29 replies to this topic

[cherylannes]

Hello All,

I have been away from the board, so I missed out on all the stimulating conversations one of my posts generated.  Sorry michael, didn't mean to hijack your situation.

RCT, you ask a very valid question - i.e. "who are these BCR ABL positive but healthy individuals" - I am asking the same question to some experts and hope to get back to you.  For now I will say that at every CML conference I go to, most of the CML experts who speak always relate back to the statement that BCR ABL is detectable in otherwise healthy individuals.  I always took that to mean that BCR ABL is a "marker" of the disease, but not the definitive cause of the disease.  Below I am going to post a few links to various newer papers - Trey, you might like that they are post 1990's....So still relevant in today's world of TKI's....

That being said, now that there are more trials and interests in getting patients to stop TKI after a certain number of years in stable CMR, there is heavy investing going on in more sensitive testing being developed.  At ASH this year we heard about the exciting advancement of DNA PCR.  This is really interesting because it personalized PCR testing at the patient level.  It is very expensive to do, for now, anyway, but when it is used, mostly in the stopping TKI trials going on in Europe and Australia, it can detect very low levels of BCR ABL.  Quite fascinating is that it has detected these levels in CML patients who are a few years post stopping TKI without relapse.  The other interesting thing is the level of this detectable residual disease seems to fluctuate and there are many months when no level is detected, and then BCR ABL becomes detectable again only with the DNA PCR.  When very sensitive (but non DNA) PCR testing is done on these same individuals, they show undetectable throughout....This clearly needs to be studied more, but the implications are quite fascinating.....

In Toronto Ontario they are developing PCR testing that will go down to 15 log reduction, right now they are very good at going down to a 9 log reduction.  Then of course they are also developing Mass Spect PCR.  The worry with these sensitive tests, and this is straight from the investigators mouth, everybody will potentially test positive for BCR ABL.....So, we have heard some discussion at ASH this year of the role of NK cells and what happens to the range and functionality of these cells during TKI treatment...Link below....

So, what am I saying?  Keep an open mind with regards to this, I do not have all the answers, neither does science yet, but, it is exciting and relevant for now...

Some links:

http://bloodjournal....full/103/8/3245

[PDF]

Download - Case Report Detection of BCR-ABL Positive Cells in an ...

http://www.nature.co...eu2010101a.html

NK Cells:

http://ash.confex.co...Paper31045.html

http://bloodjournal....short/116/5/772

Older paper, but important early research none-the-less:  http://www.ncbi.nlm..../pubmed/1690865

http://www.nature.co...l/1203584a.html

http://onlinelibrary...430410/abstract

[Tedsey]

Nice to hear from you again Cherylannes!  This makes me think of a post from someone who reported Dr Druker, et. al. believe CML is not dependent upon BCR-ABL for survival.  So, if it is ever supported that this fusion protein is found in people without CML, is BCR-ABL the best marker to follow the disease?  Maybe we are looking in the wrong place?  Well, it may come down to percents and ratios.  Who knows?  Since there are so many unknowns with this crazy disease, (but I feel so happy that scientists know as much as they do), I refuse to believe that any of us can adopt a gloom and doom attitude before we are told we are at the end of the line.

Thanks for all the valuable input and information you provide.

Tedsey  

[Trey]

It makes me wonder why we would need a super sensitive DNA level PCR type test to find very low levels of BCR-ABL if it is found in so many healthy people anyway.  What would be the point of finding it at such low levels, if your theory is correct that it does not mean anything.  Just wonderin'.....

Your links do not show anything new.  The first is a letter to the editor (which we have discussed previously) that talks about finding certain T-cells and KQSSKALQR in healthy individuals, not BCR-ABL.  The other references discuss people with CML.  So nothing new about BCR-ABL in healthy individuals in any of these references.

[valiantchong]

Hi,

On the BCR-ABL on healthy individual, was wondering how low is the detection or is the test valid. I was wondering why there is no official study reported on the % of BCR-ABL on healthy individual distribution, since there was one or 2 reports on this but no distribution at all.

