Michelle D. Tallquist, PhD
- Full Member
Cancer Biology Program
University of Hawaii Cancer Center
- Associate Professor in Medicine
Center for Cardiovascular Research
John A. Burns School of Medicine
University of Hawaii at Manoa
- Graduate Faculty Chair
Program in Cell and Molecular Biology
Program in Developmental and Reproductive Biology
John A. Burns School of Medicine
- Graduate Faculty
Program in Molecular Biosciences and Bioengineering
College of Tropical Agriculture and Human Resources
- PhD, Immunology
Mayo Graduate School of Medicine
In the area of cancer research, much emphasis has been placed on the reduction or elimination of the tumor cell, but as survival rates improve for a variety of cancers we are learning that other complications need to be addressed. Our research focuses on the cardiac fibroblast. We have two lines of research related to the cardiac fibroblast and cancer. First, we have identified that mutations in Nf1, which can lead to neurofibromatosis also cause susceptibility to cardiac fibrosis. Second, several cancer therapies such as doxirubicin have a detrimental side effect of causing fibrosis. We believe our studies on the activation of the fibroblast could lead to further understanding on the long term survival of cancer patients.
Cardiac fibrosis emerges as the default repair response to acute or chronic injury such as myocardial infarction, hypertrophy, chemotherapy, or inflammation. The process entails excessive deposition of scar tissue produced by locally recruited and activated fibroblasts. Fibrosis impairs cardiac compliance and alters cardiac function. Despite its clinical and pathophysiological significance, no interventions currently exist to directly treat or reverse cardiac fibrosis. Our long-term goal is to identify and understand signaling pathways that control the behavior of fibroblasts under pathological and non-pathological conditions.
- Kanisicak O, Khalil H, Ivey MJ, Karch J, Maliken BD, Correll RN, Brody MJ, J Lin SC, Aronow BJ, Tallquist MD, Molkentin JD. (2016). Genetic lineage tracing defines myofibroblast origin and function in the injured heart. Nat Commun, Jul 22;7:12260. doi: 10.1038/ncomms12260. PubMed PMID: 27447449.
- Nurnberg ST, Cheng K, Raiesdana A, Kundu R, Miller CL, Kim JB, Arora K, Carcamo-Oribe I, Xiong Y, Tellakula N, Nanda V, Murthy N, Boisvert WA, Hedin U, Perisic L, Aldi S, Maegdefessel L, Pjanic M, Owens GK, Tallquist MD, Quertermous T. (2015). Coronary Artery Disease Associated Transcription Factor TCF21 Regulates Smooth Muscle Precursor Cells That Contribute to the Fibrous Cap. PLoS Genet, May 28;11(5):e1005155. doi: 10.1371/journal.pgen.1005155. PubMed PMID: 26020946; PubMed Central PMCID: PMC4447275.
- Pinto AR, Ilinykh A, Ivey MJ, Kuwabara JT, D'Antoni ML, Debuque R, Chandran A, Wang L, Arora K, Rosenthal NA, Tallquist MD. (2016). Revisiting Cardiac Cellular Composition. Circ Res, Feb 5;118(3):400-9. doi: 10.1161/CIRCRESAHA.115.307778. PubMed PMID: 26635390; PubMed Central PMCID: PMC4744092.
- Baek ST, Tallquist MD. (2012). Nf1 limits epicardial derivative expansion by regulating epithelial to mesenchymal transition and proliferation. Development, Jun;139(11):2040-9. doi: 10.1242/dev.074054. PubMed PMID: 22535408; PubMed Central PMCID: PMC3347692.
Publication list via PubMed
- M. Tallquist, PI
2R01HL074257 (parent grant and diversity supplement)
National Institutes of Health
"PDGF Receptor Signaling in Mammalian Development"
July 1, 2003 â€“ June 30, 2017