Use of CME (Continuing Medical Education) to impact self-reported changes in the evaluation and management of anaemia in geriatric patients: An important topic for those of us with CLL (chronic lymphocytic leukemia)

Honestly, most of my fellow family doctors (FP) know very little hematology. This may be even more true of other primary care providers.

The ABFM board exams for family doctors dedicated a whopping 1% of all the questions to hematology- that is for everything from a simple iron deficiency anemia to a life threatening acute leukemia. Not much incentive to become expert.

As one of the few FP who lives and breathe heme with a deep and abiding personal stake in making sure that all things blood related are done right, and also as doctor with a long background in teaching, in fact a masters of science degree in Medical Education (all my initials are MDCM FCFP, DABFP, MS Ed), this publication on teaching my colleagues about the importance of anemia in the elderly and all the work that lead up to it definitely was a topic in my wheelhouse.

I was lucky to be involved in all ages of this effort: helped with the content development and served as faculty for all the live presentations to thousands of primary care providers across the country and worked on the very cool mobile app: Anemia Algorithm. Click here for the iPhone and here for the Android downloads (>15,000 total downloads). Finally I co-authored what culimated in the actual peer reviewed publication. 

The take away message of all our educational effort is that anemia (or if you prefer the British: anaemia) is not a normal part of aging, shouldn't be ignored and is often related to bone marrow issues that can be helped by a hematologist. 

Sadly, MDS (myelodysplastic syndrome) is too often missed by my fellow doctors. MDS are a group of bone marrow disorders in which the bone marrow is dysfunctional, cancerous, and does not produce adequate healthy blood cells resulting in either anemia or infections or bleeding problems or in more difficult cases,  dangerous combination of all three, depending on what hematopoietic stem cell line or lines are effected. This is an increasingly real and common concern for us CLL patients as we live longer, especially those of us who have had chemotherapy. Past history of chemotherapy is a long recognized risk factor for developing MDS. Please take a listen to this ASH 2012 prior post on CLL and MDS from one of my co-authors, Dr. David Steensma who is a recognized world expert on MDS and geriatric anemia. My other co-authors are Jill Hays and Kathy Farmer with whom I worked at Primary Care Network on CME, and Betsy Dennison who besides doing CME and patient education, works with the CLL Society. I am lucky to be part of such a fine team of researchers and educators.

We wanted to measure if we made a difference through continuing medical education in patients' lives, and looks like we did. That is the subject of our publication.

Subsequently, I have stepped away from much of what I do in non-CLL related medical education to be able to volunteer more of my time to the nonprofit CLL Society, but I wanted to share some of the past work that I have done to educate my fellow doctors over the past several years. I am very proud of these educational endeavors and they clearly inform all that I do on the blog and even more so now on our new website, CLLSociety.org. The new website is dedicated to educational efforts that move the bar higher by first surveying and assessing what is needed in the CLL community, teaching to those needs and following up to see if we made impact.

As a doctor, a patient and an educator, I and the rest of the CLL Society team try to reach beyond journalism to education, support, research, and advocacy, not just posting pleasant videos that report good news, but digging to point out the good and bad that might have serious treatment implications for us CLL patients. We have an vision: smart patients get smart care.

CLL Support Group on July 3, 2013 at 4 PM at the Moore Cancer Center

Please join me tomorrow at UCSD at 4 PM on the 2nd floor of the Moore Cancer Center in the "Commons" for my talk to the CLL support group based on my experience as a doctor turned patient dealing with cancer.

I plan to start with a brief overview of CLL, discussing in general terms diagnosis, lab tests, prognostic factors, symptoms, complications, management, and how treatment is changing. The last half of my talk will be about my personal experiences as a patient ending with my participation in OSU clinical trial with ibrutinib.

It will feature video clips from my interviews with Drs Kipps, Wiestner, Byrd and Pagel at past ASH meetings.

After my 45 minutes, we all have a chance to meet and exchange stories and information.

Hope you can make it.

ASH 2012: Dr. David P Steensma: Myelodysplastic Syndrome with a Focus on Secondary MDS in CLL

Dr. David Steensma is a world leader in not only basic laboratory and clinical research on MDS, but also in examining the impact that anemia has on the life of older patients.

MDS or myelodysplastic syndrome is bone marrow failure and in a minority cases, turns into an acute leukemia.

