The purpose of the Core C Biostatistics is to assure that studies conducted through this P01 to develop novel therapeutic strategies in myeloid malignancies are conceptualized under robust principles of statistical design and are analyzed appropriately.
Specific Aim 1. To provide biostatistical collaboration for clinical research protocols. Biologically motivated clinical research protocols in this P01 are conducted through Core D as in vivo human experiments on behalf of the projects. Support by Core C includes all aspects of the design, conduct, analysis, and reporting of the clinical studies, as well as oversight of the electronic data capture mechanism.
Specific Aim 2. To provide biostatistical collaboration for the laboratory research studies. This includes all aspects of the design, conduct, analysis, and reporting of such studies, as well as the association between laboratory results and clinical outcomes both in prospective clinical studies of new agents and in retrospective studies involving sequencing and identification of mutations and their associations with both clinical features of disease and with clinical outcomes. 3. To provide biostatistical collaboration for animal studies, including all aspects of the design and analysis of murine studies.

Public Health Relevance

Core C Biostatistics will assure that all experiments conducted through this P01 in myeloid malignancies will have robust statistical designs and appropriate statistical analysis, to optimize our ability to identify novel therapeutic strategies and improve our understanding of the biology of myeloid malignancies.

National Institute of Health (NIH)
National Cancer Institute (NCI)
Research Program Projects (P01)
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Special Emphasis Panel (ZCA1-RPRB-C (J1))
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Brigham and Women's Hospital
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Hanoun, Maher; Zhang, Dachuan; Mizoguchi, Toshihide et al. (2014) Acute myelogenous leukemia-induced sympathetic neuropathy promotes malignancy in an altered hematopoietic stem cell niche. Cell Stem Cell 15:365-75
Adamia, Sophia; Bar-Natan, Michal; Haibe-Kains, Benjamin et al. (2014) NOTCH2 and FLT3 gene mis-splicings are common events in patients with acute myeloid leukemia (AML): new potential targets in AML. Blood 123:2816-25
Heckl, Dirk; Kowalczyk, Monika S; Yudovich, David et al. (2014) Generation of mouse models of myeloid malignancy with combinatorial genetic lesions using CRISPR-Cas9 genome editing. Nat Biotechnol 32:941-6
Adamia, Sophia; Haibe-Kains, Benjamin; Pilarski, Patrick M et al. (2014) A genome-wide aberrant RNA splicing in patients with acute myeloid leukemia identifies novel potential disease markers and therapeutic targets. Clin Cancer Res 20:1135-45
Bruedigam, Claudia; Bagger, Frederik O; Heidel, Florian H et al. (2014) Telomerase inhibition effectively targets mouse and human AML stem cells and delays relapse following chemotherapy. Cell Stem Cell 15:775-90
Santos, Margarida A; Faryabi, Robert B; Ergen, Aysegul V et al. (2014) DNA-damage-induced differentiation of leukaemic cells as an anti-cancer barrier. Nature 514:107-11
Schneider, Rebekka K; Ademà, Vera; Heckl, Dirk et al. (2014) Role of casein kinase 1A1 in the biology and targeted therapy of del(5q) MDS. Cancer Cell 26:509-20
Liu, Suiyang; Yin, Li; Stroopinsky, Dina et al. (2014) MUC1-C oncoprotein promotes FLT3 receptor activation in acute myeloid leukemia cells. Blood 123:734-42
Liss, Adam; Ooi, Chia-Huey; Zjablovskaja, Polina et al. (2014) The gene signature in CCAAT-enhancer-binding protein * dysfunctional acute myeloid leukemia predicts responsiveness to histone deacetylase inhibitors. Haematologica 99:697-705
Ng, C E L; Sinha, A; Krivtsov, A et al. (2014) KRas(G12D)-evoked leukemogenesis does not require *-catenin. Leukemia 28:698-702

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