Graduate Studies Faculty

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Evan F. Lind, Ph.D.

Assistant Professor
Admin Unit: SOM-Molecular Microbiology & Immunology Department
Phone: 503 494-1347
Mail Code: L220
Programs:
Cell & Developmental Biology
Molecular Microbiology & Immunology
Program in Molecular & Cellular Biosciences
Cancer Biology
Research Interests:
AML, Leukemia, Hematopoietic Stem Cells, Infection, Autoimmunity, T Cells, Cancer AML, Leukemia, Hematopoietic Stem Cells, Infection, Immunology, Cancer, T cells, Dendritic Cells, Inflammation
Preceptor Rotations
Dr. Lind has not indicated availability for preceptor rotations at this time.
Faculty Mentorship
Dr. Lind is available as a mentor for 2016-2017.
Profile

The goal of my research is to better understand how inflammation regulates the dynamics of hematopoiesis.  Hematopoietic precursor cells must sense and then respond to infection by proliferating to increase bone marrow output, but the signals involved are still poorly defined.  We will test the hypothesis that inflammation caused by pathogens or autoimmunity can result in DNA damage and somatic mutations found in acute myeloid leukemia (AML).  Specifically, we will determine whether proliferation in the precursor pool induced during inflammatory responses increases the risk of genetic damage.  Interestingly, hematopoietic precursors in the DNA damage repair disease Fanconi Anemia (FA) have been shown to be sensitive to apoptosis induction by inflammatory molecules such as tumor necrosis factor alpha (TNFa)and interferon gamma (IFNg).  One question we will address is how inflammatory stimuli act upon the hematopoietic stem cells in vivo during systemic viral infection in an animal model of FA.  Data generated form these experiments should give insights into links between inflammation and bone marrow failure and leukemic transformation in FA. Further, we will use mouse models with mutations in genes identified to play a role in human myelodysplastic syndromes and leukemia (IDH1, Flt3, Jak2 and others) to study how inflammation due to pathogenic bacterial and viral infection may impact disease development.  Our studies will better inform us of the interaction between the immune system and blood precursors in the bone marrow in normal and neoplastic settings.  In the future this may allow for immune-based therapeutic interventions for hematological disorders.