It is not an uncommon complication of CLL, both, as Dr. Steensma explains, secondary to the genetic and epigenetic changes inherent in the disease itself, and to the treatments, especially the alkylating agents that damage the DNA. In CLL, these included chlorambucil (Leukeran), cyclophosphamide (Cytoxan or the C in FCR), and bendamustine (Treanda).

This is a strong argument for younger patients to avoid those drugs known to damage the bone marrow, but Dr. Steensma offers some more subtle analysis and advice.

We also discuss the radiation risk of MDS from all those CT scans we get in clinical trials.

A good friend of mine is now more than two years out post transplant at MDACC for his CLL/MDS combo one-two knockout punch and he is doing great with no molecular evidence of either disease (MRD negative). And very little graft versus disease.  You can read his story at this link.

This is my last video interview from ASH 2012, but ASCO is just around the corner with more news and interviews.

Dr. Steensma clarifies and explains the risk of MDS in simple terms.

Einstein is quoted as saying: "Make things as simple as possible, but not simpler."

Dr. Steensma does exactly that.

ASH 2012: Dr. Adrian Wiestner: Final Thoughts

The thoughtful Dr. Wiestner of the NIH has some provocative things to say in this brief 2 minute wrap up of our interview.

He says that there may be a significant role for chemotherapy in the future for some carefully selected CLL patients.

He reminds us that these new drugs should force us to re-examine our bedrock views about cancer cocktails. They should force us to revisit all our traditional approaches.

That is a hard thing to do, but a good thing. Doctors are by nature conservative and slow to change.

But there is a sea change coming and Dr. Wiestner suggests that this is a time to really consider what  old baggage can be tossed and what we might need on this voyage.

IMPORTANT: Dr. Wiestner's trial at the NHLBI still has openings for treatment naive 17p del patients. Check out http://www.clinicaltrials.gov/ct2/show/NCT01500733?term=CLL+17p+Ibrutinib&recr=Recruiting&rank=2 . This is a great opportunity at the NIH for those who qualify and I understand a number of fellow Canadians have already enrolled.

Soon I will share his updated data on this research.

Right now, here is the second part of the ASH 2012 interview:



I still have a few surprises from ASH 2012, before I start posting from ASCO 2013 later this month.

I am happy to share that my good friend and fellow CLL survivor and patient advocate, Andrew Schorr of Patient Power and I will be combining forces to offer up several interviews on CLL and other blood and solid cancer from ASCO in Chicago.

I am looking forward to working with Andrew and his professional and pro-patient team.

I have so much I want to share here: more on non-chemo approaches, important discussions on the place of cross-overs in clinical trials, new data from the AACR meeting, what we can learn from the death and autopsy of those who didn't make it, new trials starting up and old trials closing down.

So much to share.

On a personal note, May 7th marked my one year anniversary of my taking ibrutinib. I still remember my disbelief that my nodes seemed to be shrinking in those first few days, but they were. And still are. a year later, albeit, in a less dramatic fashion.

So much has happened in this last year. My mission here and elsewhere is push that we patients can get the best possible care, and that involves more research, great doctors, and wise and brave patients.

We have all those and we sure have moved the bar forward in the last year!

ASH 2012: Dr. Adrian Wiestner of the NIH (NHLBI) on his Research Findings with Ibrutinib and Reflections on the Changing Therapy for CLL

Even though the Annual Meeting of the American Society of Clinical Oncologists or ASCO is only a month away, there is still much valuable information to share from the ASH 2012 Annual Meeting six months ago and there is no one better than Dr. Adrian Wiestner from the NIH (NHLBI) to teach us.

At the upcoming ASCO meeting, there will undoubtedly be fresh reports that improve our understanding of the underlying biology and treatment of chronic lymphocytic leukemia (CLL), but let us pause to remember just how quickly the treatment landscape is changing by taking some parting glances at the data from ASH 2012.

Let me explain what I understand to be the main differences between ASCO and ASH, two giant cancer conferences vying to attract the best groundbreaking research papers and the oncology crowds that follow them.

I have been attending the annual meetings of the American Society of Hematology (ASH) for many years. Approximately 15,000 hematologists from around the world meet every December in major American cities offering a convention center big enough to handle the crowds and interesting enough diversions for the docs and their families. Last year it convened in Atlanta; this year we’ll converge on the Big Easy.

