Secondary Hematologic Malignancies

Japanese researchers suggested in a retrospective study of patients treated with Temodar for Glioma, that there is an increased occurrence of secondary Myelodysplasia, leukemias and particularly Acute Lymphoblastic Leukemia.  It is interesting to look further, beyond the simple observation and speculate as to what leads to such a transformation at the gene level.
Leukemias are a disease not only of pathways, but of deep derangement at the Histone-DNA level and include particularly not only protein complexes similar to core binding factors, but also regulator genes which appear to be specifically amplified in leukemias!
It is pertinent to also look closer at Proteins Kinases affecting or interacting with DNA.  Temodar is an Alkylating agent per the researcher's report.
The interval between the treatment and the occurrence is also interesting, and suggests that the secondary Leukemia results from a secondary amplification of proliferative genes after the onslaught on cellular receptors by the chemical stimulus. The NK-kB, c-JUN must be in play.  Blocking these pathways could prevent such malignant occurrence. We will soon find that secondary malignancy could be prevented by simply blocking some tumor growth factors.  We don't need to accept these complications any more.  I learned that my first patient who was diagnosed with Hodgkin disease, a curable disease, died later on with an Acute Leukemia.  She was free of Hodgkin disease. Our current follow-up is inadequate in this regard, as we sit and wait for secondary leukemia to set in.  Lets look into blocking Tumor growth factors to stop secondary leukemias!