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Susan Kay Murphy, PhD

Murphy
Associate Professor in Obstetrics and Gynecology
Campus Mail: 701 W. Main Street, Suite 510, Room 5140, Durham, NC 27701
Phone: (919) 681-3423
Email: susan.murphy@duke.edu

My research interests are largely centered around epigenetics and the role of epigenetic modifications in health and disease. My research projects include studies of gynecologic malignancies, including working on approaches to target ovarian cancer cells that survive chemotherapy and later give rise to recurrent disease.  I have ongoing collaborative projects in which we investigate the nature of the Developmental Origins of Health and Disease (DOHaD) hypothesis. DOHaD reflects the idea that our early environment plays an important part in shaping our risk of developing neurodevelopmental disorders or other chronic health problems. I am currently focused on preconception exposures in males with studies of the impact of cannabis use on the sperm epigenome and heritability of these effects. My lab is also working on the effects of in utero exposures, with our primary work revolving around the Newborn Epigenetics STudy (NEST), a mother-infant dyad cohort recruited from central North Carolina between 2005 and 2011 and whom we have followed since early pregnancy.

Education and Training

  • Ph.D., Wake Forest University, 1998
  • B.A., University of North Carolina - Charlotte, 1992

Selected Grants and Awards

Publications

Dietz, L. G., A. A. Wylie, K. A. Rauen, S. K. Murphy, R. L. Jirtle, and P. D. Cotter. “Exclusion of maternal uniparental disomy of chromosome 14 in patients referred for Prader-Willi syndrome using a multiplex methylation polymerase chain reaction assay.” J Med Genet 40, no. 4 (April 2003): e46. https://doi.org/10.1136/jmg.40.4.e46.

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Dietz, L., A. A. Wylie, K. A. Rauen, S. K. Murphy, R. L. Jirtle, and P. D. Cotter. “Exclusion of maternal uniparental disomy of chromosome 14 in Prader-Willi syndrome referrals using a rapid methylation PCR assay.” In American Journal of Human Genetics, 71:553–553. UNIV CHICAGO PRESS, 2002.

Scholars@Duke

Freking, Brad A., Susan K. Murphy, Andrew A. Wylie, Simon J. Rhodes, John W. Keele, Kreg A. Leymaster, Randy L. Jirtle, and Timothy P. L. Smith. “Identification of the single base change causing the callipyge muscle hypertrophy phenotype, the only known example of polar overdominance in mammals.” Genome Res 12, no. 10 (October 2002): 1496–1506. https://doi.org/10.1101/gr.571002.

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Li, Tao, Thanh H. Vu, Kok-Onn Lee, Youwen Yang, Chuyen V. Nguyen, Huy Q. Bui, Zhi-Lan Zeng, et al. “An imprinted PEG1/MEST antisense expressed predominantly in human testis and in mature spermatozoa.” J Biol Chem 277, no. 16 (April 19, 2002): 13518–27. https://doi.org/10.1074/jbc.M200458200.

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Murphy, S. K., A. A. Wylie, A. J. McVie-Wylie, D. Pulford, C. M. Nolan, T. C. Orton, and R. L. Jirtle. “Development and characterization of a conditional M6p/Igf2r knockout mouse.” American Journal of Human Genetics 69, no. 4 (October 1, 2001): 363–363.

Scholars@Duke

Evans, H. K., A. A. Wylie, S. K. Murphy, and R. L. Jirtle. “NNATresides in a micro-imprinted domain on human chromosome 20q11.2.” American Journal of Human Genetics 69, no. 4 (October 1, 2001): 346–346.

Scholars@Duke

Evans, H. K., A. A. Wylie, S. K. Murphy, and R. L. Jirtle. “The neuronatin gene resides in a "micro-imprinted" domain on human chromosome 20q11.2.” Genomics 77, no. 1–2 (September 2001): 99–104. https://doi.org/10.1006/geno.2001.6612.

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Keller, M. A., S. K. Murphy, and G. D. Parks. “RNA replication from the simian virus 5 antigenomic promoter requires three sequence-dependent elements separated by sequence-independent spacer regions.” J Virol 75, no. 8 (April 2001): 3993–98. https://doi.org/10.1128/JVI.75.8.3993-3998.2001.

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Murphy, S. K., A. A. Wylie, and R. L. Jirtle. “Imprinting of PEG3, the human homologue of a mouse gene involved in nurturing behavior.” Genomics 71, no. 1 (January 1, 2001): 110–17. https://doi.org/10.1006/geno.2000.6419.

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Wylie, A. A., S. K. Murphy, T. C. Orton, and R. L. Jirtle. “Novel imprinted DLK1/GTL2 domain on human chromosome 14 contains motifs that mimic those implicated in IGF2/H19 regulation.” Genome Res 10, no. 11 (November 2000): 1711–18. https://doi.org/10.1101/gr.161600.

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