ASH emphasizes an exhausting array of exciting basic laboratory research, in addition to the clinical trial data and many practical “how to treat” symposia.

This upcoming conference will be my first ASCO meeting.

ASCO, as the name suggests, is more clinical in its orientation and much bigger. Gimongous! At twice the size of ASH, the 30,000 attendees annually trek to Chicago where the McCormick Place Convention Center has room for them all. Wear comfortable shoes because there will be a lot of walking. Plan your days carefully and pick a track on breast cancer or brain tumors and be prepared to run from room to room.

My chief interest of course remains my personal torch, CLL; but I also plan to expand my reporting on other B-cell lymphomas specifically, and hematologic cancers in general, with some important diversions to cover the latest on a few common solid tumors.

What I don’t yet know is how much will be revealed at the ASCO meeting about the emerging basic lab science related to CLL, especially the importance of clonal evolution and the critical role of the microenvironment.

What I do anticipate is more mature clinical trial data on ibrutinib (PCI-32765), idelalisib (CAL-101), ABT-199, and GA-101 and also a host of preliminary studies on other TKIs (tyrosine kinase inhibitors or small molecules, usually oral meds, that block pro-survival pathways in cancer) and the new mAbs (monoclonal antibodies trying to improve on rituximab) that are in early development.

Concerning the leading TKIs, here are my questions:

What is the durability of the response? 

What have we learned about the significance of the almost universal finding of a low level of residual disease with these new TKIs?

What do we know about the longer term adverse event profiles, including the risk of Richter’s Transformation, secondary cancers, immune function, and infections?

Maybe most importantly, what have we have learned from the few CLLers who have relapsed? Who are they? What are the risk factors? Is there anything we can do to improve the already good odds?

Concerning the newer dugs and the mAbs, I want to hear which pathways offer us the best promise of a lengthy trouble-free survival.

I posed some of these same questions last December at ASH 2012 and there is no one better to teach us than the thoughtful Dr. Adrian Wiestner from the NIH.

His deep, inventive, commercial free, and government-sponsored research includes a focus on non-chemo approaches to CLL.

Ibrutinib specifically, and kinase inhibitors in general, all induce dramatic responses in CLL with a very favorable adverse event profile. That is great news for all with CLL, but especially those with difficult to treat disease, such as those of us with 17p del or refractory disease.

In the first part of my ASH 2012 interview, Dr. Wiestner discusses some of what is known and what questions he is hoping to answer. You get a sense of why he is so exited about these new lines of therapy.

And he correctly predicted the rapid enrollment in the phase III RESONATE trials comparing ofatumumab and ibrutinib. It just closed accrual with its 350 subjects, every one of whom deserves our gratitude.

Enjoy Dr. Wiestner.

On a personal note, I remain with my mild iron deficient anemia. Maybe that explains my increased fatigue. The rest of my lab remains super. I am off to OSU today for yet more lab, more ibrutinib, and radiotherapy also known as CT scans. Only kidding, but CTs every 3 months is excessive!

The treat on this trip besides the Mark Rothko exhibit at the Art Museum in Columbus and seeing old friends and smelling the spring flowers at the Metro Parks, is that I get to tour Dr. Byrd’s lab and the new cancer hospital under construction (again sensible shoes and this time I will need a hard hat), meet some other CLLers, and best of all, have a chance to break bread with Drs. Byrd and Flynn.

More soon from Dr. Wiestner from ASH 2012 and prep for ASCO 2013.

ASH 2012: Dr. Richard Furman Discusses What is Known and What Isn't About the New Treatments in Trials

In the final part of Dr. Furman's interview from ASH 2012, the doctor who had the most early experience with GS-1101 (idelasilib) and ibrutinib discusses the still limited experience of disease progression with these new small molecules. He reminds of the real risks of bone marrow damage (MDS) and transformation to a more aggressive cancer (Richter's) and offers an interesting hypothesis on why Richter's might be found more often with these treatments.

He reviews the open pivotal for idelasilb (GS1101) and the associated crossovers, plus the trial for ibrutinib versus ofatumumab.

But there are other trials out there too that he didn't mention, especially for patients in special categories, such as 17p deletion or age  > 65.

