Monica and I got to go to the Duke Lemur Center in Durham, NC today for business. It was great! I took some pictures through the fences with my iPhone camera, and this was the best of them. I’m afraid I can’t tell you what type of lemur this is, but I’ll find out.
Just before the meeting at the Lemur Center, I had a checkup at the Bone Marrow Transplant Clinic. I’ll have the results of my tests on Wednesday. It’s been almost two years since I had a skeletal survey, so I scheduled that for September. The skeletal survey is a series of xrays of the long bones, skull and ribs and spine. I asked about a recent report I read that suggests that PET scans should be used for monitoring myeloma. My doctor does those if there’s activity such as an increasing m-spike and nothing shows up on xrays. The PET can show plasmacytomas and other activity.
I’ve been told that standard radiographs aren’t much good at detecting bone damage until there’s been a significant amount of destruction, so it’s not a good early warning indicator. I’d like to have a PET scan just to see what’s lurking. I know they’re expensive. A few years ago I called around to get the costs at various places because I wanted one, but was told by my insurance company that they weren’t covered for myeloma. At the time, the cheapest PET scan I could find was about $3,000.
Did you know you can do that? If you’re not insured, or your coverage isn’t very good, call around to see who has the best deals on tests or procedures. The costs can vary quite significantly between institutions. Another money-saving tactic is to find out what’s covered under what setting. For example, my insurance has me pay 20% of services performed in hospitals. That’s why I have most of my chemo and all of my Zometa infused at a nearby doctor’s office. When I do that, it’s just a $30 copay. Investigate all of your options!
I was told about about a research project that’s underway. I have no affiliation with the group, so please do your due diligence. If you participate, let us know how it went.
We are currently looking for people that have suffered “oral mucositis” (mouth inflammation or sores) as a result of cancer treatment to participate in 45 min telephone interviews.
The purpose of this research is to understand what does or does not work as treatment for this condition.
The interviews can be scheduled this week and next and participants receive $100.
Please respond with interest to contacts below. If this is not you, please refer or post for others that may have interest.
Kind Regards
Jan Mallery-Groom RN
Clinical Project Manager
+510-922-9710
recruitingresourcesllc.com
I don’t have a lot to blog about here because my myeloma has been stable since last fall. There’s not much there at all. If you don’t have myeloma, I have only a little bit more than you do.
These labs were done 12/08/2008
IFE SERUM
(2) MONOCLONAL IgA-LAMBDAS DETECTED BY IFE.
SPE M-SPIKE 1 0.17 g/dL
SPE M-SPIKE 2 0.12 g/dL
IG FREE LIGHT CHAINS SERUMReference
IG FREE LIGHT CHAIN KAPPA *0.16mg/dL [0.33-1.94]
IG FREE LIGHT CHAIN LAMBDA 1.85mg/dL [0.57-2.63]
IG FLC KAPPA/LAMBDA RATIO *0.09 [0.26-1.65]
IMMUNOGLOBULIN PROFILE
IMMUNOGLOBULIN G *374mg/dL [588-1573]
TEST REPEATED TO CONFIRM
IMMUNOGLOBULIN A *415mg/dL [46-287]
TEST REPEATED TO CONFIRM
IMMUNOGLOBULIN M *31mg/dL [57-237]
TEST REPEATED TO CONFIRM
IMMUNOGLOBULIN E 13 IU/mL [4-269]
Gene Variants Can Predict Early or Late Mortality in Multiple Myeloma
Elsevier Global Medical News. 2008 Nov 11, MG Sullivan
Genetic variants in the DNA of patients with multiple myeloma appear to strongly influence survival, a groundbreaking new genomic study has concluded.
In this first pass at identifying genetic markers for survival, treatment response, and complications in the disease, a group of 3,400 variants predicted early or late mortality 76% of the time, Dr. Brian Van Ness said in an interview about the initial report (BMC Medicine 2008 Sept. 8 [doi: 10.1186/1741-7015-6-26]).
“Clearly, inherited genetics influenced survival,” said Dr. Van Ness
of the University of Minnesota, Minneapolis. “What we have not yet done is identify which specific variants are responsible for these differences. Our hypothesis is that it won’t be a single variant driving response or survival, but a complex interaction of many.”
After narrowing down the initial 3,404 candidate single nucleotide polymorphisms (SNPs), Dr. Van Ness and his colleagues are now focusing on 1,000 SNPs found to be most strongly associated with the outcome
measures. More studies are on the way using this genetic panel, he said.
Indeed, just 2 weeks after the first study appeared, a coinvestigator, Dr. Gareth Morgan of London’s Royal Marsden Hospital, published findings on the association between certain SNPs and the incidence of
treatment-associated venous thromboembolism (VTE). The analysis showed that some of the variants associated with thalidomide-related VTE occurred in pathways important in drug transport and metabolism.
“The effects of the SNPs associated with thalidomide-related VTE may be functional at the level of the tumor cell, the tumor-related microenvironment, and the endothelium,” Dr. Morgan and his colleagues wrote (Blood 2008 Sept. 19 [Epub ahead of print]).
“Another study, currently submitted, has identified an association between some of the variants and the development of severe myeloma bone disease,” Dr. Van Ness said.
