Abstract

The ultimate objective of the research projects in this application is to improve our understanding of mechanisms of disease in human myeloid leukemias, and to explore new therapeutic options relating to the disease pathways under investigation. It is anticipated that the laboratory and murine will inform the clinical project, and that the clinical insights will feed back to the animal and laboratory projects for further assessment. Members of the Biostatistics core will provide assistance to all the research projects contained in this program.
The specific aims of Core C Biostatistics are: 1. To provide biostatistical collaboration for clinical research protocols. This includes all aspects of the design, conduct, analysis, and reporting of the clinical studies. 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 analysis of laboratory results in conjunction with, or as outcomes of, the clinical studies of Project 5. 3. To provide biostatistical collaboration for animal studies, including all aspects of the design and analysis of such studies. 4. To assist in the oversight of data management, other clinical support services, and the tracking of samples to Projects for analysis with data returned and computerized for statistical analysis.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA066996-12
Application #
7882406
Study Section
Special Emphasis Panel (ZCA1)
Project Start
Project End
Budget Start
2009-04-01
Budget End
2010-03-31
Support Year
12
Fiscal Year
2009
Total Cost
$66,730
Indirect Cost

  Institution

Name
Dana-Farber Cancer Institute
Department
Type
DUNS #
076580745
City
Boston
State
MA
Country
United States
Zip Code
02215

  Publications

Patel, Sanjay S; Kuo, Frank C; Gibson, Christopher J et al. (2018) High NPM1-mutant allele burden at diagnosis predicts unfavorable outcomes in de novo AML. Blood 131:2816-2825
Montero, Joan; Letai, Antony (2018) Why do BCL-2 inhibitors work and where should we use them in the clinic? Cell Death Differ 25:56-64
DeAngelo, Daniel J; Brunner, Andrew M; Werner, Lillian et al. (2018) A phase I study of lenalidomide plus chemotherapy with mitoxantrone, etoposide, and cytarabine for the reinduction of patients with acute myeloid leukemia. Am J Hematol 93:254-261
Fink, Emma C; McConkey, Marie; Adams, Dylan N et al. (2018) CrbnI391V is sufficient to confer in vivo sensitivity to thalidomide and its derivatives in mice. Blood 132:1535-1544
Wroblewski, Mark; Scheller-Wendorff, Marina; Udonta, Florian et al. (2018) BET-inhibition by JQ1 promotes proliferation and self-renewal capacity of hematopoietic stem cells. Haematologica 103:939-948
Konopleva, Marina; Letai, Anthony (2018) BCL-2 inhibition in AML: an unexpected bonus? Blood 132:1007-1012
Donovan, Katherine A; An, Jian; Nowak, Rados?aw P et al. (2018) Thalidomide promotes degradation of SALL4, a transcription factor implicated in Duane Radial Ray syndrome. Elife 7:
Lee, J Scott; Roberts, Andrew; Juarez, Dennis et al. (2018) Statins enhance efficacy of venetoclax in blood cancers. Sci Transl Med 10:
Liu, Bee Hui; Jobichen, Chacko; Chia, C S Brian et al. (2018) Targeting cancer addiction for SALL4 by shifting its transcriptome with a pharmacologic peptide. Proc Natl Acad Sci U S A 115:E7119-E7128
Kahn, Josephine D; Miller, Peter G; Silver, Alexander J et al. (2018) PPM1D-truncating mutations confer resistance to chemotherapy and sensitivity to PPM1D inhibition in hematopoietic cells. Blood 132:1095-1105

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