This content was current as of the date it was released. In science and medicine, information is constantly changing and may become out-of-date as new data emerge.
Take Away Points:
- Every one of us with CLL has a different type of CLL that may behave differently.
- The biology of our particular CLL should aid in determining our choice of therapy.
- Our personal preferences in therapy should also inform our treatment choices.
- For some specific patients, FCR and even F alone was an excellent choice.
- A small subset of CLL patients never needs treatment and may have a normal life expectancy.
Hematology in general and CLL specifically are full of jargon and acronyms that can be both overwhelming and daunting. With time and experience, you’ll become familiar with the terminology and acronyms. We will try to explain each medical term the first time it appears in an article, but we will use the true terminology so that you gain comfort and familiarity with the medical terms that you will see in your lab reports and in medical articles. We will also provide a glossary for your reference.
Dr. Adrian Wiestner from ASH 2013:
In this short video with Dr. Adrian Wiestner of the National Institute of Health (NIH), he discusses the tremendous variability of our disease.
Due to the breadth of the subjects covered in our recorded interview, this article discusses a number of interrelated but distinct topics that touch on the issue of personalized therapy.
This is a more complex article and may be difficult for the newly diagnosed who is still unfamiliar with the jargon and the basic therapeutic landscape. It is meant to provide the experienced readers with some background information to inform their approach to choosing their own individualized therapy in cooperation with their provider.
New Versus Old:
I asked Dr. Wiestner about the debate among hematologists treating CLL on the role of such proven “gold standard” therapies such as FCR (fludarabine, cyclophosphamide, and rituximab) compared to the growing importance of novel targeted therapies, mostly not approved at the time of the interview.
Times have changed quickly and for the better since this interview. In addition to the monoclonal antibody obinituzumab, we now have the approvals of ibrutinib and idelalisib.
F and FCR:
He starts with a historical perspective by pointing out that for those very few patients who had extremely durable remissions with fludarabine (F) as a single agent, this was the right choice for those select few. And this is true for a therapy that is no longer used by itself and has been long eclipsed by the clinically proven better response and overall survival (OS) rates for the chemo-immunotherapy combination of FCR. Again quoting from the research published in 2011:
“The CLL8 trial has demonstrated that an association of rituximab, fludarabine and cyclophosphamide is effective in prolonging progression-free survival and overall survival of patients with symptomatic CLL, therefore establishing the new standard of treatment for physically fit patients.”
You read more at: http://informahealthcare.com/doi/abs/10.1586/era.11.118
FCR by the way was the first therapy proven to prolonged overall survival (OS). Since then several others have joined it.
Moreover with FCR a small but significant group of patients have no detectable disease many years later after only one six month or less course of therapy. For that small group, FCR has certainly offered them a long disease-free ride.
Dr. Wiestner and others argue that those that did so well were those we could have predicted would do well regardless of therapy. Others would counter that FCR is the best options for many patients.
Whether these extremely durable remissions constitutes a cure or whether chemo-immunotherapy is ever a wise choice are both topics worthy of vigorous debate that awaits more published data and will be discussed elsewhere on the site.
We talk about just how heterogeneous is CLL, both from a historical perspective and from the viewpoint only recently provided by deep sequencing.
Dr. Wiestner argues eloquently why we need therapy guided both by the biology of the cancer and the patient’s preferences.
“No CLL patient is exactly the same as another CLL patient.”
This is truly personalized medicine.
The Good Cancer?
In the last segment of the interview Dr. Wiestner reminds of the subset of CLL patients that may never need therapy and have the same life expectancy as their matched cohort.
In this article from BLOOD about prognostic subgroups in CLL, we find this encouraging statement about one population of CLL patients who are:
“…very low-risk, harboring del13q14 only, whose 10-year survival (69.3%) did not significantly differ from a matched general population.”
Yes, the research is saying that this group of patients with CLL lived as long as a matched cohort with no CLL. As I argue in my article on the GOOD CANCER, no cancer is good, but there are certainly some of us that have a subtype of CLL that is not all bad.
Many strong reasons that argue for individualized therapies.
While a full discussion of the evolving use of prognostic and predictive factors is beyond the scope of what we are discussing here, the Blood article provides important insights and elsewhere on the website one can will find different options to learn more.
In the end, we need to consider our cancer’s biological tendencies and staging, our own health besides our CLL and of course our personal preferences, and then in consultation with our doctor, make a shared medical decision about our best treatment.
Here’s my opinion: No cookbook, no “gold standard”, but an individualized approach to our care.
Brian Koffman 3/1/15 with help from EK.