Re: Successful Chemo for 11q?

[Guest guest]

Yes. FCR

In a message dated 13/02/2011 15:57:20 GMT Standard Time,

zz646@... writes:

Any Regimes seem to produce more durable results

for the ATM or 11q deletion?

Thanks,

Skip

[Guest guest]

Thank you.

I got a 50% node reduction after 6 cycles and rapid growth

after just a few months...so looking for more options.

Skip

__________________

On Sun, Feb 13, 2011 at 11:48 AM, TERJOHA wrote:

Yes. FCR

__________________

Any Regimes seem to produce more durable results

for the ATM or 11q deletion?

Thanks,

Skip

__________________

[Guest guest]

One of the most important findings coming out of the German CLL Study Group 4

trial, and one of the few means iFISH has for altering therapy is that patients

with deletion 11q did much better with FC versus F chemotherapy. As a result,

deletion 11q patients are the one population I use FCR in.

Rick Furman, MD

>

> Any Regimes seem to produce more durable results

> for the ATM or 11q deletion?

>

> Thanks,

>

> Skip

>

[Guest guest]

I know that is the gold standard but I had virtually no response thru 3

cycles of FCR ...then we raised the R from the standard of 375 to 500

....showed immediate reduction, yet at the end of the remaining 3 cycles

ended with about 50% node reduction and was back to prechemo level after

only 4-5 months of chemo holiday. Currently on Benda/Retux and it is

working much better but still looking for fallback options...not

optimistic this will be longlasting at the end of the full regime.

On Sun, Feb 13, 2011 at 12:49 PM, rrfman wrote:

One of the most important findings coming out of the German CLL

Study Group 4 trial, and one of the few means iFISH has for altering

therapy is that patients with deletion 11q did much better with FC

versus F chemotherapy. As a result, deletion 11q patients are the one

population I use FCR in.

Rick Furman, MD

[Guest guest]

Dear Dr. Furman,

Would you be kind enough to give us an update on Pci32765 and Cal 101? Are you

still feeling as confident in the two kinase inhibitors?

Thank you

Re: Successful Chemo for 11q?

Yes. FCR

In a message dated 13/02/2011 15:57:20 GMT Standard Time,

zz646@... writes:

Any Regimes seem to produce more durable results

for the ATM or 11q deletion?

Thanks,

Skip

[Guest guest]

You might want to look at HDMP and Rituxan. PubMed has a few articles. Kipps

at UCSD designed the protocol, some hem/oncs use it locally.

11q is known for a shortened treatment response and poor prognosis. I have it

too, and expect the same results you just obtained with FCR.

Ann

Re: Successful Chemo for 11q?

Thank you.

I got a 50% node reduction after 6 cycles and rapid growth

after just a few months...so looking for more options.

Skip

__________________

On Sun, Feb 13, 2011 at 11:48 AM, TERJOHA wrote:

Yes. FCR

__________________

Any Regimes seem to produce more durable results

for the ATM or 11q deletion?

Thanks,

Skip

__________________

[Guest guest]

The best option for most patients in this setting would be a clinical trial. I

remain very optimistic that CAL-101 and PCI-32765 (and others to come) will be

the treatments of the future.

Rick Furman

>

> One of the most important findings coming out of the German CLL

> Study Group 4 trial, and one of the few means iFISH has for altering

> therapy is that patients with deletion 11q did much better with FC

> versus F chemotherapy. As a result, deletion 11q patients are the one

> population I use FCR in.

>

> Rick Furman, MD

>

[Guest guest]

There is a misunderstanding about del 11q and treatment. It is the presence

of rituxin in the treatment mix that makes the difference. The German CLL8

trial demonstrated that del 11q went from being a poor risk factor with FC

to a standard risk factor with FCR. This is not to say that there are not

some cases that will relapse rapidly (the median is not the message), but

on average with FCR del 11q does no worse than trisomy 12 or a normal

karyotype.

There is no evidence that the presence of an alkylating agent makes any

difference, but we have no data of FR versus F in this situation and no

evidence that I know of that bendamustine works in this situation. I would

expect

the new enzyme inhibitors to be effective, but it is still early days in

their development and they are only available in clinical trials.

Terry Hamblin MD

[Guest guest]

My question is: are the different responses we see, at least here on lists, due

in part to different flavors of 11q? and in that case, IF known should FCR be

considered differently in those patients ?

While at dx I was pronounced 'lucky' to have gorgeous markers. As if any

cancer can be termed thusly. That being said I was not surprised at slow steady

rise in

various whites, and same lowering of the reds, short hand here. However two

years into this waiting game nodes proliferated, and grew. spleen became a

problem.

