, and despite just about every bad marker.

This is the best news.

How deep and durable my response will be is my next challenge, but for now there is much to quietly celebrate and good cause to be optimistic.

So I under react, stay both calm and hopeful and move forward.

It has been wonderful to be home for a few weeks with my family and friends and patients and cat and the Pacific Ocean.

This weekend, I am off to Houston to lecture on CLL, transplants and anemia. The weekend after is Dallas, then back to OSU for more lab and to pick up 28 more days of ibrutinib.

Life is sweet.

Dangerously tired but all is well with me and my ibrutinib

Just like you shouldn't text when driving or call your boss when drinking, I shouldn't blog on three hours sleep.

My trip home stated with a 3AM wake up to get to the Cloumbus airport around 4:20AM for my 5:50 AM flight to Chicago as the first leg of my trip home.

Yesterday I got good news. Went for a beautiful walk in Inniswood Garden to celebrate. Pictures to follow.

More good news.

Hgb is back up to a low normal 13.8. No downward trend.

My reticulocytes are just fine at 1.8 (some unproven but possible concerns that BTK inhibition might effect retics which are baby red cells and therefore eventually lead to anemia).

My WBC climbed from 9.8 to 12.1, which was mostly from my ALC going from 2.9 to 4.1. This are very small changes, but could represent more shifting of cancer cells from my nodes to the blood stream. One of the pleasant ironies of ibrutinib treatment is that, at lead in the early phases of treatment, no matter what your lymphocytes do, go, up down or stay stable, it is possible and logical to have a positive interpretation. Nice that is virtually impossible to get any bad news.

Eosinophils are high again following a weekly saw tooth pattern. Absolute count is 1.3 which would normally get my attention.  Seeing it is not trending up, I am not worrying.

Platelets are still super at well over 400,000, partially reflecting the reality that  a spleen less, so they enjoy a longer life span with much less filtering

Neuts are 5. That's nice.

No change in my nodes on exam, but seeing as most are gone or have shrunken in just three weeks of therapy to less than 1x 1 cm, it is hard to detect meaningful change.

I still some gut issues- heartburn, cramps, mild nausea. Nothing dramatic.

Next week, after flying across the country yet again, I get will two CT scans, more extensive lab work, my next 28 days' worth of inbrutinib and the associated diary, and  IV ofatumumab, all on the same day.

From there, the next day I fly to Orlando to lecture before I get to rest at home.

Also, as my follow-up visit is on day 30 and I only get 28 days of pills, I will have been of my magic pills for two full days, something I am not looking forward to.

More on this subject in another post. This may not be an insignificant issue.

New Clinical Trial for Ibrutinib (PCI-32765): Exclusion Criteria and More

The phase 3 pivotal trial to get ibrutinib (PCI-32765) approved by the FDA is gearing up.

A Phase 3 Study of Ibrutinib Versus Ofatumumab in Patients With Relapsed or Refractory Chronic Lymphocytic Leukemia (RESONATE™)

This is big news.

Let me get personal first.

My prior failed transplant would have knocked me out of any chance at the drug in this and maybe any other trials until approval.

Please read the exclusion criteria for this critical study listed below.

Exclusion Criteria:

• Known CNS lymphoma or leukemia.
• No documentation of cytogenetic and/or FISH results reflecting 17p del status in patient records prior to first dose of study drug.
• Any history of Richter's transformation or prolymphocytic leukemia.
• Uncontrolled Autoimmune Hemolytic Anemia (AIHA) or idiopathic thrombocytopenia purpura (ITP).
• Prior exposure to ofatumumab or to ibrutinib.
• Prior autologous/allogeneic transplant
• History of prior malignancy, with the exception of certain skin cancers and malignancies treated with curative intent and with no evidence of active disease for more than 3 years.
• Serologic status reflecting active hepatitis B or C infection.
• Unable to swallow capsules or disease significantly affecting gastrointestinal function.
• Uncontrolled active systemic fungal, bacterial, viral, or other infection.
• History of stroke or intracranial hemorrhage within 6 months prior to the first dose of study drug.
• Requires anticoagulation with warfarin.

Exclusion Criteria: Prior autologous/allogeneic transplant

I would be out of luck and running low on options, but instead I am so fortunate because I am here at OSU, four weeks away from my first dose of ibrutinib.

I saw that one coming, and so jumped at this opportunity here in Columbus. One of my more prescient moves.

Transplants cuts off many options, especially clinical trials, so if ibrutinib doesn't work for me, then my path is narrowed and obscured.

Exclusion Criteria: Prior exposure to ofatumumab or to ibrutinib.

Please note that any prior ofatumumab also excludes you.

Exclusion Criteria: No documentation of cytogenetic and/or FISH results reflecting 17p del status in patient records prior to first dose of study drug.

The 17p deletion exclusion seems to be a double negative.

The way I am reading it, it seems to say that unless you are 17p deleted, you CAN NOT enter the trial.

If so, that was not a turn I expected. I thought Pharmacyclics (PCYC) would go after the much larger population (market) of all new and old patients with CLL not just those with "Relapsed or Refractory Chronic Lymphocytic Leukemia".

It certainly suggests a great degree of confidence in the drug to handle the nastiest 17p del cohort. The company is betting are betting the farm on that wildest and most dangerous horse and the one most in need of taming. And maybe secretly hoping for the same wide off label use that is seen with rituximab helping to generating seven billion US dollars in annual sales.

I hear the results out the NIH trial on 17p del patients, though very preliminary, are very promising on that tough group.

