Chronic myelomonocytic leukemia

Decitabine is specifically indicated for the treatment of multiple types of myelodysplastic syndromes and chronic myelomonocytic leukemia. As anticipated, use of decitabine is associated with bone marrow suppression including neutropenia and thrombocytopenia which are the most frequently observed serious adverse effects. 

As well as NONOates, other NO donors also showed anticancer activity independently. Sodium nitroprusside (SNP), a metal-NO complex, showed cytotoxic effects on the cells of some patients with malignant lymphoma (ML), acute myelocytic leukemia (AML) or chronic myelomonocytic leukemia (CMMoL), but not with multiple myeloma [109]. SNP and cytosine arabinoside (Ara-C) did not share the drug resistance. Interestingly, SNP had no effect on lymphocytes of healthy volunteers. These results suggest that SNP has an anti-tumor effect on human hematological malignant cells. 

DAC (decitabine) II syndrome, chronic myelomonocytic leukemia MDS, chromic SuperGen/... 

Immune hemolytic anemia has been reported in a 67-year-old man taking mercaptopurine for chronic myelomonocytic leukemia (17). Serology showed a positive direct antiglobuhn test and confirmed the presence of mercaptopurine drug-dependent antibodies. He improved and the direct antiglobulin test was no longer positive 20 days after mercaptopurine withdrawal. 

The longer-term effects of immunosuppression, and in particular the residual hematological and immunological abnormalities in patients with aplastic anemia treated with antilymphocjde globulin, have been documented there is toxicity to hemopoietic cells, eventually leading to clonal marrow diseases years after treatment (37). Paroxysmal nocturnal hemoglobinuria, refractory sideroblastic anemia, chronic myelomonocytic leukemia, or acute leukemia can develop 4-10 years after treatment (40). 

There have been reports of acute leukemia (SEDA-10, 125) and neutropenia (SEDA-5, 151) during PUVA and one dubious report of preleukemia (SEDA-4, 105). Transformation of stable chronic myelomonocytic leukemia to acute myeloid leukemia has been attributed to PUVA (SEDA-14,124). These events may aU have been purely coincidental and not causally related, as PUVA does not appear to increase the risk of non-cutaneous mahgnancies (16). 

CML patients characteristically exhibit relative and absolute monocytosis in peripheral blood reminiscent of chronic myelomonocytic leukemia. Another distinct but rare fusion that has been described in t(9 22)-positive CML is one that results in the formation of a large 230kDa fusion protein as a consequence of a fusion between exon 19 (c3) of BCJ and exon 2 (a2) of ABL. The BCR breakpoints for this fusion are located in the micro breakpoint cluster region (jX-BCl ) located between exons 19 and 20 (see Figure 39-14). The p230 fusion is characteristic of a peculiar form of CML with prominent neutrophilic proliferation. The clinical course of p230-positive CML is reportedly indolent in the majority of cases. ... 

Azacitidine is a DNA demethylation agent, that causes hypomethylation of DNA and direct cytotoxicity on abnormal hematopoietic cells in bone marrow. Azacitidine is indicated in the treatment of myelodysplastic syndrome subtypes refractory anemia or refractory anemia with ringed sideroblasts (if accompanied by neutropenia or thrombocytopenia or requiring transfusions), refractory anemia with excess blasts, refractory anemia with excess blasts in transformation, and chronic myelomonocytic leukemia. 

Factor-Receptor PDGFR Translocation Cell membrane Chronic myelomonocytic leukemia... 

DAC (decitabine) II myelomonocytic leukemia Chronic myelogenous MDACC NCI/MDACC... 

Melo JV, Myint H, Galton DA, Goldman JM. P190BCR-ABL chronic myeloid leukaemia the missing linlc with chronic myelomonocytic leukaemia Leukemia 1994 8 208-11. 

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