On the DNA testing on CML individual that will showed, does this mean the CML is coded into the DNA, and irreversible ? Does this mean all CMLers are bound to "doom", since it is already coded in the DNA, which means it will bound to multiply........??

[rct]

valiantchong:

There is no testing of "healthy individuals".  There is no detection level because there is no testing.  There is no study reporting on the distribution of BCR/ABL in the healthy population because there is no testing.

I'm sorry, I don't like being a grump, I really don't.  cherylannes says "...I don't have all the answers...", and that she will get back to us with the answers.  Fact is, she won't, because there isn't an answer, BECAUSE THEY DO NOT TEST HEALTHY INDIVIDUALS FOR BCR/ABL.  I have had consultations, been to seminars, see all kindsa CML experts, many of the same folks mentioned in these threads on this forum, they know of no testing of healthy individuals, they know of no reason to, and they agree that if this were the case I would be getting tested for things all the time, because I want My Mrs cured, and all of the rest of you.

cheralyannes says "...keep an open mind...".  I have an open mind.  I'm willing to listen patiently to, I've sought out those that would know and do, and my open mind has not found one "expert" anywhere that has tested, tests, or advocates the testing of, "healthy individuals" for the presence of BCR/ABL without leukemia.  It just isn't happening.  The links posted above:

1.) T-Cells.  Whole nother ball game, not at all about guys like me with BCR/ABL and no CML.

2.) The asymptomatic guy in Jamaica.  How many people went years asymptomatic before CML was diagnosed?  Whole bunch, that's how many.  This thing just comes up way too often as some evidence of something or other.

3.) Natural Killer(NK) Cells. How bout that, they figured out that CML peoples have defective ones.  I'm shocked.  I'm also not amused, there is NOTHING in this at all about healthy individuals with CML.

4.) NK Cells in patients being treated with Dasatanib.  I'm pretty sure they all have CML if they are taking Dasatanib.  NOTHING about healthy individuals and BCR/ABL.

5.) NK Cells in CML patients in varying states of remission.

6.) See number 5 again.

7.) CML patients have functional deficiencies in there NK Cells.  I prolly coulda told them that.  No mention of healthy individuals and BCR/ABL.

I can not say it enough without sounding like a grouch, so just one more time in this thread before they probably punt me from this forum for good:

There is no such thing as testing healthy individuals, i.e., me, for the presence of BCR/ABL without leukemia, and posting lots of links to lots of research having nothing to do with healthy individuals having BCR/ABL just doesn't make it true.

I apologize if this offends anyone.

rct

[cherylannes]

RCT,

You are not offensive, but tiring.  I know I do not have all the answers, you THINK you have all the answers...You do not...

Go back and read the study, they are comparing CML patients to Healthy Donors....The Healthy Donors do not have CML but have low level detection of BCR ABL....We've gone over this before, BCR ABL pops up because the body is not perfect, it makes millions of errors each day when copying DNA.  In nearly almost all of the cases our body catches the errors and fix them.  THIS IS GREAT NEWS.....This means we can FIX IT!  The trick is to find out how it is that our bodies sometimes fail at the job of fixing it....

So, yes RCT they do test healthy non CML people, because they are looking for the differences and similarities....

Honestly I do not know how to make this any clearer to you.  Stay in your dark cave if you must, but stop trying to pull other people down with you....

As for the links to the articles, I should have given you clearer instructions, you are supposed to be able to read them and then link, that is make associations between the information in all of them.  In case you forgot, this is what researchers do....Not all the articles were meant to highlight a comparison of healthy donors to CML patients....

You've done a find job of misconstruing the information provided....

So RCT, I am calling you out on this next thing you posted:  RCT Said:   I have had consultations, been to seminars, see all kindsa CML experts, many of the same folks mentioned in these threads on this forum, they know of no testing of healthy individuals, they know of no reason to, and they agree that if this were the case I would be getting tested for things all the time, because I want My Mrs cured, and all of the rest of you.

