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Kelly A. Frazer

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Kelly A Frazer is a Professor of Pediatrics in the Medical School at the University of California, San Diego, Chief of the Division of Genome Information Sciences[1] and Director of the Institute for Genomic Medicine.[2]

Kelly A Frazer
Alma materUniversity of California, San Francisco
Known for
Scientific career
InstitutionsUniversity of California, San Diego
Doctoral advisorDavid R. Cox
Other academic advisorsEdward Rubin

Education

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Frazer did her undergraduate studies at the University of California, Santa Cruz. She then attended the UCSF Medical Center at the University of California, San Francisco and received her PhD in 1993.[citation needed]

Research

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Over the past thirty-three years Frazer has researched and discovered insights into the molecular underpinnings of a wide variety of human diseases and complex traits.[3][4] As a postdoctoral fellow she and Edward Rubin pioneered cross-species DNA sequence comparisons between humans and mice resulting in the discovery of evolutionarily conserved non-coding regulatory sequences in the human genome.[5][6] As Vice President of Genome Biology at Perlegen Sciences Frazer worked with David Cox and others to generate the content for the HapMap Phase II project[7] and determined that common structural variants are largely in linkage disequilibrium with common SNPs.[8] She joined UC San Diego as a faculty member in August 2009[9] and has developed novel methods for identifying and functionally characterizing regulatory variants underlying GWAS signals[10][11][12][13] and has contributed to a greater understanding of mutational signatures in cancer.[14][15]

References

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  1. ^ "Home - Division of Genome Information Sciences - UC San Diego Department of Pediatrics".
  2. ^ "Home". igm.ucsd.edu.
  3. ^ Frazer, KA; Murray, SS; Schork, NJ; Topol, EJ (2009-04-10). "Human Genetic Variation and Its Contribution to Complex Traits". Nature Reviews Genetics. 10 (4): 241–251. doi:10.1038/nrg2554. PMID 1929382. S2CID 19987352.
  4. ^ Frazer, KA (September 2012). "Decoding the human genome". Genome Research. 22 (9): 1599–1601. doi:10.1101/gr.146175.112. PMC 3431476. PMID 22955971.
  5. ^ Loots, G. G.; Locksley, R. M.; Blankespoor, C. M.; Wang, Z. E.; Miller, W.; Rubin, E. M.; Frazer, K. A. (2000-04-07). "Identification of a coordinate regulator of interleukins 4, 13, and 5 by cross-species sequence comparisons". Science. 288 (5463): 136–140. Bibcode:2000Sci...288..136L. doi:10.1126/science.288.5463.136. ISSN 0036-8075. PMID 10753117.
  6. ^ Frazer, KA; Pachter, L; Poliakov, A; Rubin, EM; Dubchak, I (2004-07-01). "VISTA: computational tools for comparative genomics". Nucleic Acids Research. 32 (Web Server issue): W273–W279. doi:10.1093/nar/gkh458. PMC 441596. PMID 15215394.
  7. ^ Frazer, KA; Ballinger, DG; Cox, DR; Hinds, DA (2007-10-18). "A Second Generation Human Haplotype Map of Over 3.1 Million SNPs". Nature. 449 (7164): 851–861. Bibcode:2007Natur.449..851F. doi:10.1038/nature06258. hdl:2027.42/62863. PMC 2689609. PMID 17943122.
  8. ^ Hinds, DA; Kloek, AP; Jen, M; Chen, X; Frazer, KA (2005-12-04). "Common deletions and SNPs are in linkage disequilibrium in the human genome". Nature Genetics. 38 (1): 82–85. doi:10.1038/ng1695. PMID 16327809. S2CID 24205661.
  9. ^ "UCSD Announces Chief of Division of Genome Information Sciences in Pediatrics".
  10. ^ Harismendy, O; Notani, D; Song, X; Rahim, NG; Tanasa, B; Heintzman, N (2011-02-10). "9p21 DNA Variants Associated With Coronary Artery Disease Impair Interferon-γ Signalling Response". Nature. 470 (7333): 264–268. Bibcode:2011Natur.470..264H. doi:10.1038/nature09753. PMC 3079517. PMID 21307941.
  11. ^ DeBoever, C; Li, H; Jakubosky, D; Benaglio, P; Reyna, J; Olson, KM (2017-04-06). "Large-scale profiling reveals the influence of genetic variation on gene expression in human induced pluripotent stem cells". Cell Stem Cell. 20 (4): 533–546.e7. doi:10.1016/j.stem.2017.03.009. PMC 5444918. PMID 28388430.
  12. ^ Panapoulos, M; D'Antonio, M; Benaglio, P; Williams, R; Hashem, SI (2017-04-11). "iPSCORE: a resource of 222 iPSC lines enabling functional characterization of genetic variation across a variety of cell types". Stem Cell Reports. 8 (4): 1086–1100. doi:10.1016/j.stemcr.2017.03.012. PMC 5390244. PMID 28410642.
  13. ^ Greenwald, WW; Li, H; Benaglio, P; Jakubosky, D; Matsui, H; Schmitt, A (2019-03-05). "Subtle changes in chromatin loop contact propensity are associated with differential gene regulation and expression". Nature Communications. 10 (1): 1054. Bibcode:2019NatCo..10.1054G. doi:10.1038/s41467-019-08940-5. PMC 6401380. PMID 30837461.
  14. ^ DeBoever, C; Ghia, EM; Shepard, PJ; Rassenti, L; Barrett, CL; Jepsen, K (2015-03-13). "Transcriptome sequencing reveals potential mechanism of cryptic 3'splice site selection in SF3B1-mutated cancers". PLOS Computational Biology. 11 (3): e1004105. Bibcode:2015PLSCB..11E4105D. doi:10.1371/journal.pcbi.1004105. PMC 4358997. PMID 25768983.
  15. ^ D'Antonio, M; Tamayo, P; Mesirov, JP; Frazer, KA (2016-07-19). "Kataegis Expression Signature in Breast Cancer Is Associated With Late Onset, Better Prognosis, and Higher HER2 Levels". Cell Reports. 16 (3): 672–683. doi:10.1016/j.celrep.2016.06.026. PMC 4972030. PMID 27373164.
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