Nancy Andrews

Positions:

Nanaline H. Duke Professor of Pediatrics

Pediatrics
School of Medicine

Dean Emerita of the School of Medicine

School of Medicine
School of Medicine

Professor of Pediatrics

Pediatrics
School of Medicine

Professor of Pharmacology & Cancer Biology

Pharmacology & Cancer Biology
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

B.S. 1980

Yale University

M.S. 1980

Yale University

Ph.D. 1985

Massachusetts Institute of Technology

M.D. 1987

Harvard University

Grants:

School of Medicine 2017 Biddle

Administered By
School of Medicine
Awarded By
Mary Duke Biddle Foundation
Role
Principal Investigator
Start Date
End Date

Expansion of Animal Resources for Large Animals (Vivarium Expansion project)

Administered By
School of Medicine
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Genes that modify Iron loading in mice

Administered By
Pharmacology & Cancer Biology
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Identification of Novel Genes That Modulate Systemic Iron Homeostasis

Administered By
Pathology
Awarded By
National Institutes of Health
Role
Mentor
Start Date
End Date

Regulation of Iron Homeostasis

Administered By
Pharmacology & Cancer Biology
Awarded By
National Institutes of Health
Role
Principal Investigator
Start Date
End Date

Publications:

Research in academic medical centers: two threats to sustainable support.

Reductions in federal support and clinical revenue jeopardize biomedical research and, in turn, clinical medicine.
Authors
Levine, AS; Alpern, RJ; Andrews, NC; Antman, K; Balser, JR; Berg, JM; Davis, PB; Fitz, JG; Golden, RN; Goldman, L; Jameson, JL; Lee, VS; Polonsky, KS; Rappley, MD; Reece, EA; Rothman, PB; Schwinn, DA; Shapiro, LJ; Spiegel, AM
MLA Citation
Levine, Arthur S., et al. “Research in academic medical centers: two threats to sustainable support..” Sci Transl Med, vol. 7, no. 289, May 2015. Pubmed, doi:10.1126/scitranslmed.aac5200.
URI
https://scholars.duke.edu/individual/pub1073942
PMID
26019216
Source
pubmed
Published In
Sci Transl Med
Volume
7
Published Date
Start Page
289fs22
DOI
10.1126/scitranslmed.aac5200

Tmprss6 is a genetic modifier of the Hfe-hemochromatosis phenotype in mice.

The hereditary hemochromatosis protein HFE promotes the expression of hepcidin, a circulating hormone produced by the liver that inhibits dietary iron absorption and macrophage iron release. HFE mutations are associated with impaired hepatic bone morphogenetic protein (BMP)/SMAD signaling for hepcidin production. TMPRSS6, a transmembrane serine protease mutated in iron-refractory iron deficiency anemia, inhibits hepcidin expression by dampening BMP/SMAD signaling. In the present study, we used genetic approaches in mice to examine the relationship between Hfe and Tmprss6 in the regulation of systemic iron homeostasis. Heterozygous loss of Tmprss6 in Hfe(-/-) mice reduced systemic iron overload, whereas homozygous loss caused systemic iron deficiency and elevated hepatic expression of hepcidin and other Bmp/Smad target genes. In contrast, neither genetic loss of Hfe nor hepatic Hfe overexpression modulated the hepcidin elevation and systemic iron deficiency of Tmprss6(-/-) mice. These results indicate that genetic loss of Tmprss6 increases Bmp/Smad signaling in an Hfe-independent manner that can restore Bmp/Smad signaling in Hfe(-/-) mice. Furthermore, these results suggest that natural genetic variation in the human ortholog TMPRSS6 might modify the clinical penetrance of HFE-associated hereditary hemochromatosis, raising the possibility that pharmacologic inhibition of TMPRSS6 could attenuate iron loading in this disorder.
Authors
Finberg, KE; Whittlesey, RL; Andrews, NC
MLA Citation
Finberg, Karin E., et al. “Tmprss6 is a genetic modifier of the Hfe-hemochromatosis phenotype in mice..” Blood, vol. 117, no. 17, Apr. 2011, pp. 4590–99. Pubmed, doi:10.1182/blood-2010-10-315507.
URI
https://scholars.duke.edu/individual/pub757605
PMID
21355094
Source
pubmed
Published In
Blood
Volume
117
Published Date
Start Page
4590
End Page
4599
DOI
10.1182/blood-2010-10-315507

Build it and hope that enough of them will come.

Authors
MLA Citation
Andrews, Nancy C. “Build it and hope that enough of them will come..” J Clin Invest, vol. 119, no. 10, Oct. 2009, pp. 2860–61. Pubmed, doi:10.1172/jci41105.
URI
https://scholars.duke.edu/individual/pub757617
PMID
20069718
Source
pubmed
Published In
J Clin Invest
Volume
119
Published Date
Start Page
2860
End Page
2861
DOI
10.1172/jci41105

Genetic variation in Mon1a affects protein trafficking and modifies macrophage iron loading in mice.

We undertook a quantitative trait locus (QTL) analysis in mice to identify modifier genes that might influence the severity of human iron disorders. We identified a strong QTL on mouse chromosome 9 that differentially affected macrophage iron burden in C57BL/10J and SWR/J mice. A C57BL/10J missense allele of an evolutionarily conserved gene, Mon1a, cosegregated with the QTL in congenic mouse lines. We present evidence that Mon1a is involved in trafficking of ferroportin, the major mammalian iron exporter, to the surface of iron-recycling macrophages. Differences in amounts of surface ferroportin correlate with differences in cellular iron content. Mon1a is also important for trafficking of cell-surface and secreted molecules unrelated to iron metabolism, suggesting that it has a fundamental role in the mammalian secretory apparatus.
Authors
Wang, F; Paradkar, PN; Custodio, AO; McVey Ward, D; Fleming, MD; Campagna, D; Roberts, KA; Boyartchuk, V; Dietrich, WF; Kaplan, J; Andrews, NC
MLA Citation
Wang, Fudi, et al. “Genetic variation in Mon1a affects protein trafficking and modifies macrophage iron loading in mice..” Nat Genet, vol. 39, no. 8, Aug. 2007, pp. 1025–32. Pubmed, doi:10.1038/ng2059.
URI
https://scholars.duke.edu/individual/pub757631
PMID
17632513
Source
pubmed
Published In
Nature Genetics
Volume
39
Published Date
Start Page
1025
End Page
1032
DOI
10.1038/ng2059

Understanding heme transport.

Authors
MLA Citation
Andrews, Nancy C. “Understanding heme transport..” N Engl J Med, vol. 353, no. 23, Dec. 2005, pp. 2508–09. Pubmed, doi:10.1056/NEJMcibr053987.
URI
https://scholars.duke.edu/individual/pub757647
PMID
16339100
Source
pubmed
Published In
The New England Journal of Medicine
Volume
353
Published Date
Start Page
2508
End Page
2509
DOI
10.1056/NEJMcibr053987