Clarify what you are saying.  What exactly was your question?  Did it go something like this " Is there currently screening going on in healthy individuals to test for BCR ABL"?  If so, the answer is NO, a thousand times NO!  We KNOW THAT.  The question should be does research require that you sometimes ask for healthy non CML volunteers to provide samples for testing of BCR ABL.  The answer is yes - as indicated in a couple of the articles...

@ Valiantchong, there is absolutely testing in healthy donors for comparative purposes with in a research context as some of the articles pointed out....No one has ever suggested that it is a routine screening..

So, back at RCT - Lighten up and think of the possibilities....There is an immune component to this disease, some doctors at Fox Chase know this as well as they are treating some CML patients on low dose Peg IFN.....Precisely for the immune response...One patient I am in touch with over there has an interesting story to tell.  He is a retired surgeon, was having checkup every six months, so he could almost pin point the day his BCR ABL went wonky...He was dxed with a very low level of BCR ABL went through treatment with all the TKI's trying to find the one that didn't give him horrible side effects.  During which time he achieved and sustained CMR, finally they switched him to 45ug of Peg IFN once every two weeks, his quality of life is amazing, and he is still CMR.....Different strokes for different folks....We are not a one size fits all....

No hard feelings....

Cheers!

[cherylannes]

Trey,

The first link shows this:

BCR-ABL-specific T cells can be detected in healthy donors and in chronic myeloid leukemia patients following allogeneic stem cell transplantation

Rezvani et al have recently reported the presence of leukemia-associated antigen-specific memory CD8⁺ T cells in human leukocyte antigen (HLA)-A2-positive healthy individuals and chronic myeloidleukemia (CML) patients before and after stem cell transplantation(SCT).¹ CD8⁺ cells specific for HLA-A2-restricted proteinase-3(PR1) and Wilms tumor (WT1) peptides were undetectable usingspecific tetramers in all but 2 cases, both healthy individuals.Tetramers of HLA-A2 with BCR-ABL junctional peptide sequenceswere not used. Using quantitative polymerase chain reaction (qPCR) to measure interferon-gamma mRNA production in response to peptide-pulsed targets, Rezvani et al showed that CD8⁺ T cells with specificity for PR1 and WT1 peptides were present in both healthy individuals and CML patients. In contrast, T cells with specificity for the b3a2 BCR-ABL junctional peptide sequence GFKQSSKAL were identifiable only in the patient population.

Using tetramers of HLA-A3 and the BCR-ABL junctional sequenceKQSSKALQR, we have previously reported that BCR-ABL-directed CD8⁺ cells are circulating in some HLA-A3-positive CML patients.² We recently have extended this study to a larger population of both CML patients and healthy subjects³ (N.B. et al, manuscript submitted, 2003). Using this HLA-A3 tetramer and also a tetramer of HLA-B8 and the junctional sequence GFKQSSKAL, we found that 3 of 18 assessable HLA-A3- and/or HLA-B8-positive healthy subjects had circulating tetramer-positive CD8⁺ cells directed against BCR-ABL. Representative plots are given in Figure 1. These findings are in contrast to the findings of Rezvani et al.¹ However, in line with their findings, we foundthat 9 of 13 HLA-A3- and/or HLA-B8-positive CML patients had evidence of a tetramer-positive CD8⁺population, which in most cases was present on several occasions. These 9 cases included 2 HLA-A3-positive cases who had undergone allogeneic SCT several years previously and who were consistently PCR negative for BCR-ABL.

In the case report, you will see references to other reports of healthy donors showing levels of BCR ABL...

The third link:  Note HD stands for Healthy Donors - just saying.....

