One year ago today I had my first bone marrow biopsy at DFCI. This was my first bone marrow biopsy ever, approximately 3 years after my initial MGUS diagnosis. On this fateful day, I had no fear. I wasn't worried about the procedure as it was supposed to be a 'simple' aspiration. Little did I know this would be 4 aspiration pulls and a biopsy. This experience turned out to be the worst of my three bone marrow biopsies to date. Luckily, my last two were not so bad. Sadly, my left leg STILL hurts off and on to this day from the nerve damage!
Let's all remember... July 3, 2012 ;) Bone Marrow Biopsy and Aspiration: Ouch
Wednesday, July 3, 2013
Friday, June 28, 2013
Summer & Zometa
Summer is here!
My plans for this summer are to....
Work on my fitness ;)
Read
Beach
In addition, I have my 6 month follow up for the Natural History Study of MGUS & SMM in August and my 3 month labs and appointment with Dr. R in July. I received my MD note from my last appointment in April. Some of the statements are a little unsettling... I guess I knew all of the information written but it's hard to see in black and white. A few quotes:
"Elizabeth is clinically stable and doing well overall. It should be noted that she has been fully evaluated by my colleagues in Endocrinology and she does not have any other explanation for her osteopenia. This, therefore, raises the possibility of early myeloma-related bone disease. At this juncture, bisphosphonate therapy has not been recommended by her endocrine consult team because of the risk to any potential pregnancy that she is planning. At this juncture, therefore, Elizabeth is not keen to proceed with bisphosphonate therapy."
"Elizabeth otherwise continues to do relatively well and in this context, I have recommended she continue with her regimen of simple analgesics for antipyretic effects. In this regard, aspirin may be an excellent choice. This may have the additional advantage of being useful as an anti-inflammatory and thus has some clinical benefit for her. In this context, we have recommended two to three tablets a day provided GI tolerance permits.
Otherwise, we will follow a policy of careful observation. In terms of her bone disease, this will require simply careful observation at this stage given her reluctance to in any way consider bisphosphonate at this point in time."
"It should be noted that she will continue on vitamin D and other supplements as needed. Elizabeth will return to see me again in the next several months. We will continue to monitor her course very carefully and she knows to call should she have outstanding issues or concerns".
Sort of feel blindsided by this note because I thought everyone was in agreement that I would not start zometa at this time. This makes it sound like I'm refusing to start, which makes me uneasy. Definitely need to inquire a bit more about this in July.
Monday, June 17, 2013
FISH Abnormalities
I've had all these blog posts in my drafts for quite a while and I am finally getting around to finishing them! Thrilling, right? It's amazing what I get accomplished when I am avoiding the things I actually need to do... (read: grading, report cards, etc. etc.)
Fluorescence in situ hybridization (FISH) is a type of chromosome analysis that detects abnormalities of specific chromosomes. I have abnormal -13, t(11;14), and 14q32(IGH sep).
My reports:
December 2012:
+11 (CCNA-XTx3) normal
13q- normal
-13 abnormal
17p- normal
-17 normal
t(11;14) abnormal
14q32(IGH sep) abnormal
-14(3'/5'IGHx3: normal
Interpretation:
The result is abnormal and indicates a plasma cell clone with monosomy 13 and CCND1/IGH fusion, t(11;14). Insufficient plasma cells were observed with probes for chromosomes 3, 7, 9, and 15. This result indicates persistence or relapse of this patient's plasma cell clone.
July 2012:
+9 normal
+15 normal
+11 (CCNA-XTx3) normal
13q- normal
-13 abnormal
17p- normal
-17 normal
t(11;14) abnormal
14q32(IGH sep) abnormal
-14(3'/5'IGHx3: normal
Interpretation:
The result is abnormal and indicates plasma cell clone with monosomy 13 and CCND1/IGH fusion, t(11;14). At diagnosis, the combination of -13 and t(11;14) has uncertain prognostic significance in multiple myeloma. The prognostic significance for these abnormalities in MGUS, amyloidosis, or smoldering multiple myeloma is unknown (Fonseca et al., Blood 202: 4569-4575, 2003).