So always remember to check what clinical trials might be a fit for you at http://clinicaltrials.gov when you are considering treatment. Don't count on your doctor to know all the latest. See my prior post on clinical trials.

Dr. Furman candidly outlines what is known and not known about how these drugs work.

What I really like is the strategy he outlines of using these drugs one after another as stepping stones to a normal life expectancy.



More to come from ASH 2012.

ASH 2012: Dr. Rick Furman Discussed the Very Early Experiences with Idelalisib and Ibrutinib

This video is a real treat as it shows us the recent history of the small molecules that are changing our future.

And the narrator, Dr. Richard Furman, the head of the CLL and Waldenstrom's Macroglobulinemia program at Weill Medical College was not only there at the beginning, he was the investigator for these phase 1 trials for ibrutinib and idelalisib.

He tells of the broken promises of a prior generation of small molecules. He reminds of the bravery of the volunteers who entered the unknown world of these new drugs with little more than hope that these pills would be different than all the rest that preceded them. He points out how the amazing changes that lead to the record fast accrual for the follow-up phase 2 trials. He explains why the climbing lymphocyte count was not a big concern and how it is so different than the rising counts encountered with the tumor flare seen with lenalidomide.

So much has changed in the last few years. What a brave new world we have entered. A place chock full of both hope and unknowns.

This was filmed at ASH 2012 in December.



I have nearly caught up on all my other non CLL medical writing so I can soon turn my attention to more on non-chemo answers for CLL, but this interview should help those looking more than my musical interludes when they tune in on my CLL adventure.

Part 2 with Dr. Furman to follow, then a long interview with my friend, Dr. Adrian Wiestner.

And I will be going to ASCO in May in Chicago though at this point it is uncertain whether I will be  bringing my video staff.

ASH 2012: Dr. Wierda and Practical Advice on CAR-T Trials

In part two and final part of my interview from ASH 2012 with Dr. Wierda from MD Anderson (please  see part one first to get oriented) talks about some of the practical issues, upcoming trials, and possible role of CAR-T in conjunction with the new TKIs (tryosine kinase inhibitors).

In effect, Dr. Wierda is painting a picture where a small molecule such as ibrutinib or idelalisib or ABT-199 or AVL-292 or others in the pipeline is being used to reduce the amount of disease (cytoreduction) and then adding CAR-T therapy instead of the riskier allogeneic transplant to get rid of the nagging residual disease that seems to be left by all these drugs, and with that two step chemo-free process  offering the real possibility of a cure for our CLL.

As he stated, this are still many active area of research. Here's some issues that are near and dear to me.

Why the small molecules seem to move so slowly at ridding the body of all traces of disease- maybe we are just not waiting long enough or maybe it doesn't matter? It doesn't seem to matter in many patients with CML treated with imatinib (Gleevec). Will it be the same with CLL?

Can CAR-T therapy replace allo-transplants and become a practical, affordable path to a cure? A one-two knock out punch?

What about the rare relapses in CAR-T therapy with the cancerous clonal evolving to express no CD-19 and thus are no longer targets for the the engineered T-cells?

What are the bridges to these new therapies while we are waiting for answers?

Let's here a surprisingly practical discussion with one of the doctors who is not only discussing but creating this new future.



Dr. Wierda had to run off after this segment, so there is no part 3.

But Drs. Furman and Wiestner still have important things to teach us from interviews at ASH 2012 that I will be posting soon.

ASH 2012: Dr. Bill Wierda on CAR-T Therapies and "Off the Shelf" T-Cells

Dr. Bill Wierda out of MD Anderson Cancer Center (MDACC) is doing important cutting edge immunological research in CLL and looking to improve and make CAR-T therapy a safer and more generic treatment option.

In the first part of my interview from ASH 2012, he explains how he is moving forward in engineering T- cells to target the CLL clone and spare the normal B-cells.

These are early days, but there is surely a vision of an exciting future that is becoming clearer and brighter. Think of these souped-up T-cells doing the work of an allogeneic transplant without all the associated risks. Imagine them seeking and destroying our cancer cells and passing harmlessly by our normal cells.

Dr. Wierda does not minimize the risks or the work left to be done, but the journey has begun. There have been startling successes at U. of Penn and MDACC and UCSD and collaborating on finding better targets to attack and quicker and cheaper ways to engineer these killing machines.