BCR and BCR-ABL regulation during myeloid differentiation in healthy donors and in chronic phase/blast crisis CML patients

M Marega, R G Piazza, A Pirola, S Redaelli, A Mogavero, I Iacobucci, I Meneghetti, M Parma, E M Pogliani and C Gambacorti-Passerini

Abstract

Chronic myeloid leukemia (CML) is caused by the BCR-ABL hybrid gene. The molecular mechanisms leading from chronic phase (CP) to blast crisis (BC) are not understood. However, both the presence and the levels of BCR-ABL seem to be important for CML progression. BCR-ABL is under the transcriptional control of BCR promoter. Here we focused on the gene expression control of BCR and BCR-ABL upon myeloid differentiation in healthy donors (HDs), CP and BC patients. As previously reported, BCR-ABL is downregulated during myeloid maturation in CP patients. A similar pattern was detected for BCR (but not for ABL) in CP-CML and in HD, thus suggesting that the two genes may be under a similar transcriptional control. In BC this mechanism is similarly impaired for both BCR-ABL and BCR. These data indicate the presence of an 'in trans' deregulated transcription of both BCR and BCR-ABL promoters, associated with CML progression.

In all of the links provided we are supposed to be seeing how various researchers, within a research context that is, are looking at healthy donor specimens looking for comparisons and trying to figure out how it is that BCR ABL goes so awry in just a few of us, relatively speaking (1 in 100,000) when seemingly many non CML people can test positive for BCR ABL....

Non of this should be disturbing to anyone, it all makes sense.  We know that the body makes millions of errors a day in copying DNA and going through cell divisions, yet the good news is that the body mostly catches the mistakes....GREAT, if we could understand this better than we can understand how it goes wrong for some of us and how we can fix it.

CML IS NOT A PERMANENT DISEASE - for this I am happy! 

No hard feelings....

Cheers!

[Trey]

Finding T-cells specific for WT1 and PR1 in healthy individuals is not the same as finding BCR-ABL in them.  Healthy cells have both WT1 and PR1, just not in the same quantity as leukemic cells.

The second study clearly states that the healthy individuals only showed BCR, not BCR-ABL.  Everyone has BCR on chromosome 22.

Still no evidence to support the theory.

[cherylannes]

From the first link:

"We would, however, underline their caution against extrapolating their negative findings on CD8 responses against BCR-ABL in healthy individuals to HLA types other than HLA-A2, since the response against BCR-ABL may vary according to HLA type. Further studies on the HLA-specific response to BCR-ABL are required.

In the other link:

"Here we focused on the gene expression control of BCR and BCR-ABL upon myeloid differentiation in healthy donors (HDs), CP and BC patients. As previously reported, BCR-ABL is downregulated during myeloid maturation in CP patients. A similar pattern was detected for BCR (but not for ABL) in CP-CML and in HD, thus suggesting that the two genes may be under a similar transcriptional control."  This means that they looked at both BCR and BCR ABL in HD and in CML CP....and in CML BC.....

I am not miffed at all about what you and RCT are claiming.  It isn't my theory...It is the theory of some of the researchers....I just think it is exciting!!!

We all win if the theory works out or not, because either way it adds another piece to the puzzle....

[rct]

cherylannes wrote:
RCT,
You are not offensive, but tiring.  I know I do not have all the answers, you THINK you have all the answers...You do not...
Go back and read the study, they are comparing CML patients to Healthy Donors....The Healthy Donors do not have CML but have low level detection of BCR ABL....We've gone over this before, BCR ABL pops up because the body is not perfect, it makes millions of errors each day when copying DNA.  In nearly almost all of the cases our body catches the errors and fix them.  THIS IS GREAT NEWS.....This means we can FIX IT!  The trick is to find out how it is that our bodies sometimes fail at the job of fixing it....
So, yes RCT they do test healthy non CML people, because they are looking for the differences and similarities....
Honestly I do not know how to make this any clearer to you.  Stay in your dark cave if you must, but stop trying to pull other people down with you....

Ok, all the DNA stuff aside, which I have sat in front of a pretty prominent genetic researcher at a Gildas Club presentation who made it crystalline clear that the issue is that we live our lives through literally TRILLIONS of replications WITH NO ERROR WHATSOEVER and the BAM on that 10 trillionth one we have a FAIL, and CML begins.  That is exactly counter to what your experts claim.

