All FISH (Fluorescence in situ hybridization) testing "should" be listed as the number of cells (actually, the number of interphase nuclei- the region of the cell containing DNA) harboring the abnormality out of 100-200. This is the percent of cells with that specific abnomality. Most, but all labs should be using a method to identify only the myeloma cells (cytoplasmic immunoglobulin (cIg-FISH) or like assay), because we really are not interested in non-myeloma cells. The percent of cells with the abnormality is primarily used to determine if the abnormality is real- above the false positive rate of the test. However, as Dr. Voorhees noted there is data from France suggesting that large percentages of Del 17 by FISH may portend a worse prognosis.
Your bone marrow pathology FISH reports should contain this information.
Forums
Re: Plasma cell percentage & speed of progression
Yes, I too have been reading the abstracts/research/trials from Herve Avet-Loiseau's group out of France and the cytogenetic stratification based on chromosomal abnormalities impacting outcomes.
Which is how I came to ask the initial question about plasma cell burden in terms of disease progression and what 'advanced' meant. Given that they were designating the chromosomal changes as being seen in 'advanced' disease state, in the articles.
Ahhhh, I see ..." the number of interphase nuclei" ... I did see that term on the FISH report.
It does indicate that 4-11% of cells contained the abnormalities based on amplification, deletion, gains, etc. I am now able to determine I CAN make the presumption that since it was FISH that indeed the percent of plasma cells that had the abnormalities was from purified cells as you had noted.
Unfortunately, as a newly diagnosed patient, I am an exceptionally fascinating case for science but not for survival. Of the 3 prognostic markers they indicate as poor (gain 1q/del 1p) bad (14q32) and worse (17p) I have all of them.
It is aggressive and rare in the newly diagnosed, so I am reading, and clinically true given that in the 6 weeks since original diagnosis, the SPEP and B2 microglobulin both shot up a hundred and thousand fold, respectively a significant increase and the lesions have progressed from one site, only in skull to jaw to tibia.
That is also my reason for inquiring if the percent of cells matter or simply the present of those chromosomal changes is ultra-high risk (new term I am now reading) for multiple myeloma. I suspect, ultra-high risk is due to bortezomib having been shown to be effective against some of the other cytogentic translocation abormalities, like 13q and t (4:14) moving the formerly high risk into an effective therapeutic regimen...but I am digressing....
What the FISH report does not indicate is the percent for the specific genetic change for each. There is simply a cummulative total of the cells presenting those cytogenetic abnormalities.
Given, the information from France, what would you be requesting from the lab...to sort all this out and delineate the plasma cells quantatatively per chromosomal change?
Thanks so much for your time.
Which is how I came to ask the initial question about plasma cell burden in terms of disease progression and what 'advanced' meant. Given that they were designating the chromosomal changes as being seen in 'advanced' disease state, in the articles.
Ahhhh, I see ..." the number of interphase nuclei" ... I did see that term on the FISH report.
It does indicate that 4-11% of cells contained the abnormalities based on amplification, deletion, gains, etc. I am now able to determine I CAN make the presumption that since it was FISH that indeed the percent of plasma cells that had the abnormalities was from purified cells as you had noted.
Unfortunately, as a newly diagnosed patient, I am an exceptionally fascinating case for science but not for survival. Of the 3 prognostic markers they indicate as poor (gain 1q/del 1p) bad (14q32) and worse (17p) I have all of them.
It is aggressive and rare in the newly diagnosed, so I am reading, and clinically true given that in the 6 weeks since original diagnosis, the SPEP and B2 microglobulin both shot up a hundred and thousand fold, respectively a significant increase and the lesions have progressed from one site, only in skull to jaw to tibia.
That is also my reason for inquiring if the percent of cells matter or simply the present of those chromosomal changes is ultra-high risk (new term I am now reading) for multiple myeloma. I suspect, ultra-high risk is due to bortezomib having been shown to be effective against some of the other cytogentic translocation abormalities, like 13q and t (4:14) moving the formerly high risk into an effective therapeutic regimen...but I am digressing....
What the FISH report does not indicate is the percent for the specific genetic change for each. There is simply a cummulative total of the cells presenting those cytogenetic abnormalities.
Given, the information from France, what would you be requesting from the lab...to sort all this out and delineate the plasma cells quantatatively per chromosomal change?
Thanks so much for your time.