Take a look at my recent post with Dr. Kipps on ROR1 to set the stage.

This work is particularly important because since it was recorded, it has been revealed that some patients with CAR-T directed against CD19 are relapsing because the clone is losing its CD19. Clever nasty cancer.

Poor patients now not only have an aggressive CLL relapsing, they also have no B cells and next to none antibodies, probably forever.

More to come soon.

Exciting and promising and challenging times.

ASH 2012: Dr. Tom Kipps ROR1

In this short final segment from my ASH 2012 interview, Dr. Kipps explains an exciting new target for CLL, ROR1 that seems to almost exclusively exist on cancer cells, making it an extremely attractive target for a vaccine, a monoclonal antibody, or CAR-T therapy.



Please excuse the bursts of static.

Soon I will be ASH 2012 interviews with Drs. Wierda on CAR-T,  Dr. Furman on his experience in the early trials with the TKIs, and an overview with Dr. Wiestner.

Pretty exciting stuff.

ASH 2012: Dr. Tom Kipps on Genetics, Epigenetics, and Targeted Therapy

In the third of a four part interview with my CLL doctor, Dr. Tom Kipps out of UCSD, we hear him present a vision of the future of "personalized" cancer therapy in general and CLL in particular.

But he also tells us what targeted therapies are available right now in clinical trials near you.

In CLL, it is less about the genetic code and more about the epigenetics. This crucial and relatively recent understanding has been critical in advancing therapies because the pinpoint DNA damage seen in CML such as the telltale fused Philadelphia chromosome are frustratingly less of a glaring target in CLL. However, when the researchers instead started identifying the overly activated pathways in our clonal B cells, the progress sped up in decoding and quickly thereafter, controlling our disease. Dr. Kipps walks you through the difference in these approaches.

Dr. Sharman talks about this insight in one of my prior post, and here Dr. Kipps makes it all easy to understand. He also explains combination therapies, the importance of the new and old generations mAbs (monoclonal antibodies) including 1st generation rituximab, 2nd generation ofatuzamab, and the promise of the powerful 3rd generation GA-101 or another mouthful of a name, obinutuzumab, all directed at CD20, re-use of some drugs already approved for other cancers, and CAR-T therapy

Eleven minuted well spent. Dr. Kipps breaks it all down into bite size pieces.

Learn and enjoy:



Part Four with Dr. Kipps will be coming soon and I still have Drs. Wiestner and Furman in the video vault. ASH 2012 was an amazing meeting, jam-packed with hope and good news for those of us with CLL.

Personal notes:

I am still waiting for my final bone marrow biopsy report from OSU done Feb 5, 2013. FISH and cytogenetics should be back by now, and I hate the suspense.

Back home from studying hematology for hematologists at the 17th Annual International Congress on Hematologic Malignancies – Focus on Leukemias, Lymphomas, and Myeloma in Manhattan and the MDACC hematology board reviews, so I can be more fluent in speaking about the buzz around small molecules such as ibrutinib, ABT-199 and idelalisib in treating other B-cell lymphomas in particular and blood cancers in general.

I will also return to posting more on the personal and human aspects of dealing with an incurable cancer, but for right now, my priority is to get all the remaining ASH 2012 videos online over the next few weeks.

Next weekend, I am off to Washington DC to lecture to the National Sleep Foundation on "The Sleepy Patient". Then I am home for several weeks in a row. Yeah!

In the spring and fall, I will be flying all over the place again teaching other doctors about anemia (MDS or myelodysplastic syndrome that can be a challenging late complication of CLL and some of the chemotherapy used to treat it), gout and thyroid disease. I will be posting my ASH 2012 interviews with Dr. Steensma on MDS here soon.

For any health care providers reading this blog, and to anyone else interested, for another few weeks until March 6, 2013, at Primary Issues, an online medical journal, you can receive ACCME accredited CME on the recognition and early lab testing of CLL or just learn from my article and interviews with Drs. Wiestner and Kipps done at ASH 2011. That San Diego meeting 14 months ago is where I made the fateful decision to enroll in the clinical trial NCT01217749 at OSU that has served me so well.

My love is teaching and my special love is teaching hematology and making sure that the patients and their providers are teamed together to offer the best possible care for each individual case. That's what I want to do more and more.