Past all that, if you want to make it clearer to me, I'll leave my dark cave that has no literature at all about this when you provide me with literature about this.

cherylannes wrote:

As for the links to the articles, I should have given you clearer instructions, you are supposed to be able to read them and then link, that is make associations between the information in all of them.  In case you forgot, this is what researchers do....Not all the articles were meant to highlight a comparison of healthy donors to CML patients....
You've done a find job of misconstruing the information provided....

The information provided has nothing to do with healthy individuals being tested for BCR/ABL yet not presenting with CML that requires medication, specifically, the TKIs that these people take.  If you see that in the information, I would be happy to have you point it out to me, because I don't see it.

If the information isn't there, I don't know why, in response to reasonable discussion regarding the "....in healthy individuals" you would post these links in support of that discussion.  Sorry, I'm missing that.  The information provided is as I wrote about each abstract.  I will say this to you directly:

None of those articles has anything at all to do with testing healthy individuals for BCR/ABL translocation that causes CML yet they do not have CML.

cherylannes wrote:
So RCT, I am calling you out on this next thing you posted:  RCT Said:   I have had consultations, been to seminars, see all kindsa CML experts, many of the same folks mentioned in these threads on this forum, they know of no testing of healthy individuals, they know of no reason to, and they agree that if this were the case I would be getting tested for things all the time, because I want My Mrs cured, and all of the rest of you.
Clarify what you are saying.  What exactly was your question?  Did it go something like this " Is there currently screening going on in healthy individuals to test for BCR ABL"?  If so, the answer is NO, a thousand times NO!  We KNOW THAT.  The question should be does research require that you sometimes ask for healthy non CML volunteers to provide samples for testing of BCR ABL.  The answer is yes - as indicated in a couple of the articles...
@ Valiantchong, there is absolutely testing in healthy donors for comparative purposes with in a research context as some of the articles pointed out....No one has ever suggested that it is a routine screening..

Read your own posts cherylannes, read them carefully.  Understand why a new person, valiantchong for instance, with no knowledge of where that person is in their journey.  Read your posts, understand that no matter what you say here in this thread, you will again allude to the idea that this occurs in healthy individuals. I will sit with Druker and You any time you want, and we will ask the question together, and I am absolutely confident that he, and any other doctor of reknown I choose, will provide the answer that I have provide to others:  There Is No Testing, this is a non issue, and further, testing of "healthy individuals" while attempting to provide data proving/disproving theoretical NK Cell activity or uptake of TL(small a) -1 HSA and all that other IN NO WAY indicates anything to be used for comparison to the entire community. In other words, sure, they test healthy individuals for stuff, but you(the imperial) must be very very careful in how you context that testing and the intended outcomes from that testing.

In short:  Nobody is testing healthy individuals at all in any way to see why the healthy indiduals have the BCR/ABL translocation but do not present with CML.  That is not happening.  I am calling you out on this, because whether you like it or believe it or not, your posts very delicately, without any facts whatsoever, indicate that, followed by reasearch links that have nothing to do with that concept.

cherylannes wrote:

So, back at RCT - Lighten up and think of the possibilities....There is an immune component to this disease, some doctors at Fox Chase know this as well as they are treating some CML patients on low dose Peg IFN.....Precisely for the immune response...One patient I am in touch with over there has an interesting story to tell.  He is a retired surgeon, was having checkup every six months, so he could almost pin point the day his BCR ABL went wonky...He was dxed with a very low level of BCR ABL went through treatment with all the TKI's trying to find the one that didn't give him horrible side effects.  During which time he achieved and sustained CMR, finally they switched him to 45ug of Peg IFN once every two weeks, his quality of life is amazing, and he is still CMR.....Different strokes for different folks....We are not a one size fits all....
No hard feelings....
Cheers!

