Drugs that target topoisomerase II, such as etoposide and anthracyclines may induce the second type of t-AML. It occurs in a Fenoprofen Calcium median of 2 years and is not preceded by MDS. Cytogenetic analysis shows a high frequency of rearrangements of chromosome band 11q23 but also recurrent balanced rearrangements t, t and inv. The prognosis is poor in t-AML, excepted in case of t, t and inv which follow the same course as p-AML and the karyotype is more frequently modified with at least 2 abnormalities or more. p-AML are also heterogeneous entities, classified according to bone marrow cell morphology and karyotype with the recent addition of several gene mutations. AML was among the first diseases to be treated and monitored according to somatic acquired chromosomal abnormalities, including the first successful targeted treatment against a pathological gene product in AML3. Thus, even though the major pathological hallmarks of prion disease are spongiform degeneration and gliosis in the brain, prion infection and the conversion of PrPC to PrPSc are not necessarily restricted to brain areas but can also occur in peripheral lymphoid tissues such as spleen and lymph nodes. The conversion of PrPC to PrPSc and the spread of the prion agent from peripheral sites of infection to the brain and vice versa are key events in the pathogenesis of prion diseases. However, in some pathological contexts such as inflammation, prion infectivity and PrPSc can be found in tissues that are not normally associated with prion infection. Indeed, chronic Glyburide inflammatory conditions such as nephritis, hepatitis or mastitis can lead to changes in the distribution of scrapie infectivity in the organism although the mechanisms involved are poorly understood. Recently, we found that co-infection of scrapie-infected mouse fibroblast cells with the Moloney Murine Leukemia retrovirus strongly enhanced the release and spread of scrapie infectivity in cell culture. Specifically, we found that PrPSc and infectivity were associated with Mo-MuLV viral particles as well as exosomes and observed that Mo-MuLV infection strongly stimulated the release of exosomes. In agreement with our findings, the small-ruminant caprine arthritis encephalitis lentivirus was also found to enhance PrPSc accumulation in coinfected, cultured sheep microglial cells as well as culture supernatant. Similarly, Ligios et al. showed that the lentivirus Maedi Visna virus, a common cause of lymphofollicular mastitits in sheep, leads to an inflammatory response which is associated with an increase in prion propagation and secretion of prions into milk. Taken together, the data suggest that retroviral coinfection might facilitate the spread of prions in vivo by significantly increasing the level of PrPSc released from infected tissues.