{
"METABOLOMICS WORKBENCH":{"STUDY_ID":"ST000308","ANALYSIS_ID":"AN000488","VERSION":"1","CREATED_ON":"January 5, 2016, 3:49 pm"},

"PROJECT":{"PROJECT_TITLE":"Leukemia stem cells studies","PROJECT_TYPE":"Glycolysis/TCA/Nucleotide analysis (tissue/cells)","PROJECT_SUMMARY":"Define the function of AMPK metabolic sensor in leukemia stem cells","INSTITUTE":"Baylor College of Medicine","DEPARTMENT":"Molecular and Human genetics","LABORATORY":"Nakada Lab","LAST_NAME":"Nakada","FIRST_NAME":"Daisuke","ADDRESS":"Houston, TX","EMAIL":"nakada@bcm.edu","PHONE":"713-798-1175"},

"STUDY":{"STUDY_TITLE":"13C mass isotopomer analysis (LCMS flux studies) MLL-AF9 (part I)","STUDY_TYPE":"1,2-13C2 Flux analysis","STUDY_SUMMARY":"How cancer cells adapt to metabolically adverse conditions in patients and strive to proliferate is a fundamental question in cancer biology. Here we show that AMP-activated protein kinase (AMPK), a metabolic checkpoint kinase, confers metabolic stress resistance to leukemia-initiating cells (LICs) and promotes leukemogenesis. Upon dietary restriction, MLL-AF9-induced murine acute myeloid leukemia (AML) activated AMPK and maintained leukemogenic potential. AMPK deletion significantly delayed leukemogenesis and depleted LICs by reducing the expression of glucose transporter 1 (Glut1), compromising glucose flux, and increasing oxidative stress and DNA damage. LICs were particularly dependent on AMPK to suppress oxidative stress in the hypoglycemic bone marrow environment. Strikingly, AMPK inhibition synergized with physiological metabolic stress caused by dietary restriction and profoundly suppressed leukemogenesis. Our results indicate that AMPK protects LICs from metabolic stress and that combining AMPK inhibition with physiological metabolic stress potently suppresses AML by inducing oxidative stress and DNA damage. Research is published: http://www.sciencedirect.com/science/article/pii/S1934590915003744","INSTITUTE":"University of Michigan","DEPARTMENT":"Molecular and Human genetics (Baylor College of Medicine)","LABORATORY":"Nakada Lab (Baylor College of Medicine)","LAST_NAME":"Saitoh","FIRST_NAME":"Yusuke","ADDRESS":"Houston, TX","EMAIL":"Yusuke.Saitoh@bcm.edu","PHONE":"713-798-1175","NUM_GROUPS":"7","TOTAL_SUBJECTS":"18","STUDY_COMMENTS":"1. Collect leukemia cells from MLL-AF9 leukemia mouse bone marrow. 2. Leukemia cell were cultured in RPMI1640 medium for 16hr. 3. Cell pellets were resuspend in pre-warmed labeling medium containing 1,2-13C2-glucose(2g/L) and incubated for 5min (sample 5) or 60min(sample 60).","PUBLICATIONS":"http://www.sciencedirect.com/science/article/pii/S1934590915003744"},

"SUBJECT":{"SUBJECT_TYPE":"Animal","SUBJECT_SPECIES":"Mus musculus","TAXONOMY_ID":"10090"},
"SUBJECT_SAMPLE_FACTORS":[
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"COLLECTION":{"COLLECTION_SUMMARY":"None available, see publication","SAMPLE_TYPE":"Cells"},

"TREATMENT":{"TREATMENT_SUMMARY":"None, see publication"},

"SAMPLEPREP":{"SAMPLEPREP_SUMMARY":"See attached file."},

"CHROMATOGRAPHY":{"CHROMATOGRAPHY_TYPE":"HILIC","INSTRUMENT_NAME":"Agilent 1260","COLUMN_NAME":"Phenomenex Luna NH2 (150 x 1mm, 3um)"},

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