Not much to report

I saw Dr. Kipps in late July, and he said he was pleased with my current status.  I do have lots of nodes, but they all seem to have shrunk, as far as he could tell based upon a manual manipulation of the nodal areas.  My biggest problem still is the abdominal area, and he couldn't tell much in that region without a scan.  Dr. Coutre wants me to have my next scan at the end of the year.  So we have to get together on a date for that one.  In the meantime, I'll see Dr. Kipps in January, 2013.

So, I supppose no news is good news.

I did ask Dr. Kipps about the ROR vaccine that would be created to perhaps 'cure' CLL.  He said that they are looking for a 2014 start date for a trial, since they have to jump through a lot of hoops with the FDA and other organizations.  You know, 'first do no harm'.  So that is good news, though I wish they would start sooner than two years from now.  But I guess we must be patient...

Cruise Control

I went down to Stanford last week for my latest appointment with Dr. Coutre.  The lab numbers were not in yet (even though I got there over an hour early!), so I don't know how the lab is going to assess my progress or lack thereof.  (Is it progress if the numbers progress to a worse level, or is it progress if my counts are stable and/or improved.  I vote for the latter.)

From a purely subjective standpoint, I feel fine and am able to do pretty much what I want physically.  I think it has taken me about six months to pretty much fully recover from my hospital stays.  That's a long time, and thinking back, I was pretty much wiped out in January and February.  I couldn't drive, I couldn't make it to the end of the street even with a cane.  Now I am driving to Stanford and elsewhere, I did some roof repairs that necessitated me carrying shingles up the ladder, and ripping off damaged shingles, and even using new plywood to replaced some damaged sections.  (The whole problem started unnoticed some time ago when I lost a single shingle to a wind storm, and didn't notice it.)

My attitude to the lack of numbers from Stanford is that since I've not heard from Dr. Coutre, all's pretty much well.  At least I like to think so.  I see him in a month.  I'll repeat my scans in December or January.

In addition, I'll see Dr. Kipps next month in San Diego.  I'll get to fly the no-frills Southwest, which has the only non-stop from Sacramento to San Diego.  I hope things go well there.  Dr. Kipps is more of a worrier than Dr. Coutre, so I expect a somber analysis from Kipps.  But I will get to pump him on new treatments.  Of course the one trial I'm interested in apart from CAL-101/GS-1101 is a trial educating the T-lymphocytes to attack and destroy CLL cells.  A cure would be very, very nice.  To get back to the business of living without having to worry about my immune system.

Perhaps an impossible dream for me, but one can only hope, can't one?

Two Weeks Off!

The clinical trial protocol of flavopiridol (Alvocidib) is a long one, with the full course lasting nine months. (I started in late July and if all goes well, I'll have my last infusion the end of March, 2010.) It consists of six cycles of four weekly infusions, followed by a two week 'holiday'. It has been suggested that the infusions should just run continuously so that the drug can work continously to kill CLL cells, but the trial protocol is set up with the two-week break.

Being the patient, I can say that I will not protest too much that I get a two-week break. Part of the procedure using flavopiridol is that one cannot have too high of a potassium level. I've discussed this before, but the dying CLL cells dump the cell contents in the blood, and this can cause acute renal failure which has been fatal in at least one patient in the phase I component of the study. Starting off with a low normal level of potassium (3.9 or thereabouts) means that there is room to go up without doing anything drastic in terms of managing the potassium level.

So, I try to manage this by drinking lots of water spaced throughout the three days before going down to San Diego for the next infusion. (There is a danger of drinking too much all at one time. Search on 'water intoxication.') I also go on a low potassium diet, which I have devised. This is basically a 'white' diet consisting of white bread, white cake, white cookies, muffins, etc. Few vegetables and no meats are low in potassium. Also, no chocolate. The 'diet' is more comprehensive, of course. And, of course, don't do anything without checking with your doctor as I have.

This means that my diet is severely restricted for the Sunday, Monday and Tuesday before the Wednesday infusion. (I fast on the day of the infusion because anything I eat will just come up later. And I will have an aversion to that food for a long time. As it is now, the thought of raspberry juice is revolting, since I used to buy a raspberry Snapple and wash down pills with that. Bleech! Sorry, Snapple.)

So...I can have a normal diet for Friday and Saturday. Only two days a week. Of course, things could be a lot worse.

Anyway...I had a wonderful two-week break the last two weeks of November. This included Thanksgiving. My wife is a great cook and we had a turkey breast (thank you mister or miss turkey for giving up your life for my meal) with the usual fixings. I had Thanksgiving and the day after off from work, so my wife and I spent one day up in the foothills of the Sierra poking around various antique shops.

We try to do two trips a year in Amador City and Sutter Creek. These two are delightful towns that are only 30 miles from Sacramento, but with a totally different feeling. It's a beautiful drive up highway 16 east of Sacramento, then south on highway 49. It's especially pretty in the fall with the changing leaves on the trees, the cold air, the wood smoke in the air, and the happy tourists clogging the streets.

We spent the day looking at and for various fun things to look at or to buy. Sutter Creek has a crafts fair most weekends from Thanksgiving to Christmas. Both towns have some unique shops that carry things you don't ordinarily find. My wife's favorite shop is in Amador City, and features antique lace. Now, as a guy, I don't know why anyone would want to wear 100-year-old fabric, but my wife puts together some attractive looks mixing old lace and modern clothes.

It may not be the best way to administer the flavopiridol, but having a two-week break from the tedium of flying to and from San Diego, and spending the day in the infusion room isn't all bad from my point of view!

I'm more than halfway through the regime. So far, it has been working pretty well.

Might a Major Development in CLL Treatment Be in Sight?

I was perusing the Web looking for interesting CLL news, when I decided to look at Dr. Kipps’ Blood Cancer Research Fund site (www.bcrf.org). The site now posts news from “Blood”, the periodical of the American Society of Hematology (www.hematology.org).

I noted an interesting editorial from Dr. Byrd on the discovery by researchers of the National Institutes of Health of a single antigen on CLL cells that may be common to all CLL cells. (An antigen is a protein that is the target of an antibody.) Dr. Byrd practically gushes with enthusiasm for the possibilities for CLL and other blood cancers from this discovery (http://bloodjournal.hematologylibrary.org/cgi/content/full/114/20/4324). In fact, his editorial is entitled, “Hunting for the Achilles’ Heel of CLL”. He terms the value of the process in identifying the antigen common to CLL cells as ‘immense’.

That sound like extremely good news!

What the researchers did was to look at people who were cured of their CLL by allogenic stem cell transplants (SCT). They then compared the blood to the patient’s blood and CLL cells that were preserved from the time before they had their transplants. (Research such as this is the reason donating blood for research is so important.)

Using sophisticated techniques, they were able to identify an antibody to an antigen that was present on the CLL cells in these patients before their transplants. The antibody wasn’t present in the patients (otherwise they presumably would have never developed CLL in the first place), but was produced from the donor’s stem cell derived B lymphocytes. It appears that, once the donor’s stem cells start producing those lymphocytes in the transplant patient, somatic hypermutation (which is the process where by all antibodies are produced by the body), starts working to produce an antibody which then starts to destroy CLL cells.

Byrd envisions development of this work to leading to therapies that may improve the curative potential of stem cell transplants. He also suggests that this may find a place in non-transplant therapies in treating CLL and other blood cancers. Avoiding the very expensive, very complex, very disruptive, and dangerous STC would be highly desirable!