From what I understand and have been told, monosomy 13 and t(11,14) are both common abnormalities and are seen within MGUS, SMM, and MM patients. Also, t(11, 14) "may" be a more "favorable" risk factor. And monosomy 13 is not quite as terrible as doctors once thought. So, good news right? Dr. R said that for me they wouldn't have much prognostic significance as they would sort of cancel each other out... one more favorable, one a little less ideal. At the NCI/NIH Dr. L said that they "are just letters and numbers, we don't entirely know what they mean..." and basically, not to worry too much. I posted my results and this is one very helpful response:
Monosomy 13 (loss of 1 of the 2 copies of chromosome 13) in the absence of other high risk markers is not considered high risk in this day and age. It would be considered an intermediate risk factor. It should be noted that 40 - 50% of patients will have a 13q deletion (only a portion of 1 copy of chromosome 13 missing) or monosomy 13 and 40 - 50% of patients do not have high risk disease! You also have chromosomes 11 and 14 fused together. This is also a more common cytogenetic abnormality and is considered a better risk marker.
The statement, "This result indicates persistence or relapse of this patient's plasma cell clone", means that they were able to detect myeloma chromosome abnormalities in both of the bone marrow samples, suggesting that there were still myeloma cells left around in Dec 2012. If there were no myeloma cells left, the chromosome abnormalities would not have been detected. The blood and urine tests and numbers of myeloma cells on the 2 biopsies will give you a better sense of how things have changed in that period of time.
Chromosomal Abnormalities May Identify Smoldering Myeloma Patients At Higher Risk of Progression
According to the study the (11,14) translocation would put me into the "standard risk" group. This group had a median progression time of 4.6 years, a median survival time from SMM diagnosis of 12.3 years, and an overall survival time from MM diagnosis of 7.2 years.
YIKES.
That, of course, is not going to happen because I am not a statistic.
And lots of other information... lots of it is outdated.
MMRF: Genetic Abnormalities in Multiple Myeloma
14q32 Translocations and Monosomy 13 Observed in Monoclonal Gammopathy of Undetermined Significance
Choosing to ignore this study, plus it's super old:
Monosomy 13 is associated with the transition of monoclonal gammopathy of undetermined significance to multiple myeloma.
Fluorescence in situ hybridization (FISH) is a type of chromosome analysis that detects abnormalities of specific chromosomes. I have abnormal -13, t(11;14), and 14q32(IGH sep).
Weird FISH.
My reports:
December 2012:
+11 (CCNA-XTx3) normal
13q- normal
-13 abnormal
17p- normal
-17 normal
t(11;14) abnormal
14q32(IGH sep) abnormal
-14(3'/5'IGHx3: normal
Interpretation:
The result is abnormal and indicates a plasma cell clone with monosomy 13 and CCND1/IGH fusion, t(11;14). Insufficient plasma cells were observed with probes for chromosomes 3, 7, 9, and 15. This result indicates persistence or relapse of this patient's plasma cell clone.
July 2012:
+9 normal
+15 normal
+11 (CCNA-XTx3) normal
13q- normal
-13 abnormal
17p- normal
-17 normal
t(11;14) abnormal
14q32(IGH sep) abnormal
-14(3'/5'IGHx3: normal
Interpretation:
The result is abnormal and indicates plasma cell clone with monosomy 13 and CCND1/IGH fusion, t(11;14). At diagnosis, the combination of -13 and t(11;14) has uncertain prognostic significance in multiple myeloma. The prognostic significance for these abnormalities in MGUS, amyloidosis, or smoldering multiple myeloma is unknown (Fonseca et al., Blood 202: 4569-4575, 2003).
From what I understand and have been told, monosomy 13 and t(11,14) are both common abnormalities and are seen within MGUS, SMM, and MM patients. Also, t(11, 14) "may" be a more "favorable" risk factor. And monosomy 13 is not quite as terrible as doctors once thought. So, good news right? Dr. R said that for me they wouldn't have much prognostic significance as they would sort of cancel each other out... one more favorable, one a little less ideal. At the NCI/NIH Dr. L said that they "are just letters and numbers, we don't entirely know what they mean..." and basically, not to worry too much. I posted my results and this is one very helpful response:
Monosomy 13 (loss of 1 of the 2 copies of chromosome 13) in the absence of other high risk markers is not considered high risk in this day and age. It would be considered an intermediate risk factor. It should be noted that 40 - 50% of patients will have a 13q deletion (only a portion of 1 copy of chromosome 13 missing) or monosomy 13 and 40 - 50% of patients do not have high risk disease! You also have chromosomes 11 and 14 fused together. This is also a more common cytogenetic abnormality and is considered a better risk marker.
