The Hematologic Malignancies Research Program at the University of New Mexico Cancer Center is a highly interactive transdisciplinary program with 25 Program Members from 4 Departments in the UNM School of Medicine (Medicine, Molecular Genetics and Microbiology, Pathology, and Pediatrics), 2 Departments on the UNM Main Campus (Mathematics, and Physics and Astronomy), and Los Alamos and Sandia National Laboratories. Research conducted by program members spans from the most basic interdisciplinary research, to translational investigations using human tissues and animal model systems, to the design of cancer clinical trials. The goals of the program are to: 1) use comprehensive genomic technologies and model systems to study the transcriptional regulation of hematopoiesis and the gene expression patterns of normal and leukemic cells in order to discover novel underlying genetic lesions in leukemia that may serve as new therapeutic targets;2) functionally characterize, image, and model signaling and adhesion pathways in normal and leukemic cells in order to understand how unique genetic abnormalities perturb these pathways to promote leukemogenesis and to identify targets for therapeutic intervention;and 3) translate program science and discoveries to novel diagnostic and therapeutic strategies and clinical trials at the UNM Cancer Center and within the NCI Cooperative Groups. Program members have used sophisticated genomic and computational technologies to develop gene expression classifiers for outcome prediction in leukemia and discover novel therapeutic targets in this disease (JAK2 mutations, CRLF2 activation, Metnase) that are being translated to clinical trials. These and other targets are also being studied in pre-clinical murine xenograft models to define the biochemical consequences of how these mutations perturb signaling pathways and to develop and test novel therapeutics. The development of advanced live cell imaging and spatiotemporal modeling technologies in the program are supporting high profile studies of receptors and signaling pathways involved in leukemogenesis. Since 2005, the program's funding and intra- and inter-programmatic interactions have significantly increased. Program members hold 3 interdisciplinary, multi-investigator, programmatic grants (one of 10 NIH National Centers for Systems Biology {P50GM085273;PI: Oliver);an LLS Specialized Center for Research in Leukemia {7388-06;PI: Willman);and a NCI Strategic Partnerships Grant {U01CA114762;PI: Willman)) and launched the first NCI TARGET Project to identify new therapeutic targets in high-risk pediatric ALL. Program members and their collaborators at St. Jude Children's Hospital and in the Children's Oncology Group have been notified of the awarding of a NCI ARRA TARGET Grant and a NCI ARRA Grand Opportunities Grant to continue to translate their work to leukemia clinical trials. As of September 2009, program members held $9,967,007 in total annual direct funding (representing a 44% increase in funding since 2005) of which $9,131,453 was peer-reviewed;annual direct NCI funding to the program has increased 55% to $2,448,182. In 2008, program members published a total of 64 cancer-relevant publications, of which 41 were intra-programmatic and 19% were inter-programmatic.

Public Health Relevance

The Hematologic Malignancies Research Program integrates a team of transdisciplinary basic, translational, and clinical scientists who use highly sophisticated genomic, computational, imaging, and modeling approaches in human leukemia specimens and animal model systems to study how novel underlying genetic mutations in leukemia perturb gene expression and signaling and adhesion pathways to promote leukemogenesis. Discoveries are actively being translated to new diagnostic strategies and therapeutic modalities at the UNM Cancer Center and within the NCI Cooperative Oncology Groups.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Center Core Grants (P30)
Project #
5P30CA118100-09
Application #
8545065
Study Section
Subcommittee G - Education (NCI)
Project Start
Project End
Budget Start
2013-09-01
Budget End
2014-08-31
Support Year
9
Fiscal Year
2013
Total Cost
$15,077
Indirect Cost
Name
University of New Mexico Health Sciences Center
Department
Type
DUNS #
829868723
City
Albuquerque
State
NM
Country
United States
Zip Code
87131
Castleman, Moriah J; Pokhrel, Srijana; Triplett, Kathleen D et al. (2018) Innate Sex Bias of Staphylococcus aureus Skin Infection Is Driven by ?-Hemolysin. J Immunol 200:657-668
Barton, Matthias; Filardo, Edward J; Lolait, Stephen J et al. (2018) Twenty years of the G protein-coupled estrogen receptor GPER: Historical and personal perspectives. J Steroid Biochem Mol Biol 176:4-15
Prossnitz, Eric R (2018) GPER modulators: Opportunity Nox on the heels of a class Akt. J Steroid Biochem Mol Biol 176:73-81
Perez, Dominique R; Nickl, Christian K; Waller, Anna et al. (2018) High-Throughput Flow Cytometry Identifies Small-Molecule Inhibitors for Drug Repurposing in T-ALL. SLAS Discov 23:732-741
Pallikkuth, Sandeep; Martin, Cheyenne; Farzam, Farzin et al. (2018) Sequential super-resolution imaging using DNA strand displacement. PLoS One 13:e0203291
Leng, Shuguang; Picchi, Maria A; Kang, Huining et al. (2018) Dietary Nutrient Intake, Ethnicity, and Epigenetic Silencing of Lung Cancer Genes Detected in Sputum in New Mexican Smokers. Cancer Prev Res (Phila) 11:93-102
Peretti, Amanda S; Dominguez, Dayna; Grimes, Martha M et al. (2018) The R-Enantiomer of Ketorolac Delays Mammary Tumor Development in Mouse Mammary Tumor Virus-Polyoma Middle T Antigen (MMTV-PyMT) Mice. Am J Pathol 188:515-524
Brandsma, Arianne M; Schwartz, Samantha L; Wester, Michael J et al. (2018) Mechanisms of inside-out signaling of the high-affinity IgG receptor Fc?RI. Sci Signal 11:
Zheng, Handong; Wu, Dandan; Wu, Xiang et al. (2018) Leptin Promotes Allergic Airway Inflammation through Targeting the Unfolded Protein Response Pathway. Sci Rep 8:8905
Ray, Anita L; Berggren, Kiersten L; Restrepo Cruz, Sebastian et al. (2018) Inhibition of MK2 suppresses IL-1?, IL-6, and TNF-?-dependent colorectal cancer growth. Int J Cancer 142:1702-1711

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