I am hoping to find some funding do more of these interviews and news coverage for patients and healthcare providers alike, to expand beyond the big ASH meeting to ASCO and IWCLL and more. Next up will be ASCO at the end of May, where I bet there will be important updates on ibrutinib, idelalisib, ABT-199, obinutuzumab and others.

ASH 2012: Dr. Tom Kipps Explains BCR, Chemokines, and the Power of Blocker Drugs

This is part two of my ASH 2012 interview where my doctor, Dr. Kipps out of UCSD, makes the importance of BCR and chemokines to the B cells understandable. Even a vegan like me can understand his Thanksgiving dinner analogy. He too talks about the debt of gratitude owed to all the patients who enroll in the clinical trials.



More to come soon.

On a personal note, I am home a day early from five days in Manhattan at a hematology conference where my family doctor brain was crammed full of new malignant hematology facts and figures so that I can talk about more than CLL to the experts that I am privileged to meet. I was, for obvious reasons, the only family doctor there, and had to check "other" on my registration form as there were not expected any PCPs to show up. If you newbies to CLL think the acronyms for CLL are bad, hematologist are the perpetual masters of an expanding array of coded alphanumeric soups. I was constantly multi-tasking as I was learning the new material and scouring the web at the same time to decode the heme shorthand for all their therapies.

I did take time off to have some gourmet vegan and raw vegan meals at Pure Food and Wine, Candle 79, and Candle Cafe, dance and sing at a neo-Hassidic shabbat service at the beautiful B'nai Jeshurun,

and catch the very last day of the gritty ash-canny George Bellows exhibit at the Met (and of course revisit the masterpieces by Van Goghs and Caravaggios) all artists whose lives ended far too early, but whose influence will be eternal.

Despite the biting cold and the wind that careens channeled by the steel skyscraping canyons, just walking around Central Park (where I saw an extremely rare golden (or red) tail hawk) or by the skaters at Rockefeller Center or inside the bustle of the well preserved centarian, Grand Central Station, or with my fellow gawkers at Time Square, there is no place on earth like New York City.

After a wonderful visit with dear friends in Springfield, Missouri and undergoing a critical and demanding but extraordinarily successful external review for all the medical education work that I do, I had the help of a friend who drove me 80 miles to Joplin, MO to get the very last seat on an overbooked flight out of Missouri before the ice storm hit the midwest (all the local flights were unavailable and the next flights out were likely two days away). 

I got home a day early to warm and sunny California.

Home for a week, then off the Washington, DC.

ASH 2012: Dr. Tom Kipps Explains why Understanding CLL Biology Helps us Focus Therapies: Bcl-2 and ABT-199; as well as my Reporting on the Suspended Trials

This is the first of a four part interview with my doctor, Dr. Tom Kipps, where he unpacks for us the complexities of why Bcl-2 is such an attractive target in CLL.

This is not a theoretical construct, but is directly pertain to a powerful drug that is in clinical trials right now: ABT-199. That power is a double edged sword and I discuss the recent news about the trial suspensions later in this post.

It turns out that of the all the B-cell cancer, CLL is guilty of the greatest overproduction of this Bcl-2 which is a strong cellular anti-suicide messenger. Twin that with the contravening fact that CLL cells also overproduce the powerful pro-apoptotic (programmed cell death) compound BIM. But BIM is held in check by the excess Bcl-2.  Block Bcl-2 and then the BIM goes bam and the cancer cell suicides.

Vey good.

That is where ABT-199 comes in. But I will let Dr. Kipps explains.



Now all this power to take the safety off the suicide bomber inside every CLL cell comes with a heavy cost. If it is too effective, especially in someone with a high tumor burden (read very high lymphocyte count and huge nodes) and /or there is a significant dose escalation, the cell death toll can exceed the body's ability to cope with all the waste produced by the broken down cells. This is the dreaded tumor lysis syndrome( see this nice explanation by Dr. Sharman), and it can not only kill the patient, it can kill the development of a life saving drug.

Very bad.

I have waited until there was a reliable public source for confirmation before posting this information on my blog and I got it today from Bloomberg news.

I quote:

AbbVie Inc., the drug company that split off from Abbott Laboratories at the start of the year, suspended five studies on its experimental leukemia and lymphoma medicine after two patient deaths.