No hard feelings are taken.  I don't have to lighten up and think of any possiblilities, I am...hip deep in this every single day.  I appreciate whatever they are doing with Interferon.  I'll say this gently in all caps as I can:  THAT HAS NOTHING TO DO WITH ORDINARY FOLKS HAVING BCR/ABL BUT NOT CML.  Period.

rct

[cherylannes]

RCT

Gilda's club - thanks for clarifying the source of your very important information....

I cannot help you with your reading comprehension skills...

RCT said: " In short:  Nobody is testing healthy individuals at all in any way to see why the healthy indiduals have the BCR/ABL translocation but do not present with CML.  That is not happening.  I am calling you out on this, because whether you like it or believe it or not, your posts very delicately, without any facts whatsoever, indicate that, followed by reasearch links that have nothing to do with that concept."

YOU ARE RIGHT NO ONE IS TESTING HEALTHY INDIVIDUALS, how many times must I say this...It is not routine screening, they are comparing samples obtained from healthy donors to CML patients...

None of this is my theory....

RCT, back to the Philadelphia Chromosome conference that was held in Philadelphia in September 2010 and the report that I posted here specifically the presentation given by Dr.  Felix Mitelman - gave an interesting talk about how he started cataloguing all of the chromosomal aberrations in cancers. He tells us that originally the Philadelphia Chromosome was referred to as Ph1, but the 1 was later dropped because there wasn't a Ph 2 - meaning that there is only one chromosomal aberration driving this disease. However, he did say as long as the disease is stable in the chronic phase, otherwise if the disease progresses other chromosomal abnormalities will be discovered, but those abnormalities are also what we see in acute leukemia's.
Dr. Mitelman also spoke about a suggestion made in 1914 by Th. Buveri was that chromosome change may cause leukemia!!!! (follow this link... http://www.nature.co...e080605-06.html) He also pointed out that 80% of the "normal" people have the fusion gene (BCR ABL) but they will not develop full blown CML - they still do not understand why this is so. Are there genetic - epigenetic windows of vulnerability? Is there something in the microenvironment that controls the aberration?

I am writing to him for more clarification....

RCT, with all due respect you may be up to your HIPs in CML everyday....Thank you for the support you give your wife and your knowledgeable posts here, but I am living with the disease.

There are certain XML experts and researchers who I find very credible, not all of them, but most of them. 

[janner25]

This has been some interesting reading and I have gone back and forth with whether or not to chime in - but I figure - Hey - why not .

I am one of those people who was diagnosed with no symptoms in October 2010 - simple WBC elevations - BCR-ABL test done by PCR.  Since I was diagnosed, I have come to this board for support (which has been tremendous) but also I will admit, has caused me some questioning about my diagnosis.  I never had a BMB done - so I question could I really have CML without all these tests done.  (And yes, I'm going for a 2nd opinion on March 7th - can't get here soon enough).  So am I in denial?  Quite possibly.  Am I doing well?  Absolutely!

I only bring this up because I am new to this...the terminology - the research - all of it.  RCT is right in that it could give people like me - who's high WBC was 28000 (not sure how to read the PCR results so don't know anything on that level - just said chronic phase) - false hope that maybe I'm one of those people who have BCR-ABL but are truly healthy.  I have been assured I do indeed have it.  I know it is on people like me to learn everything I can about this disease and learn what research is out there so I can be my biggest advocate.  I also think that this type of forum is difficult because we have so much to share that things get lost in translation.  I use this board for a kinship (which I think I have found so thank you everyone) but also for information that I unfortunately may not have the time for in my day to day life.  I read things, I get excited...but reality is...I still have CML.