-
suzierose - Name: suzierose
- When were you/they diagnosed?: 2 sept 2011
Re: Plasma cell percentage & speed of progression
Risk, as your own research has told you, is currently a moving target. Made so by a number of factors:
1) Our increasing knowledge of myeloma as a whole;
2) Evolving technology (cytogenetics, to FISH, to cIgFISH, to the recent integration of gene expression patterns (MyPRS), and maybe soon to gene sequencing;
3) Introduction of novel therapies like Revlimid (lenalidomide) and Velcade (bortezomib) that may overcome some (but not all) advesrse risk factors, and
4) Continued studies that define other relevant lab tests or imaging (beta 2-M, albumin, LDH, CRP, MRI lesions, PET/CT).
However, even this information is limited and there is a lot that we do not yet understand that goes in to the risk on a patient-to-patient basis. To this end, frequently the true risk of a patients disease reveals itself with treatment and relapse.
Hopefully, we can continue to increase our knowledge of disease so that we eventually truly will personalize therapy. Today, we have made great strides in using risk to help us define appropriate therapy - Risk Adapted Therapy. Everyday we are moving away from just two groupings of patient Standard and High Risk to incorporate new risk categories; whether we include an intermediate risk, or add an ultra-high risk. However, this is still based on wide generalizations of people/patients as populations. And as you are learning with all the great strides we have made in myeloma, certain risk categories have not felt gains to the same degree.
Your FISH is only part of your story, though with del17 ("the ugly"- if you are a Clint Eastwood fan, yes) and amplification of 1q ("the bad"), it does suggest that your disase is going to be more difficult to control in the long term. Based on your comments you are still fighting to control disease. We wish you the best of luck and quick control of diease.
1) Our increasing knowledge of myeloma as a whole;
2) Evolving technology (cytogenetics, to FISH, to cIgFISH, to the recent integration of gene expression patterns (MyPRS), and maybe soon to gene sequencing;
3) Introduction of novel therapies like Revlimid (lenalidomide) and Velcade (bortezomib) that may overcome some (but not all) advesrse risk factors, and
4) Continued studies that define other relevant lab tests or imaging (beta 2-M, albumin, LDH, CRP, MRI lesions, PET/CT).
However, even this information is limited and there is a lot that we do not yet understand that goes in to the risk on a patient-to-patient basis. To this end, frequently the true risk of a patients disease reveals itself with treatment and relapse.
Hopefully, we can continue to increase our knowledge of disease so that we eventually truly will personalize therapy. Today, we have made great strides in using risk to help us define appropriate therapy - Risk Adapted Therapy. Everyday we are moving away from just two groupings of patient Standard and High Risk to incorporate new risk categories; whether we include an intermediate risk, or add an ultra-high risk. However, this is still based on wide generalizations of people/patients as populations. And as you are learning with all the great strides we have made in myeloma, certain risk categories have not felt gains to the same degree.
Your FISH is only part of your story, though with del17 ("the ugly"- if you are a Clint Eastwood fan, yes) and amplification of 1q ("the bad"), it does suggest that your disase is going to be more difficult to control in the long term. Based on your comments you are still fighting to control disease. We wish you the best of luck and quick control of diease.
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Dr. Ken Shain - Name: Ken Shain, M.D., Ph.D.
Beacon Medical Advisor
Re: Plasma cell percentage & speed of progression
Dear Suzierose,
Dr. Shain has highlighted an important caveat to my previous post regarding the percentages of plasma cells that harbor any given cytogenetic abnormality. The cytoplasmic immunoglobulin-FISH assay does overcome this technical problem. As such, if FISH testing was done by this technique (as opposed to FISH on the whole marrow population), the percentage of chromosome abnormalities should be reflective of the pure plasma cell population. This new testing is done at most but not all centers. The report should qualify which assay was run.
Good luck!
Pete V.
Dr. Shain has highlighted an important caveat to my previous post regarding the percentages of plasma cells that harbor any given cytogenetic abnormality. The cytoplasmic immunoglobulin-FISH assay does overcome this technical problem. As such, if FISH testing was done by this technique (as opposed to FISH on the whole marrow population), the percentage of chromosome abnormalities should be reflective of the pure plasma cell population. This new testing is done at most but not all centers. The report should qualify which assay was run.
Good luck!
Pete V.
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Dr. Peter Voorhees - Name: Peter Voorhees, M.D.
Beacon Medical Advisor
14 posts
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