Tom Paul | CaringBridge
Breakfast of Champions

Tom Paul

First post: 10/11/2016 Latest post: 5/14/2017
Thanks for visiting.

In the spring of 2015 I felt that, physically, I was beginning to "slow down."  I knew I needed to exercise more, eat better, etc., etc.  I observed people 20 years older than I continuing an active lifestyle and I began to wonder if I'd ever get "back in shape."  

By May (2015) my Fitbit was telling me that after walking two blocks, my heart rate was 147.   I'd hope for a red light so that I could stop, rest,  and not cross to the next block.  Something was clearly not right.  I went to my doctor and told him I thought there was something wrong with my heart.  Did a few tests.  My hemoglobin was 6.8 grams per deciliter ("low" is less than 13.5).  Colonoscopy, endoscopy, pill significant bleeding.

I was diagnosed with high-risk IgG kappa multiple myeloma with 17p deletion (bone marrow cancer) in July of 2015.  After doing a little homework, I applied for and was assigned to a clinical trial studying the efficacy of elotuzumab (defined below)  in newly diagnosed, previously untreated patients.  My chemotherapy consisted of elotuzumab, along with the standard RVD (Revlimid, Velcade and Dexamethasone).      After six months of heavy chemo, I took a six-week break, and began maintenance doses of the same drugs, which would theoretically continue for the rest of my life (myeloma has no cure).  As of July, 2016 I had achieved a "complete response;"  in remission from cancer.

In September, it became clear that the maintenance dosages were not quite doing the trick, and my immunoglobulin IgG and kappa free light chains were ramping up again.  Since the dosages in the clinical trial are prescribed, I can't go back to the dosages that were working, unless insurance covers it, which it didn't.  In early October, I began a regimen of  carfilzomib, Revlimid and dexamethazone.   And lots of it.  That was completely ineffective.  A stem cell transplant scheduled for early November was postponed, and I was admitted to inpatient chemotherapy on 10/28 for a 96 hour infusion of  Cisplatin, Doxorubicin,Cyclophosphamide, and Etoposide, with (evil) Velcade, Revlimed and Dexamethazone.  The side effects (finally lost my hair) were significant, and a month later, I did it again (but at home -- kind of a challenge, but better than a hospital stay).  

I spent the month of January at Mayo Clinic getting a stem cell transplant.  My oncologists recommended another, because of the aggressive nature of "my myeloma."  So as I'm sick and tired, and 20 pounds lighter, I get to think about doing it again.

 In a nutshell, the transplant was effective; no cancer cells were detected in my bone marrow 2 months post=transplant.  And a second transplant (see the Day 88 update) was still on the table, because we've been here before (i.e., remission).  However, the transplant was cancelled because the cancer had returned rather than go through a second transplant just to end up where I am now, we're going to do something different (see day 110 update).
That's the short version.  So far.  

What follows is some information related to some of the big words in the paragraph above.  Consider it a work in progress...


What is 17p deletion?  
We have 46 chromosomes—22 pairs of chromosomes that affect the body as a whole and one pair that determines and regulates gender.  I have a problem with one of the number 17 chromosomes. Chromosomes look like an X,  with a smaller upper half and a large bottom half. The smaller top part is designated as "p."  A portion of the upper part of chromosome 17 is missing.  Each area of a chromosome carries  specific information (genes).   Since a portion of the chromosome is lost (deleted) those genes are no longer present. Within the band of the chromosome that I am missing is a gene that allows a cell to recognize and eliminate cells that don't make the quality grade. It is called p53 and is in a class of genes called tumor suppressor genes. I am  missing that, so my cells are unable to use this pathway to prevent and control any malignant cells.  It is the most treatment resistant form of Multiple Myeloma.

Elotuzumab (now marketed as Empliciti) a monoclonal antibody,  one of the new generation of chemo drugs that works with your own immune system to attack cancer cells.  It directly activates immune cells known as Natural Killer (NK) cells and helps NK-mediated killing of myeloma cells.  

A steroid.  If you're "in the system," as I'll call it, I know that I need say no more.  It used to prevent me from sleeping...not so much at this point.

Revlimid (lenolidamide)
Common chemo drug, chemically similar to thalidomide.

Carfilzomib (marketed as Kyprolis)
This is a proteasome inhibitor.  It replaced my Velcade (bortezomib), which in many cases, including mine,  causes peripheral neuopathy.  Proteasomes are cellular complexes that break down proteins. In myeloma, the proteins that normally kill cancer cells are broken down too quickly.  This drug interrupts this process and lets those proteins kill the cancer cells.  I'm back on Velcade now to try and beat this thing back again.

Immunoglobulin and Kappa Free Light Chains
For the moment, if you want to know more about these, check out Wikipedia....

CaringBridge is a nonprofit social network dedicated to helping family and friends communicate with and support loved ones during a health journey. Learn more about CaringBridge.

To interact with Tom’s website, sign in or register today.

By registering with CaringBridge, you will join over 300,000 people a day who are supporting friends and family members.

Sign In Or Register