- To my Lord Jesus and Father God for keeping me going each day and somehow always providing for all my needs
- My family and friends for their unwavering love and support.
- To the entire team at Sarah Cannon Research Institute / Tennessee Oncology / Sarah Cannon Center for Blood Cancers for helping start to beat this wretched leukemia into retreat.
- To all my new friends and family at Middle Tennessee Camp Bluebird for their cheer, support and love.
I’ve charted some of the metrics from a few months of weekly CBC tests. Treatment in the clinical trial began the first week of September and outcome so far is both expected and good. Most of my blood counts have returned to where they were about 3-6 months before I started any treatment. The neutrophil counts have been the most stubborn and variable but they do seem to be rebounding now. The ipi-145 clinical trial (now in cycle 4) will continue open-ended for me so the values should hopefully continue to normalize.
I’ve now completed 3 28 day treatment cycles in the Phase 1 clinical trial for IPI-145. Most of my blood counts with the frequent exception of the neutrophils have been rebounding steadily. Most are back to where they were in May 2013, 3 months before I began treatment. The initial goal was to drop-kick this CLL. So far, we seem to be doing just that.
Here’s a snippet from his post about the upcoming ASH (American Society of Hematology) conference in New Orleans, LA in December. My own doc, Dr Ian Flinn will be presenting on trial data with ipi-145. I can’t wait. There is a video on page one but the audio did not play well for me. Here’s page three from the article
Bumper Crop of New Agents
The rest of the studies focus on the new agents. We have several ibrutinib trials, including a single-agent study in patients with or without 17p deletion. There will be the final analysis of bendamustine and rituximab plus ibrutinib. Do you need the chemotherapy? Do you need the bendamustine? There will be another abstract with rituximab and ibrutinib alone.
This isn’t the only exciting drug. There are phosphoinositide (PI) 3-kinase inhibitors, which appear to be very good and are very impressive, perhaps as good as ibrutinib when you combine them with a drug like rituximab. In fact, a recent study of rituximab-idelalisib vs rituximab-placebo was closed early because of a survival advantage.
We are also going to be seeing a list of new PI 3-kinase inhibitors for the treatment of CLL: a new delta inhibitor, a new gamma inhibitor, and others. We’ll have to see which of these provides an advantage over the others, if at all. But in any event, we have great new drugs that will be changing the landscape of non-Hodgkin lymphomas, Hodgkin lymphoma, and chronic lymphocytic leukemia.
This is Bruce Cheson, signing off for Medscape Hematology. I will be back with you after the ASH meeting in New Orleans. See you there. Goodbye.
From what I’ve read, this seems to be the minimum goal for success in treatment of this CLL but a definition has eluded me until now. According to the journal “blood” 2008 111: 5446-5456 Prepublished online January 23, 2008;doi:10.1182/blood-2007-06-093906 it is:
5.2. Partial remission (PR)
PR is defined by the criteria described in sections 5.2.1, 5.2.2, or
5.2.3 (if abnormal before therapy), as well as one or more of the
features listed in section 5.2.4. To define a PR, these parameters need to be documented for a minimal duration of 2 months (Table
4). Constitutional symptoms persisting for more than 1 month
should be recorded.
5.2.1. A decrease in the number of blood lymphocytes by 50%
or more from the value before therapy.
5.2.2. Reduction in lymphadenopathy (by CT scans in clinical
trials 57 or by palpation in general practice) as defined by the
126.96.36.199. A decrease in lymph node size by 50% or more either in
the sum products of up to 6 lymph nodes, or in the largest diameter
of the enlarged lymph node(s) detected prior to therapy.
188.8.131.52. No increase in any lymph node, and no new enlarged
lymph node. In small lymph nodes (< 2 cm), an increase of less
than 25% is not considered to be significant.
5.2.3. A reduction in the noted pretreatment enlargement of
the spleen or liver by 50% or more, as detected by CT scan (in
clinical trials) or palpation (in general practice).
5.2.4. The blood count should show one of the following
184.108.40.206. Neutrophils more than 1.5 ϫ 109/L (1500/uL) without need for exogenous growth factors.
220.127.116.11. Platelet counts greater than 100 ϫ 109/L (100,000/uL) or 50% improvement over baseline without need for exogenous growth factors.
18.104.22.168. Hemoglobin greater than 110 g/L (11.0 g/dL) or 50%
improvement over baseline without requiring red blood cell
transfusions or exogenous erythropoietin.
Failure is not an option! We are going to get there and hope and pray for eventual full remission.
Yesterday, I posted about a diagnostic test used for CLL called flow cytometry. Another modern test that is also used extensively is known as FISH (Fluorescence In Situ Hybridization). Like flow cytometry, it is also a fairly expensive test to have run. According to WebMD:
How FISH Works
During a FISH test using a sample of the patient’s tissue, special colored dyes are attached to specific parts of certain chromosomes in order to visualize and count them under a fluorescent microscope and to detect cancer-promoting abnormalities.
Abnormalities found in cancer cells include:
- Translocation. Part of one chromosome has broken off and relocated itself onto another chromosome.
- Inversion. Part of a chromosome is in reverse order although it is still attached to the correct chromosome.
- Deletion. Part of a chromosome is missing.
- Duplication. Part of a chromosome has been copied and the cell contains too many copies.
Translocations can help doctors identify some types of leukemia, lymphomas, and sarcoma. Duplications in breast cancer cells can help doctors choose optimal treatments.
Compared to standard cytogenetic (cell gene) tests, one advantage of FISH is that it can identify genetic changes that are too small to be seen under a microscope. Another advantage is that FISH doesn’t have to be performed on cells that are actively dividing. Because other tests cannot be performed until cancer cells have been growing in lab dishes for about two weeks, the process usually takes about three weeks. FISH results are usually available within a few days.
Wikipedia has a good article on Fluorescence In Situ Hybridization if you’re interested (or having trouble sleeping).
I got an invoice a few days ago for the latest series of flow cytometry tests. Unfortunately, these blood tests tend to be really expensive. This is a modern diagnostic method which counts individual cell types for genetic testing to classify a case of CLL and identify its potential prognostic factors via Fluorescence Activated Cell Sorting (FACS). Here’s a good introductory video that explains the process.
This article also has some good basic info if you are interested. LINK
Very very interesting. I’ve not heard of this one before. There are many CLL focused drugs out there and historically, many patients have not responded to them; particularly after a relapse. Prior to the new B cell receptor pathway inhibitors, mutations like my 17p deletion has been especially hard to manage. It seems like advances are coming every few days; the future is bright. Here’s a snippet:
Drs. Weisenthal and Bosanquet state that the SignatuRx(TM) personalized chemotherapy test can be ordered by physicians for their chronic lymphocytic leukemia patients from virtually anywhere in the world. Blood samples are sent to Dr. Weisenthal and Bosanquet’s California-based laboratory by overnight courier where the cancer cells are tested for susceptibility to treatment with up to 30 different chemotherapy drugs and drug combinations. Test reports are available in 7 to 10 days
The full article is here: Test Shown to Reduce Early CLL Deaths