Since the last competing renewal, the Hematologic Malignancies and Bone Marrow Transplantation Program, formerly the Leukemia-Lymphoma/BMT Program, has greatly expanded in laboratory based and clinical/'translational research. Multiple Investigators have joined the Program and research projects have been Initiated In leukemia biology (the genomics/ proteomics and epigenetic targeting of leukemia and lymphoma), development of targeted therapies for leukemia, myeloma and lymphoma (epigenetic, MDM- 2, Notch/ ubiquitination and/ kinase pathways) and prevention of relapse after allogeneic BMT, In addition, the cutting edge research in basic biology and outstanding translational efforts in hematopoietic stem cells and graft-versus-host disease after BMT have been further expanded. The amount of peer reviewed funding, both federal and non-federal (Leukemia Lymphoma Society, Damon Runyon, etc.) has substantially increased. Peer-reviewed funding has more than doubled from $5.2 million at the last review to $13.4 million, including $2.8 million in NCI funding, in direct funding. Over this grant period, the 36 members of this program from seven departments have published 177 publications of which 25.4% are intra-programmatic and 37.3% are inter-programmatic. Clinical research has benefitted from the recruitment of prominent clinical investigators leading to an increase in Investigator-generated therapeutic studies, We have also expanded collaborations with industry to study novel drugs. Collectively, these Initiatives are leading to enhanced accrual of patients on clinical trials.

Public Health Relevance

The goal of the Hematologic Malignancies/BMT program is to improve the diagnosis and treatment of blood cancers. Including leukemia, lymphoma, and multiple myeloma through translation of high quality, novel basic and clinical research to benefit patients.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
2P30CA046592-24
Application #
8300281
Study Section
Subcommittee G - Education (NCI)
Project Start
2012-06-01
Project End
2017-05-31
Budget Start
2012-09-21
Budget End
2013-05-31
Support Year
24
Fiscal Year
2012
Total Cost
$490,872
Indirect Cost
$174,999
Name
University of Michigan Ann Arbor
Department
Type
DUNS #
073133571
City
Ann Arbor
State
MI
Country
United States
Zip Code
48109
Harvey, Innocence; Stephenson, Erin J; Redd, JeAnna R et al. (2018) Glucocorticoid-Induced Metabolic Disturbances Are Exacerbated in Obese Male Mice. Endocrinology 159:2275-2287
Schuetze, Scott M; Bolejack, Vanessa; Thomas, Dafydd G et al. (2018) Association of Dasatinib With Progression-Free Survival Among Patients With Advanced Gastrointestinal Stromal Tumors Resistant to Imatinib. JAMA Oncol 4:814-820
Wagner, Vivian P; Martins, Manoela D; Martins, Marco A T et al. (2018) Targeting histone deacetylase and NF?B signaling as a novel therapy for Mucoepidermoid Carcinomas. Sci Rep 8:2065
Hosoya, Tomonori; D'Oliveira Albanus, Ricardo; Hensley, John et al. (2018) Global dynamics of stage-specific transcription factor binding during thymocyte development. Sci Rep 8:5605
Schofield, Heather K; Tandon, Manuj; Park, Min-Jung et al. (2018) Pancreatic HIF2? Stabilization Leads to Chronic Pancreatitis and Predisposes to Mucinous Cystic Neoplasm. Cell Mol Gastroenterol Hepatol 5:169-185.e2
Su, Wenmei; Feng, Shumei; Chen, Xiuyuan et al. (2018) Silencing of Long Noncoding RNA MIR22HG Triggers Cell Survival/Death Signaling via Oncogenes YBX1, MET, and p21 in Lung Cancer. Cancer Res 78:3207-3219
Moody, Rebecca Reed; Lo, Miao-Chia; Meagher, Jennifer L et al. (2018) Probing the interaction between the histone methyltransferase/deacetylase subunit RBBP4/7 and the transcription factor BCL11A in epigenetic complexes. J Biol Chem 293:2125-2136
Ma, Vincent T; Boonstra, Philip S; Menghrajani, Kamal et al. (2018) Treatment With JAK Inhibitors in Myelofibrosis Patients Nullifies the Prognostic Impact of Unfavorable Cytogenetics. Clin Lymphoma Myeloma Leuk 18:e201-e210
Collins, Dalis; Fry, Christopher; Moore, Bethany B et al. (2018) Phagocytosis by Fibrocytes as a Mechanism to Decrease Bacterial Burden and Increase Survival in Sepsis. Shock :
Wang, Xuexiang; Dande, Ranadheer R; Yu, Hao et al. (2018) TRPC5 Does Not Cause or Aggravate Glomerular Disease. J Am Soc Nephrol 29:409-415

Showing the most recent 10 out of 1493 publications