Article

Therapy-related myeloid leukemia.

Department of Medicine and Cancer Research Center, University of Chicago, Chicago, IL 60637, USA. <>
Seminars in Oncology (Impact Factor: 3.94). 09/2008; 35(4):418-29. DOI: 10.1053/j.seminoncol.2008.04.012
Source: PubMed

ABSTRACT Therapy-related myelodysplastic syndrome and acute myeloid leukemia (t-MDS/t-AML) are thought to be the direct consequence of mutational events induced by chemotherapy, radiation therapy, immunosuppressive therapy, or a combination of these modalities, given for a pre-existing condition. The outcomes for these patients have been poor historically compared to people who develop de novo AML. The spectrum of cytogenetic abnormalities in t-AML is similar to de novo AML, but the frequency of unfavorable cytogenetics, such as a complex karyotype or deletion or loss of chromosomes 5 and/or 7, is considerably higher in t-AML. Survival varies according to cytogenetic risk group in t-AML patients, with better outcomes being observed in those with favorable-risk karyotypes. Treatment recommendations should be based on performance status and karyotype. A deeper understanding of the factors that predispose patients to the development of therapy-related myeloid leukemia would help clinicians monitor patients more carefully after treatment for a primary condition. Ultimately, this knowledge could influence initial treatment strategies with the goal of decreasing the incidence of this serious complication.

0 Bookmarks
 · 
208 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: In the 10 years since the discovery of lysine-specific demethylase 1 (LSD1), this epigenetic eraser has emerged as an important target of interest in oncology. More specifically, research has demonstrated that it plays an essential role in the self-renewal of leukemic stem cells in acute myeloid leukemia (AML). This review will cover clinical aspects of AML, the role of epigenetics in the disease, and discuss the research that led to the first irreversible inhibitors of LSD1 entering clinical trials for the treatment of AML in 2014. We also review recent achievements and progress in the development of potent and selective reversible inhibitors of LSD1. These compounds differ in their mode of action from tranylcypromine derivatives and could facilitate novel biochemical studies to probe the pathways mediated by LSD1. In this review, we will critically evaluate the strengths and weaknesses of published series of reversible LSD1 inhibitors. Overall, while the development of reversible inhibitors to date has been less fruitful than that of irreversible inhibitors, there is still the possibility for their use to facilitate further research into the roles and functions of LSD1 and to expand the therapeutic applications of LSD1 inhibitors in the clinic.
    Medicinal Research Reviews 11/2014; · 8.13 Impact Factor
  • Leukemia Research 10/2014; · 2.69 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Therapy-related leukemia is a well-documented complication of conventional therapy for cancer. Therapy-related acute myeloid leukemia (t-AML) is grouped along with therapy-related myelodysplastic syndrome (t-MDS) and therapy-related myelodysplastic syndrome/myeloproliferative neoplasms (t-MDS/MPN) as therapy-related myeloid neoplasms (t-MN) by the 2008 WHO classification system. Therapy-related myeloid neoplasms differ clinically from their de novo counterparts in terms of response to therapy, aggressiveness of disease, and associated poor prognosis.Occurrence of extramedullary myeloid sarcomas with bone marrow involvement has been shown to be a poor prognostic indicator for patients with t-MN. The karyotype of leukemic blasts has also been reported to have a significant impact in t-MN and may predict survival and outcomes in patients. The t(8;16)(p11.2;p13.3) is a rare, balanced translocation that is frequently associated with the M4/M5 subtype of de novo acute myeloid leukemia. It has also been reported in patients with t-MN, typically with poor outcomes. Here we report a case of t-MN with myeloid sarcoma and bone marrow involvement in an adult patient with a karyotype of 47,XY,t(8;16)(p11.2;p13.3),+21 after R-CHOP chemotherapy for follicular lymphoma.
    Cancer Genetics 10/2014; · 2.42 Impact Factor

Preview

Download
0 Downloads
Available from