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Notice to Announce Additional Research Objectives and Funding for PAS-10-046: Stimulating Hematology Investigation:New Endeavors (SHINE) (R01)
Issued by: National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Purpose: The NIDDK is pleased to announce additional research objectives and funding for PAS-10-046: Stimulating Hematology Investigation: New Endeavors (SHINE) (R01).
This Notice provides two updates to PAS-10-046:
1) An additional $1,250,000 has been set aside in fiscal year 2011 to make approximately 3 – 4 awards issued under this FOA in addition to those funded within NIDDK regular funding policies
2) A new SHINE-eligible research area, “Biology and Pathophysiology of Myelodysplastic Syndrome (MDS),” has been added to the SHINEFOA
In addition to the research objectives listed in PAS-10-046,
R01 applications requesting support for research on “Biology and Pathophysiology of Myelodysplastic Syndromes (MDS)” will now be accepted under PAS-10-046.
This additional research area has been added in response to a workshop on MDS held by the American Society of Hematology August 29, 2008 and an NIDDK-hosted Hematology Research Interagency Coordinating Committee meeting on MDS, May 10, 2010. Research questions to be addressed by projects on MDS eligible for submission underPAS-10-046 include, but are not limited to:
- What is the role of hematopoietic stem cell aging and senescence in MDS predisposition and pathogenesis? Relevant studies include those that examine heritable genetic mutations affecting telomere maintenance; age-dependent changes in epigenetic control and patterns of microRNA expression that may contribute to stem cell depletion and skewing toward myeloid commitment; age-dependent changes in the capacity for DNA repair; andage-dependent changes in the hematopoietic bone marrow niche.
- What are the molecular genetic and epigenetic determinants of MDS? While development of MDS may be influenced by polygenic (multifactorial) inheritance,there is increasing evidence that acquired epigenetic abnormalities, such as global and gene-specific methylation changes that affect tumor suppressor gene expression and function, may lead to the onset and progression of MDS. Studies of such genetic and epigenetic determinants of MDS, as well as studies of the effects of transcriptional dysregulation in MDS on hematopoietic cell differentiation and function are relevant to this FOA. Relevant experimental approaches could include the application of sensitive molecular array technologies, such as those that identify SNP variants and miRNA expression patterns, to identify unrecognized sites of gene deregulation andgene expression signatures that have biological, prognostic and diagnostic significance in MDS. Whole exome or genome sequencing and genomic methylation tiling are other potentially relevant experimental approaches to identifyinggenetic and epigenetic determinants of MDS.
All other policies and aspects of this FOA remain the same.
Inquiries:
Terry Rogers Bishop, Ph.D.
National Institute of
Diabetes and Digestive and Kidney Diseases (NIDDK)
6707 Democracy Boulevard,
Room 619
Bethesda, MD 20892-5658
TEL: 301-594-7726
FAX: 301-480-3510
EMAIL: tb232j@nih.gov
Or
Daniel Wright, M.D.
National Institute of Diabetes and
Digestive and Kidney Diseases (NIDDK)
6707 Democracy Boulevard, Room 621
Bethesda, MD 20892-5658
TEL: 301-594-7714
FAX: 301-480-3510
EMAIL: dw341u@nih.gov