Exclusion Criteria:

• History of stroke or intracranial hemorrhage within 6 months prior to the first dose of study drug.
• Requires anticoagulation with warfarin.

The exclusion of those on coumadin and with bleeding in the brain is because of the history of brain hemorrhages (some fatal) that occurred in earlier phase trials. Frankly I am surprised it is not all blood thinners and anyone with a bleeding tendency similar to the exclusion in the MDACC trial with rituximab.

This important phase 3 trial NCT01578707 should be much larger to get the more statistically significant result to gain FDA approval, so there will be many more opportunities to get the drug. Take a look at the trial link, move fast if you qualify and need therapy, and watch for other similar trials if you are interested in what I believe is the best of the new bunch of small molecules.

PCI-32765 or Ibrutininb and why the great responses in CLL

I almost never just have a strictly medical post, but I thought this was such a clear and concise explanation of how ibrutinib (I better get used to PCI-32765's new name) and GS-1101 (another new name, this time for for CAL-101) that it needed to be shared by those considering one of these new agents for treating their CLL.

Dr. Rai has more experience than anyone in treating CLL and he has no time or tolerance for bogus claims or hype, so I deeply respect his opinion.

That doesn't stop me from questioning his argument in favor of combination therapy.

First. it is too early to know what is best. Dr. Wiestner at the NIH is looking at a single agent therapy and others including Dr Byrd at OSU and Dr. O'Brien at MDACC at combinations.

Second, I worry about powerful chemo selecting out the most refractory clone.

And third and most importantly, I believe that these new small molecules portent a sea change in how we treat CLL with the depth of remission not being the measure of success, but rather the duration of the response.

Let me know what you think.

The original article in Blood can be found here:BLOOD article on ibrutinib.

Thanks to Blood and HemOnc Today.

It is an exciting time in the world of CLL.

9 0Posted March 25, 2012

BTK inhibitor linked to CLL regression

de Rooij MF. Blood. 2012;doi:10.1182/blood-2011-11-390989.

The Bruton’s tyrosine kinase inhibitor PCI-32765 demonstrated inhibitive properties in primary chronic

lymphocytic leukemia, according to recent results.

The researchers based their hypothesis on the premise that small molecule drugs that target the B-cell antigen receptor (BCR) signalosome demonstrate efficacy in B-cell non-Hodgkin’s lymphoma. One such drug, the Bruton’s tyrosine kinase (BTK) inhibitor PCI-32765, also demonstrates a rapid and sustained reduction of lymphadenopathy accompanied by transient lymphocytosis in CLL. This reduction is reversible upon temporary drug deprivation, according to the researchers↓ The researchers hypothesized that the clinical response induced by PCI-32765 reflects impaired integrin- mediated adhesion and/or migration.

In the current study, it is demonstrated that the drug strongly inhibits BCR-controlled signaling and integrin alpha-4 beta-1–mediated adhesion to fibronectin and vascular cell adhesion molecule-1 of lymphoma cell lines and primary CLL cells, according to the results.

It also has been shown that the drug is an inhibitor to CXCL12-, CXCL13- and CCL19-induced signaling, adhesion and migration of primary CLL cells.

“Our data indicate that inhibition of BTK by PCI-32765 overcomes BCR- and chemokine-controlled integrin-mediated retention and homing of the malignant B cells in their growth- and survival-supporting lymph node and bone marrow microenvironment, resulting in the clinically evident CLL regression,” the researchers concluded.

PERSPECTIVE

Two important new drugs have attracted the attention of colleagues all over the world who treat patients with CLL. Both PCI-32765 and GS-1101 demonstrated an extraordinary level of activity when each was used as a single agent in previously treated CLL patients who had bulky lymphadenopathy, and had relapsed or refractory disease. PCI-32765 is an inhibitor of BTK, while GS-1101 is an inhibitor of PI-3 kinase delta isoform. These kinases are considered to be highly active inhibitors of BCR signalling and chemokine networks. The paper by de Rooij and colleagues provides clear and convincing evidence as to how PCI-32765 actually works. These researchers,by meticulous and disciplined work, demonstrate that this drug acts on the micro- environment of lymph nodes and bone marrow where the leukemic cells can live safely and proliferate, an important mechanism for maintenance and progression of the disease. When exposed to PCI-32765, the leukemic cells can no longer hide in their safe harbors of lymph nodes and bone marrow, and they also can no longer continue to proliferate. Being deprived of adhesion-capabilities, these leukemic cells must, therefore, migrate into the circulating blood. That explains why the bulky lymph nodes shrink in size dramatically and rapidly when the patient starts taking this oral medication. This paper also makes it clear as to why the numbers of lymphocytes in the circulating blood increase equally dramatically,at least initially, while the lymph nodes are shrinking. Finally, this paper explains why it will be important to move from using PCI-32765 as a single agent and toward combining it with a monoclonal antibody or chemotherapy, if a lasting and good-quality remission is the desired objective. The leukemic cells pushed out from the lymph nodes and other tissues are eminently killable by cytocidal agents while they are in the blood circulation, where they no longer have the protective chemokines that allowed them to resist while they resided in the lymph nodes. In my view, this is an important contribution that explains the mechanism of action of the exciting and promising new drugs in the treatment of CLL.

– Kanti Rai, MD

HemOnc Today Editorial Board member Disclosure: Dr. Rai reports no relevant financial disclosures.

Copyright © 2012 HemOnc Today. All rights reserved.