The initial investigation used a genetic screen developed from two DNA data sets: cells from the Coriell Institute for Medical Research, and samples obtained from multiple myeloma patients enrolled in two
randomized drug trials, as well as some unaffected spouses. The samples came from white, black, Hispanic, and Asian patients from North America and Europe. The candidate SNPs, occurring on 983 genes, were chosen based on the most recent genetic research and included on a myeloma-specific gene-testing chip.
The investigators chose extremes of survival as the first test of the panel, because this comparison was most likely to show the effects of any genetic variant. “We took the worst outcomes – people who died in
the first year of their disease – and the best outcomes – those who survived at least 3 years without progression,” Dr. Van Ness said. After repeatedly running the screen on both data sets, the team concluded that, as a whole, it discriminated the survival groups correctly 76% of the time.
Further drilling down identified several SNPs of particular interest, including some associated with drug metabolism, transport, and export; a variant that induces myeloma apoptosis; one associated with cellular
migration and angiogenesis; and several linked to proliferative responses.
Although not designed to detect racial differences, the initial screen did identify some interesting variations: 401 of the SNP variants occurred only in black patients. In whites, there was no difference in these SNPs between cases and controls.
“We know that African Americans have a two- to threefold increase in the incidence of myeloma, but we don’t yet know why,” Dr. Van Ness said. “We’ll be trying to identify those genetic variants that might uniquely increase the risk for one race to develop myeloma over another.”
Neither this initial analysis nor subsequent ones will examine the possible interplay of environment with genetics. But, Dr. Van Ness said, such studies may be forthcoming. The International Myeloma Foundation of North Hollywood, Calif., is conducting a patient survey to begin assessing what role – if any – environmental exposure plays in disease development. The 36-page survey asks patients to detail their environmental, dietary, and geographical exposures. The National Cancer Institute will collaborate with the group in evaluating the data.
The International Myeloma Foundation is also the curator of the DNA samples used in the analysis through its Bank on a Cure program. “Bank on a Cure was developed by an international group of physicians and scientists to deal with a disease that’s difficult to deal with,” Dr. Van Ness said. “It’s not a high-incidence cancer, so it’s not easy to research.”
The Bank on a Cure group developed cooperative agreements with national and international clinical trial groups, and the studies were funded by the International Myeloma Foundation. While exploration of genetic variants relevant to multiple myeloma is in its infancy, Dr. Van Ness predicted the effect could be profound.
A couple of days ago I had blood drawn at Duke in Durham, NC. I should know in a few more days what the results are. They’re a little on the slow side where getting lab reports out are concerned. I’m not sure why it has to be that way. I haven’t had any tests since June, so I’m a bit anxious about it.
I signed up for a course to learn how to shoot and edit video! I’ll let you know how it is and will be sure to share some of my work. Stay tuned.
We recently learned that our local oncologist is retiring. He’s 52 years old and has had it with the medical profession, citing increasing difficulties with insurance companies and litigious Americans as a few of the reasons for early retirement. I’m really going to miss him. He was probably the best doctor I ever had in my life. He shoots straight from the hip and tells it like it is.
I’ll continue with my quarterly visits to Duke and will see the replacement doctor at this local practice every few months.
No blood was drawn, so it’ll be September before I have any test results to share again. In the mean time, I’ll assume I’m still stable and myeloma will stay in the deeper recesses of my mind. It’s been a pleasure to have been treatment free for almost a year now. I still have myeloma, but it’s been sitting still.
This is a chart of my IgA values since before the SCT last summer. I stopped Velcade and Doxil in July, 2007 and the SCT took place at the end of August. This is quantitative serum IgA in mg/dL. The test on 10/11/2007 was the first one I had after stem cell transplant.
I’ve never once regretted having the SCT, and only wish I had done it earlier. In my case, nothing was keeping the mm under control for very long. The SCT has allowed me to be off treatment for 10 months now, which is a long time for me.
Duke allows me to look at my lab results online, and I’ve been waiting to see what my m-spikes are (I have two). So far, they’ve stayed under 0.5 g/dL when added together. That’s so much better than the 3.4 g/dL they were back in 2003.
The reference range at Duke’s lab for IgA is 46 – 287.
I got the results of the tests done Monday at Duke. The full report was faxed to my office, and I haven’t seen it yet, but here’s what I have so far.
M-Spikes (I have two m-spikes)
Last month: 0.19 and 0.12 g/dL (Total is 0.31 g/dL)
This month: 0.16 and 0.22 g/dL (Total is 0.38 g/dL)
Immunoglobulin Profile
Last month: IgA 374 mg/dL Reference: 46-287
This month: IgA 465 mg/dL Reference: 46-287 (up 91)
Last month: IgG 709 mg/dL Reference: 588-1573
This month: IgG 603 mg/dL Reference: 588-1573 (down 106)
I have July and August here. Needless to say, I was fervently hoping for a drop in the IgA and an increase in the IgG. The one good thing is that the IgG is still in the normal range, where it has never been since I learned I had MM. It was usually below 300 mg/dL.
Can someone give me a good explanation about why I have two m-spikes? I’ve asked doctors about a zillion times, and I have either forgotten what they told me or didn’t understand it well enough to even remember.
Monica and I got to go to the Duke Lemur Center in Durham, NC today for business. It was great! I took some pictures through the fences with my iPhone camera, and this was the best of them. I’m afraid I can’t tell you what type of lemur this is, but I’ll find out.