I began to read everything I could find and realized perhaps my 'markers' were

no longer gorgeous. A novice CLL er then, I found all sorts of references to

transformations into Richters. I concluded wrongly, that Richters was the

" only " rock I might encounter. And that, usually after treatments.... so what

WAS going on here? Boy was I wrong. More reading had me where I would have

bet a dozen donuts that I had acquired an 11q deletion. I went about finding

the broad array - big fish for those unfamiliar- and had it done. Not one but

three different flavors of 11 were now messed up. I had also lost one copy of

ATM... probably not both copies. While one is better than none, it seems to be

an indication that this flavor of 11q is somewhat less stable than vanilla CLL

or vanilla with nuts, (as in oh nuts) 11q with ATM in tact. I learned that my

wbc/alc would probably remain a huge nothing for quite some time, but that the

red team would probably start to leave their posts. All during this wait,

however I would continue to grow more and bigger nodes, and perhaps spleen and

liver, to say nothing of crowding out my marrow...It seems that 11q CLL

progression is not so findable in routine blood tests. It's clinical

performance however has become better known to us over time.

Without ATM, or at least without Both copies, one has to rely on the other wide

receiver, p53, and hope it gets the signal to kill and replace after treatment.

Since this type of testing is relatively new, and not widely used, it will take

time before anyone can answer these questions with any real certainty. My own

report indicated a concern for a general instability, which tells me that

treatment may not give me the gold standard results we've seen in studies.

For sure this type of testing gives out more than we can use now. An

incidental finding of a tri 8 is of somewhat dubious use to a CLL doctor, but

told me that I probably had this 'pre leukemic' marker all along. Perhaps due

to my early childhood radiation. Whatever the reason, it actually helped me to

know. FISH would not have found the trisomy 8,(they don't FISH for it in CLL,

Tri-8 is thought to be associated with mylodysplastic syndrome) Since two

tries with FISH at major research centers had not found the 11q, none of them.

nor the ATM. 11's are missed on fish many times. especially if they occur

at the end of the piece. However it is entirely possible that mine may have

morphed during that wait period. Whatever the case, I am glad I know now.

they also found a 21q, which they state is at the moment of questionable value

in evaluating cll. However since this type of testing covers the entire span,

they are found. In other words, one doesn't need to know what one might find

before looking. Perhaps in time, if this type of testing becomes more

available, those other deletions will prove useful predictors as well, or

perhaps explain the course of the disease origins. Storing that data is a

simple matter.

there are papers on this however they are PDF and can't be sent thru this list.

There are also some on pay to read journals, however a google of 11q deletions

in CLL, Gunn for starters, and go from there. Dr. Gunn IS affiliated with one

lab who performs this test, but as I understand she has worked in concert with

among others, Kipps, et al. I am not pushing any tests here.

my point is that had I waited, content that my 'doubling time' and b symptoms

were within tolerable ranges. and other such quick answers were NOT the whole

story it's likely I would have been held in W and W and may have missed a chance

to treat before I acquired still more deletions. My profile a year ago was not

terribly stable, hence as I understand it, treatment could give me not much joy

and bring on further deletions. Especially now that things are progressing

more rapidly, I am not shocked. However I have serious doubts about FCR " just

because " I happen to be an 11q kid. I've also had too many skin cancers and

viral infections to want to go whole hog into particularly F. And from what I

understand, any treatment at this point might eliminate my other copy of ATM,

leaving me hoping that p53 is wide awake, and learns new tricks in time. So

the dilemma, go see what joy I may find in FCR and then since I would have

earned the coveted 'failed' status, be welcomed into a trial that required that

status, tho perhaps in a worse place, or do nothing until one of the newer pups

is ready for mass release.

I may be off base here, but it seems a bit too easy to assume that ALL 11q's

will respond the same way. As we have seen from posts repeatedly. No, the

median is not the message, and if one is blessed with one deletion, perhaps

there are others, or there will be.

all the best ,,, beth fillman

[Guest guest]

Thanks I will look into these...also hearing good things

about Cal 101 but it is early stage.

I got no response thru 3 cycles of FCR. The Rituxin was

increased from 375 to 500mg and started getting immediate

response--MD established this higher protocol.

I'm now into 3rd cycle of Bendamustine/Rituxin and it is

shrinking tumors from the first cycle...but again not

expecting long duration until they begin to return.

Good Luck

-----Original Messages-----

On Mon, Feb 14, 2011 at 3:25 AM, TERJOHA@... wrote:

There is a misunderstanding about del 11q and treatment. It

is the presence of rituxin in the treatment mix that makes

the difference. The German CLL8 trial demonstrated that del

11q went from being a poor risk factor with FC to a

standard risk factor with FCR. This is not to say that there

are not some cases that will relapse rapidly (the median is

not the message), but on average with FCR del 11q does no

worse than trisomy 12 or a normal karyotype.

