I had a clinic appointment yesterday and got my FACS and BMBx results:
Peripheral blood flow is unchanged over the past 3 months and holding at .04% hairies.
Aspirate flow is at 4% -- up from 2% last May.
BMBx immunostaining shows 5% infiltration. That means I'm no longer in remission.
It could be that my aspirate and blood flows always had hairies, but they were just masked by Rituxan until it detached from the cells and flushed out of my system. Still, the Rituxan treatments had an effect. Prior to Rituxan, my bone marrow infiltration at 6 months post-chemo was 30%. Now it's just 5%. Likewise, my blood counts are now about the best they've been since treatment started and they got a real boost after the Rituxan treatments.
The protocol calls for another round of Rituxan treatments at 6 months post-Rituxan if the peripheral blood flow is positive, so I'll be going in to NIH next Tuesday to get some more aspirate drawn for the PCR lab, then I'll start the first of 8 more Rituxan treatments (1 a week for 8 weeks) in the early afternoon.
The basic gist is this: given that my hairies' DNA doesn't bind to the baseline PCR primer used for the hyper-sensitive MRD analysis (and any variants they may have tried), my HCL genome is likely mutated from the norm such that they don't die as easily as most, even though they have more than 100,000 CD20 antigens and bind really well with the Rituxan. The exact nature of the mutation is still not known.
Since I was slow in responding to Cladribine and didn't get a knock-out punch from Rituxan, I wonder if the assumed mutation affects lipid raft function and restricts the biochemical reaction associated with hairy cell apoptosis and antibody-dependent cellular cytotoxicity (ADCC), but there's no way to know that for sure (for now anyway). Likewise, the high and fairly steady flow in the aspirate leads me to wonder if there is a significant physiological change or maturation of the cells as they move from the aspirate into the marrow and peripheral blood that makes the pb and marrow cells easier to kill (a more normal lipid raft structure)? Regardless, the prevailing theory is that the hairies in the aspirate are clumped together in a ball and the Rituxan can't peel away enough layers of the onion to eliminate them completely.
In any case, I'm hoping this round will provide more of a wallop since the bone marrow infiltration is less than before. Still, at 4%, the aspirate flow is the same as when I started Rituxan treatments in November of '09, so it's anyone's guess as to what we'll see a year from now.
Til then, I'll keep pushing the rock!
Merry Christmas to all and a Happy New Year too!
Peripheral blood flow is unchanged over the past 3 months and holding at .04% hairies.
Aspirate flow is at 4% -- up from 2% last May.
BMBx immunostaining shows 5% infiltration. That means I'm no longer in remission.
It could be that my aspirate and blood flows always had hairies, but they were just masked by Rituxan until it detached from the cells and flushed out of my system. Still, the Rituxan treatments had an effect. Prior to Rituxan, my bone marrow infiltration at 6 months post-chemo was 30%. Now it's just 5%. Likewise, my blood counts are now about the best they've been since treatment started and they got a real boost after the Rituxan treatments.
The protocol calls for another round of Rituxan treatments at 6 months post-Rituxan if the peripheral blood flow is positive, so I'll be going in to NIH next Tuesday to get some more aspirate drawn for the PCR lab, then I'll start the first of 8 more Rituxan treatments (1 a week for 8 weeks) in the early afternoon.
The basic gist is this: given that my hairies' DNA doesn't bind to the baseline PCR primer used for the hyper-sensitive MRD analysis (and any variants they may have tried), my HCL genome is likely mutated from the norm such that they don't die as easily as most, even though they have more than 100,000 CD20 antigens and bind really well with the Rituxan. The exact nature of the mutation is still not known.
Since I was slow in responding to Cladribine and didn't get a knock-out punch from Rituxan, I wonder if the assumed mutation affects lipid raft function and restricts the biochemical reaction associated with hairy cell apoptosis and antibody-dependent cellular cytotoxicity (ADCC), but there's no way to know that for sure (for now anyway). Likewise, the high and fairly steady flow in the aspirate leads me to wonder if there is a significant physiological change or maturation of the cells as they move from the aspirate into the marrow and peripheral blood that makes the pb and marrow cells easier to kill (a more normal lipid raft structure)? Regardless, the prevailing theory is that the hairies in the aspirate are clumped together in a ball and the Rituxan can't peel away enough layers of the onion to eliminate them completely.
In any case, I'm hoping this round will provide more of a wallop since the bone marrow infiltration is less than before. Still, at 4%, the aspirate flow is the same as when I started Rituxan treatments in November of '09, so it's anyone's guess as to what we'll see a year from now.
Til then, I'll keep pushing the rock!
Merry Christmas to all and a Happy New Year too!
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