Monday, June 01, 2009

CLL: Introduction

Sorry to have been silent for so long. Two things: the side effects lasted longer this time than usual; that in itself would not have stopped me blogging, but I have also swapped my computer system. That has meant that I did not have enough 'oomph' to set it up with an internet connection. Today, feeling better, and with the help of my son, I have been able to set up a wi-fi connexion.

Anyway I have been able to do some work on the CLL chapter that I have to produce. Here is the introduction:

Most people begin their article on chronic lymphocytic leukemia (CLL) with the words “CLL is the commonest leukemia in the Western world”. It may or not be true, but with recent changes in the definition of the disease we can no longer be sure. Not only that, but the general impression that CLL is getting commoner and more benign may simply be an accident of disease discovery, with more alert physicians recognizing a disease that may or may not be there.

A new heterogeneity in CLL was discovered a decade ago and this has provided a key to opening up the complex pathophysiology of the condition and coincidentally has important prognostic value. In addition, a range of new treatments has become available during this time as well as the means of detecting minimal residual disease. As a result we now have to look at CLL differently. For some patients this will mean that we may never treat their leukaemia, but may still have to manage late complications; for others we will hold out the prospect of cure, though this will not be without hazard; for yet others there will be a sequence of treatments and remissions with the physician balancing benefit and harm with the aim of producing the longest possible, good quality life.


Anonymous said...

what do you think of FCR Lite - chemoimunotherapy where there is less F and more R? Have you heard of the latest results published? Who do you think is a good candidate for this treatment?

Anonymous said...

It will take decades just to sort out the best use of drugs now available, on the market or in trials.

For example ABT-263 is a Bcl-2 inhibitor, but it seems it doesn't work well unless another anti-apoptotic protein, Mcl-1 is also inhibited. Flavopiridol inhibits Mcl-1, but they are not used in combination even in clinical trials at present.

You are lucky if you have a complete remission or if you have minimal residual disease, which can come from FCR or other agents. If you aren't as lucky, you have few if any options. You MAY get a transplant if you aren't bulky and if you can get into a complete remission, which is not guaranteed.

It's just taking too long to get drugs through the approval process. Meanwhile, people are dying.