There is no evidence that the presence of an alkylating

agent makes any difference, but we have no data of FR versus

F in this situation and no evidence that I know of that

bendamustine works in this situation. I would expect the new

enzyme inhibitors to be effective, but it is still early

days in their development and they are only available in

clinical trials.

Terry Hamblin MD

____________________

The best option for most patients in this setting would be a

clinical trial. I remain very optimistic that CAL-101 and PCI-32765

(and others to come) will be the treatments of the future.

Rick Furman

________________________

You might want to look at HDMP and Rituxan. PubMed has a

few articles. Kipps at UCSD designed the protocol, some

hem/oncs use it locally.

11q is known for a shortened treatment response and poor

prognosis. I have it too, and expect the same results you

just obtained with FCR.

Ann

[Guest guest]

Craig,

As another fellow with 11q del. I can tell you that from my

experience, and based on my most recent understanding of the science,

if you don't shrink the nodes all the way back to normal, and that

includes the ones deep in the gut that only a CT or a very skilled

sonogram can find, you are headed fro a short remission. 11q is

already notorious for shorter remissions.

HDMR + R or O is great for nodes, easy on the marrow, but very immune

suppressive in the short term. I have seen long remissions with 11qer

with this choice.

A trial makes senses, especially as the new kinase inhibitors are very

good with nodal disease. AT101 is also good with nodes and except for

liver inflammation, seems pretty non-toxic

Maybe you should be considering a second remission transplant to go

for a cure while you in healthy and in a CR.

Let me know if I can help. We are all in this together.

, 59 yr family doc & father of 4, dx 9/05 del 11q unmutated,

CD38+, ITP 9/06 failed steroids, IVIG , Rituxan and splenectomy

controlled w cyclosporin A & Rituxan combo. RIC MUD HSCT July 1/08

was CR w BMB MRD neg. - lost graft w growing nodes at 6 months, BM

involvement and ITP again at 13 months, now controlled w IVIG

cyclosporin and recent course of R, mild anemia see

http://bkoffman.blogspot.com/

[Guest guest]

My husband has 11q and is currently in the CAL101 / Rituxan trial. He is

responding very well, with very large nodes almost disappearing in just a

week or two. Now we are hoping the R will clean out the blood, and in fact

his WBC/ALC went from 122 to 44 in one week. So far he has no side effects

and is tolerating everything very well. We are excited, but realize that

this is early days for this treatment. He was previously on Rituxan mono

therapy from Feb of 2003 until 2010 when the Rituxan did not work on his

nodes and marrow anymore. With CAL101, the drop in his nodes overnight is

very exciting, and we hope the R has enough punch left in him to bring down

the WBC/ALC over the next weeks. He started the trial on January 3. We are

cautiously optomistic!

Husband dx 2001 at age 48, 11Q, Rituxan 2/2003 to 2010, now

CAL101/Rituxan

[Guest guest]

,

If you have the time, I would like take up your invitation to call and

get your perspective on this disease.

In visiting your web link I was disappointed for you that your

transplant did not " take " . My doc is recommending a trans after this

cycle of BR but with no MUD the most optimistic forecasts I am hearing

from the Cord process is 50/50 survival with 11q w/ ATM

deletion...Inclined to take my chances and rely on new technology since

I am feeling quite well--working, exercising etc--just minor fatigue and

node growth.

So if you are inclined, would appreciate the chance to talk.

Craig

On Mon, Feb 14, 2011 at 3:24 PM, Koffman wrote:

Craig,

As another fellow with 11q del. I can tell you that from my

experience, and based on my most recent understanding of the science,

if you don't shrink the nodes all the way back to normal, and that

includes the ones deep in the gut that only a CT or a very skilled

sonogram can find, you are headed fro a short remission. 11q is

already notorious for shorter remissions.

HDMR + R or O is great for nodes, easy on the marrow, but very immune

suppressive in the short term. I have seen long remissions with 11qer

with this choice.

A trial makes senses, especially as the new kinase inhibitors are very

good with nodal disease. AT101 is also good with nodes and except for

liver inflammation, seems pretty non-toxic

Maybe you should be considering a second remission transplant to go

for a cure while you in healthy and in a CR.

Let me know if I can help. We are all in this together.

, 59 yr family doc & father of 4, dx 9/05 del 11q unmutated,

CD38+, ITP 9/06 failed steroids, IVIG , Rituxan and splenectomy

controlled w cyclosporin A & Rituxan combo. RIC MUD HSCT July 1/08

was CR w BMB MRD neg. - lost graft w growing nodes at 6 months, BM

involvement and ITP again at 13 months, now controlled w IVIG

cyclosporin and recent course of R, mild anemia see

http://bkoffman.blogspot.com/