So for whatever it's worth - thank you both RCT and Cherylann for your exchange...I just hope in the end, that someone finds a cure for everyone

[Trey]

http://www.youtube.c...h?v=NzlG28B-R8Y

[cherylannes]

Janner25,

The intention is not to give anyone here false hope of having BCR ABL and being treated for CML but not really having CML...Quite the contrary.  In fact, I am shocked that anyone would insinuate that to be even a remote objective to any of my posts.  Why would I do that?  I myself have CML.  I have had CML for over ten years, I am not in denial...I chose to believe that with all that I read, study and talk to others about this disease that it is curable. What I am trying to point out is that the researchers are trying to find out the mechanism by which BCR ABL is not taken care of by the body's natural immune/check point in the relatively small percentage of the population - US CMLers.  Recall that CML has an incidence rate of 1 in 100,000....

It is unusual to be dxed with CML without having a bone marrow done as that is the only way they can do cytogenetics and actually determine unequivocally the dx of CML.

Keep us posted on the results of your second opinion.

Things do get lost in translation....There are unfortunately communications going on "behind the scenes" that we are not privy to....in some cases these clarify things in other cases it does not...

Every case of CML is different, regardless of all the similarities.

Maybe you are just lucky that you were diagnosed very early on in the disease.  I haven't read all your posts, but I imagine you are on treatment and doing well.  There was some discussion at ASH this year that some patients, like you, who probably have low sokal risk scores, good response to drugs are going to be good candidates for the stopping TKI trials.

The message being conveyed in my posts is that researchers are taking many routes in trying to solve the puzzle of what causes CML, how CML gets a foot hold in a small percentage of the population with the intent to eventually cure this disease.  There is no false hope in any of that.

There are over 100 patients in Europe off of TKI's and not relapsing and being monitored for the past five years....That is fact and reality - and very exciting....

Cheers!

[everonward]

RCT, with all due respect you may be up to your HIPs in CML everyday....Thank you for the support you give your wife and your knowledgeable posts here, but I am living with the disease.

Cherylannes this is below the belt,  I too am living with this condition  - I do not think of it as a disease - but my darling husband lives with it too, as do my two children. 

I am not going to comment on the discussion, mainly as I live in the here and now. If they discover something from it - great- but I'm noit holding my breath.

[cherylannes]

Dear Everonward,

I was not trying to hit below the belt, that thought didn't even occur to me...I was merely pointing out why would I be trying to give false hope to anyone here????

I meant what I said to RCT, I can well understand what he does for his wife, my husband and daughter go through the same thing as your family does.  A diagnosis of CML affects the entire family, not just the patient....

Nothing I have stated on this board is negative and it shouldn't be misconstrued that way either....

But, boards are awkward places to get to know one another, regardless of how well we write the word's anyone is free to interpret them as they wish.  I think people should be a bit more benevolent in how they interpret things.  I would prefer it if we would all just imagine that we are all trying to get a long and cope with this as best as possible. 

I write from a well informed level and I write with the full expectation that the days of CML are numbered and that we are very close to curing this disease for the majority of the patients...  When my posts are challenged and insulted, like RCT did, I certainly will stand up and defend them and the integrity with which I wrote them. 

Cheers!

[CallMeLucky]

@Janner25

Hi Janner, I just wanted to comment on something you wrote, and I hope I don't burst any bubbles for you, but as you said, you have already been assured you have CML.  You stated that you didn't have any symptoms, and I know what you mean, because my diagnosis was similar to yours, I didn't have any physical symptoms either, I went in for a routine physical feeling great only to find out my WBC was 35000 and a week later it was 55000.  My point is that we did have a symptom, the high white blood count.  In my case they did chromosome testing via bone marrow and saw the Philadelphia Chromosome, I also tested positive for BCR-ABL.  The fact you test positive for BCR-ABL and had elevated WBC points to the CML diagnosis.  I think the BMB is a good idea for you to get the baseline and a second opinion is always the way to go.  I wanted to clarify because in the banter that is going back and forth about the possibility of "healthy" people having trace BCR-ABL, these are not people presenting with the elevated blood counts.  That in itself is a main symptom, just not one we generally feel until they sky rocket.  Again, I'm sorry if this is deflating in anyway, I don't want to take anything away from you and I think it would be amazing if they came back after your BMB and said it was all a mistake, I would gladly eat my words.    Sometimes I feel like I'm still waiting to get that phone call where they say, "gosh we're really sorry but all these tests were wrong, you're actually fine".  I know that isn't going to happen.  Anyway I just wanted to clarify for anyone else who reads it.  I hope you are doing well.