The patients died from tumor lysis syndrome, said Tracy Sorrentino, a spokeswoman for North Chicago, Illinois-based AbbVie. The complication stems from the rapid destruction of malignant cells after treatment that can trigger acute kidney failure. It occurs most often with large tumors such as those found in leukemia and lymphoma patients, according to the National Institutes of Health. 

They continue:

“We have every expectation that these trials will come off the partial clinical hold and we’ll be able to initiate Phase 3 trials in 2013 as planned,” she said. “ABT-199 is a highly- potent agent and can result in the tumors reducing really quickly,” she said. “We are working to refine the dose.”

After the complication was discovered, AbbVie and its partner, Roche Holding AG, suspended the dose- escalation portion of the studies to determine the amount of drug that is safest and most effective, Sorrentino said. The risk stems from the drug’s potency and can be managed if the dose is carefully controlled, she said. 

This is a very powerful oral medication that has a tremendous potential to help even the worst risk patients with CLL. I want to have this option available in the near future to the many of us who might benefit from it, but not at the cost of moving too fast in the clinical trials. I agree that now that we know the danger, we can take appropriate precautions. 

Personally, if  I wasn't already doing so great on my ibrutinib trial, I would not hesitate to enter an appropriate ABT-199 trial once they have the dose escalation reworked. If anything, they are going to be over cautious from here forward.

Hence my prior post on dotting the I's and crossing the T's that was my loud admonition to take it slow with drug trials.

Nice and easy does it every time.

ASH 2012: Dr Jeff Sharman interviewed about the new treatments in CLL

My friend and fellow CLLer, Andrew Schorr did a very nice and interesting interview of Dr. Jeff Sharman at ASH 2012.

Dr. Sharman brings up some new and provocative insights on how the researchers misstepped when searching for a specific genetic target in CLL similar to the famously fused Philadelphia chromosome of CML that Gleevec blocked and in doing so, produced low toxicity, durable remission. This breakthrough drug, this targeted oral therapy, revolutionized not just the management of CML, but the whole approach on how we treat or too often, wish we could treat cancer.

As you have heard many times, in CLL, it is more complicated. In CLL, it all about “turned on” pathways than need a brake applied rather than a specific genetic defect. However, as our knowledge of the activated cellular pathways of the cancerous B cell clone improves, so does our ability to intervene. That brings us to the new generation of small molecules including ibrutinib (PCI-32765), idelalisib (CAL-101 or GS-1101), AVL 292, ABT-199 and others in the pipeline.

He shares his experience of one of of his highly refractory patient finally responding to one of the new trial medications and another where idelalisib worked when ibrutinib failed.

He cautions us that it is way too soon to pick winners among the new molecules.

Some of Dr. Sharma’s tropes you have encountered before from the doctors I spoke with at ASH. It is good to witness the building consensus.

Some of you may know Dr. Sharman from his well-written, informative blog on blood cancers and lymphoma. Check it out if you haven't already. You should also know that he has been a pioneer in small molecule research and an energetic force in developing resources to get clinical trials done.  He talks about their paramount importance right now. He forecasts the end of the world of FCR as we know it. He reflects on how well these drugs work for even those with the worst prognostic markers.

Dr. Sharman asked me if I wanted to share the video. I am, of course, happy to get the word out however I can.

So enjoy and take heart.

Soon I will be posting my ASH interviews with Drs. Furman, Kipps, Wierda, and Wiestner.

On a personal note, I am home from a medical conference in San Francisco, but just for a few hours before I take off again to lecture in San Diego.

My health insurance has me in a ridiculous Catch 22. I can not get pre-authorized for my roll-over clinical trial at OSU that continues my lifeline of ibrutinib until I sign the informed consent, but I can't sign the consent until I am ready to roll-over into the new trial. All but two insurance companies that cover the myriad of patients from far away places that come to OSU for trials understand the fallacy of such a policy and do not insist on the signed consent, but mine is one of the two that makes it difficult.

That said, I am sure it will all work out (retroactively) with the help of some real kind, persistent, and hard working people at both OSU and Blue Shield. Just one more thing to worry about in the meantime.

On Monday I leave for cold Columbus to finish one trial and begin the new continuation trial. While there, I will be busy with a bone marrow biopsy, another photo shoot and interview. Guess which one I am not anticipating with joy. Hint: there there will be no camera or recorder involved, but there will be needles.