The statement, "This result indicates persistence or relapse of this patient's plasma cell clone", means that they were able to detect myeloma chromosome abnormalities in both of the bone marrow samples, suggesting that there were still myeloma cells left around in Dec 2012. If there were no myeloma cells left, the chromosome abnormalities would not have been detected. The blood and urine tests and numbers of myeloma cells on the 2 biopsies will give you a better sense of how things have changed in that period of time.
Chromosomal Abnormalities May Identify Smoldering Myeloma Patients At Higher Risk of Progression
According to the study the (11,14) translocation would put me into the "standard risk" group. This group had a median progression time of 4.6 years, a median survival time from SMM diagnosis of 12.3 years, and an overall survival time from MM diagnosis of 7.2 years.
YIKES.
That, of course, is not going to happen because I am not a statistic.
And lots of other information... lots of it is outdated.
MMRF: Genetic Abnormalities in Multiple Myeloma
14q32 Translocations and Monosomy 13 Observed in Monoclonal Gammopathy of Undetermined Significance
Choosing to ignore this study, plus it's super old:
Monosomy 13 is associated with the transition of monoclonal gammopathy of undetermined significance to multiple myeloma.
Sunday, June 9, 2013
Bulging Bicep - confirmed?
Back in February I was at the the National Institute of Health / National Cancer Institute in Bethesda, MD for the Natural History Study of MGUS and SMM. While there, I had blood and urine tests, a bone marrow biopsy, as well as a skeletal survey. The skeletal survey showed a possible abnormality on my left humerus that the myeloma team believe could be a lytic lesion. I joked with them, "Are you sure it's not my bulging bicep?" They concurred it was not. They wanted to investigate this abnormality further and I ended up having a CT scan of my humerus the next day.
In case you missed it.... I wrote about this experience here: Abnormal Skeletal Survey & Perfect Blood Work: NIH Day One and here: Bone Marrow Biopsy & CT Scan: NIH Day Two and here: Alliteration fan? Left (Humeral) Linear Lucent Lesion and here: Little Line = Left Linear (Humeral) Lucent Lesion
The CT scan revealed a "lucent lesion" on my humerus. The doctors at NIH said that it was probably a natural variant or groove within the bone, however I should have it compared to my PET/CTs from 2009 and 2012 from Dana-Farber to be sure, and to watch the area over time. More watching and watiting...awesome. When I saw Dr. R in April, I gave him the discs of my skeletal survey from 2009 (done when I was first diagnosed from a general hem/onc) as well as from the NIH, and the CT scan so he could compare them to the scans I'd had in Boston.
Turns out.... according to Dr. R and the radiologist at DFCI who reviewed all the skeletal surveys, PET/CTs, and the CT scan, apart from my osteopenia, this questionable "lucent lesion" identified at the NIH is in fact the insertion of the deltoid and normal.
Well, well, well... whaaaaaaaat?
Blows my mind. Who is right here?
So, apparently, this abnormality WAS in fact due to my bulging bicep...er, bulging deltoid? ;) Sweet.
In case you missed it.... I wrote about this experience here: Abnormal Skeletal Survey & Perfect Blood Work: NIH Day One and here: Bone Marrow Biopsy & CT Scan: NIH Day Two and here: Alliteration fan? Left (Humeral) Linear Lucent Lesion and here: Little Line = Left Linear (Humeral) Lucent Lesion
The CT scan revealed a "lucent lesion" on my humerus. The doctors at NIH said that it was probably a natural variant or groove within the bone, however I should have it compared to my PET/CTs from 2009 and 2012 from Dana-Farber to be sure, and to watch the area over time. More watching and watiting...awesome. When I saw Dr. R in April, I gave him the discs of my skeletal survey from 2009 (done when I was first diagnosed from a general hem/onc) as well as from the NIH, and the CT scan so he could compare them to the scans I'd had in Boston.
Turns out.... according to Dr. R and the radiologist at DFCI who reviewed all the skeletal surveys, PET/CTs, and the CT scan, apart from my osteopenia, this questionable "lucent lesion" identified at the NIH is in fact the insertion of the deltoid and normal.
Well, well, well... whaaaaaaaat?
Blows my mind. Who is right here?
So, apparently, this abnormality WAS in fact due to my bulging bicep...er, bulging deltoid? ;) Sweet.
Thursday, May 23, 2013
Whole Body MRI? Who knew.