[janner25]

Lucky - THANKS!  Don't worry - you're not busting my bubble!  I know I have it - and never considered the WBC a symptom - but you're right it was (as was my tiredness - but that is a easy thing to push to the side with 2 young boys, husband on 2nd shift, working, school, and all that goes with all that).

I consider myself one of the lucky ones...tasigna is working...the side effects are waning (except for my immune system being junk with my wonderful boys (ages 8 and 4) bringing everything home from school so I'm sick every month and on an antibiotic!)....I think you and I are also pretty young (if I remember correctly - again the 'kinship')...I will be 37 in May...so if there's a chance that I can get off the meds, I'll be happy to be one of the trial subjects - knowing that if it starts going anywhere - there are more meds to bring it back in check!  Its hard being so young to know I'll be LIVING with this for my lifetime- but again - the operative word is living with - and inspiring stories of length of living from Susan and Cherylann is exactly why I know I'll be fine.  I know that it's not in the front of my mind as much as it used to be.  I just wish I had started on this board earlier as I probably would have gone for 2nd opinion and BMB sooner than 4 months after dx.  But now is better than never!

[CallMeLucky]

I've heard of some people going for their second opinion a few years after diagnosis, so four months is nothing with this disease.  It's a lousy disease but I love one attribute of it, in the chronic phase, it is slow, so at least we get a chance to work with it, think things through, get tests, get opinions and second opinions.  Early on I was so worried it was an acute form of leukemia and how everything just changes overnight.

We are the same age, I'm 38, also with two boys 4 and 6.  I know what you mean about the idea of living with this for the rest of my life, but as you put it, trying to focus on the living with part of that statement and the fact there is a rest of my life that very well may be a long time.  I'm also open to the idea of certain trials and while I am not generally an optimistic person, the science seems to suggest that they should find a way to get on top of this even better than they already have.  I'm encouraged by the amount of research I see going on despite the fact we have a good drug.  Early on I thought why would anyone want to cure CML, they have a drug that keeps most people alive for a long time, case closed move on to another cancer that is uncontrolled, but then I realized something.  The treatment for CML has been revolutionary and sparked a tremendous amount of research and helped other cancers.  CML is simple, it is serious, but it is simple.  It makes for the perfect testing ground to try new approaches to treating cancers, like vaccines and other targeted drugs.  In many cancers there are hundreds of mutation involved, in CML chronic phase, there is one.  It is the perfect test model, and that is why I believe researchers are still so interested in it and why I believe they will continue to come up with new and better treatments.  I don't hold my breath for a cure, but how nice would a vaccine be?  You go for a few shots and then go back once in a while for a booster, side effects could be minimal, mostly around the time of the shot and then fade away.  And the next best part, if my doctor has to give it to me as a shot, it falls under my med insurance, not my prescription plan.  Well, here's to hoping!

[PhilB]

I wouldn't be holding my breath for a 'conventional' vaccine based on an approach of 'let's find someone who has BCR ABL, but doesn't develop CML and develop a vaccine from their immune cells'.  Even if we do accept that lots of healthy people have some level of BCR-ABL (and all the referenced studies directly supporting that finding do appear to be 'ancient' in CML terms which casts some doubt on the reliability of the PCR testing involved) there is no evidence I've been able to find to suggest that these 'healthy' people aren't developing CML because of an immune response rather than just the fact that the translocation occured in a non self-replicating stem cell and therefore will disappear with the death of that stem cell -  before this slow moving disease would become clinically manifest.

Maybe in years to come we'll have the technology to engineer a virus that specifically targets Ph+ cells and either kills them directly, or makes them vulnerable to a drug and then you really could have a CML vaccine.  I think that would be a long way off, but we can dream.