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Hi Lisa,
I usually don't post here, but I was browsing to see if anybody knows why Bruce's site is down (it still is). I lost my collection of AA articles because my computer crashed, but from memory, Trisomy 8 is the most common cytogenetic abnormality developed post ATG. The clone itself is the target of the immune system. The immune system tries to attack the clone, and it suppresses the normal marrow too, via collateral damage. As you are suppress the immune system with ATG + CsA, the clone is allowed to expand and it becomes more visible.The conclusion of the articles was that ATG does NOT create Trisomy 8, and patients with Trisomy 8 usually require maintenance CsA, because of the ongoing "irritation" which the clone produces. Without CsA the marrow is suppressed again, and the patient returns to severe pancytopenia and transfusion dependence.
One third of the MDS patients repond to IST (ATG + CsA) and Trisomy 8 patients belong to this group, because the pathogenesis of their pancytopenia is immune-mediated.
It is possible that some patients have a small clone under the level of detection at diagnosis, and the clone expands with the rest of the marrow. In some other patients the clone might evolve during the period of severe pancytopenia due to the stress of the Stem Cell Compartment (few stem cells are forced in overdrive, and don't have time to correct mutations).
Hope this helps.
Dan
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