Okay, so I've had scalp to toes PET/CTs, MRI of my spine, skeletal surveys, DEXA scan, and a CT of my arm...
BUT, with my crappy low bone density and humeral lucent lesion, I want a whole body MRI (wbMRI)! Sounds much more efficient than all this piecemeal baloney. Plus no radiation!
Totally going to ask about this test at my next appointment in July.
Abstract from ASCO:
Longitudinal whole body MRI (wbMRI) in monoclonal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma.
BUT, with my crappy low bone density and humeral lucent lesion, I want a whole body MRI (wbMRI)! Sounds much more efficient than all this piecemeal baloney. Plus no radiation!
Totally going to ask about this test at my next appointment in July.
Abstract from ASCO:
Longitudinal whole body MRI (wbMRI) in monoclonal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma.
Tuesday, May 21, 2013
$100,000 here, $100,000 there...
As I am a patient at Dana Farber, I get a lot of newsletters and mail from them. One newsletter I received the other day had an article about Dr. R.
The basic gist of the article was that a multiple myeloma patient Dr. R has had (since 1993...!!!) recently decided to give him $100,000 to support his research. Wow!
The basic gist of the article was that a multiple myeloma patient Dr. R has had (since 1993...!!!) recently decided to give him $100,000 to support his research. Wow!
Wouldn't it be nice to be rich? :)
The husband of the patient was quoted saying, "Causes don't raise money. People do. It was our absolute pleasure to support him, and our only hope is that when others learn of our gift, they too might be inspired to give what they can."
Monday, May 6, 2013
Things that make you go, "hmmmm"
IMF Video:
Multiple Myeloma: International Myeloma Foundation : Live! The Boca Raton Patient & Family Seminar
If you click the link and zip ahead to ~1:31:54 you will hear Dr. R say something along the lines of...antibodies...there is an emerging role of vaccination for minimal disease...moving toward tailored treatment and the goal of a functional cure...driving quality of life. Something like that. ;)
THEN ...
This next part of the discussion made me really take notice. Dr. RK, who is like the godfather of MGUS, was asked, "How do you see things moving forward?"
His response, which I found very, very interesting was this:
I think in the long, long, future what we need to address is smoldering myeloma and MGUS which are the precursors of multiple myeloma. Something has happened to that patient that allows this clone of plasma cells to escape and then it is limited in the case of MGUS and then in the patient of smoldering myeloma it's limited a little later on...the body has allowed that clone to grow larger and then for for some unforeseen reason has stopped its progression as well. So I think ultimately, if we can get to the point where we can do something about the MGUS when it appears if we can do something to wipe out that clone at that point in time we wont have to worry about anything else and that's the ultimate long, long, term goal.
Hmmm.... well, okay... So, in the "long, long" future they need need to address smoldering myeloma and MGUS and the ultimate "long, long" term goal is to do something about MGUS when it first appears? Um, how about let's make this a goal now?! :)
I watched to the end of this video... some interesting discussion around MGUS and SMM.
Multiple Myeloma: International Myeloma Foundation : Live! The Boca Raton Patient & Family Seminar
If you click the link and zip ahead to ~1:31:54 you will hear Dr. R say something along the lines of...antibodies...there is an emerging role of vaccination for minimal disease...moving toward tailored treatment and the goal of a functional cure...driving quality of life. Something like that. ;)
THEN ...
This next part of the discussion made me really take notice. Dr. RK, who is like the godfather of MGUS, was asked, "How do you see things moving forward?"
His response, which I found very, very interesting was this:
I think in the long, long, future what we need to address is smoldering myeloma and MGUS which are the precursors of multiple myeloma. Something has happened to that patient that allows this clone of plasma cells to escape and then it is limited in the case of MGUS and then in the patient of smoldering myeloma it's limited a little later on...the body has allowed that clone to grow larger and then for for some unforeseen reason has stopped its progression as well. So I think ultimately, if we can get to the point where we can do something about the MGUS when it appears if we can do something to wipe out that clone at that point in time we wont have to worry about anything else and that's the ultimate long, long, term goal.
Hmmm.... well, okay... So, in the "long, long" future they need need to address smoldering myeloma and MGUS and the ultimate "long, long" term goal is to do something about MGUS when it first appears? Um, how about let's make this a goal now?! :)
I watched to the end of this video... some interesting discussion around MGUS and SMM.
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