Active clinical trials for "Leukemia, Myeloid"

FLT3 overexpression in acute myeloid leukemia (AML) is often caused by mutations in this gene. These mutations cause constitutive phosphorylation of FLT3 proteins leading to increased proliferation and survival, decreased apoptosis and resistance to chemotherapeutic agents in AML cells. There are two major types of FLT3 mutations- internal tandem duplication (ITD) and point mutation at 835th amino residue. AMLs with FLT3 mutations have worse prognosis and are often resistant to conventional chemotherapy. Several small molecule compounds targeting FLT3 have been in the market or in clinical trials. Therefore, identification of these mutations at the time of diagnosis will provide a better prognostic prediction, might guide the treatment selection and follow-up strategies. In this study, the investigators will develop a sensitive molecular assay to detect FLT3 mutations for future clinical application. The investigators will collect 100 AML samples with at least 20 samples with known FLT3 mutations. The investigators will compare this assay with commonly used methods and standardize the procedure to meet the requirement of clinical pathology laboratory with reasonable cost.

Little is known about the epidemiologic risk factors associated with the development of acute myelogenous leukemia (AML), and less is known about the role that genetic susceptibility plays in the development of AML. We propose to conduct a population-based study to investigate genetic susceptibility in adult AML patients, both de novo and treatment-related in a well-defined geographical area. Using a case-control design, we will prospectively enroll 400 patients from Texas and 800 healthy controls. Controls will be recruited using random digit dialing, and will be matched to the cases by age, gender, and ethnicity. Epidemiological and demographic information will be obtained through personal interviews, and will be integrated with clinical information, cytogenetic data, and genotypic markers. Blood specimens will be collected on all participants, who will be genotyped for markers associated with activation and detoxification of chemical carcinogens, including chemotherapy drugs. Polymorphisms in genes such as cytochrome p450 (CYP2E1), glutathione S-transferases (GSTT1, GSTM1, GSTP1), epoxide hydrolase (HYL1), NADPH-quinone oxidoreductase (NQO1), and myeloperoxidase (MPO) will be analyzed. This study will provide insight into the role that these susceptibility markers, along with clinical epidemiological, and cytogenetic factors, play in the identification of people at risk of developing AML. Understanding how genetic predisposition and exogenous exposures interact to determine AML susceptibility will allow the development of prevention strategies in the future.