Alexander S. Nord
· Associate ProfessorUniversity of California, Davis · Neurology
Active 2023–2023
About
Alexander S. Nord, Ph.D., is a professor at the University of California, Davis, who received his Ph.D. from the University of Washington, working with Mary-Claire King on identifying the genetic causes of human diseases and disorders such as autism and schizophrenia. He completed a postdoctoral fellowship at Lawrence Berkeley National Laboratory with Axel Visel, Len Pennacchio, and Eddy Rubin, focusing on mouse models of development and functional genomics. His research interests include the genetic and epigenetic systems that control gene regulation in the brain. Dr. Nord joined UC Davis in 2014 and leads the Nord Neurogenomics Lab, where his work centers on understanding the molecular mechanisms underlying neurodevelopmental and neuropsychiatric disorders through gene regulation studies.
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Research topics
- Molecular biology
- Genetics
- Cancer research
- Biology
Selected publications
2023-03-31
supplementary-materialsOpen access<p>PDF file 69K, Paired primary and recurrent carcinomas</p>
2023-03-31
supplementary-materialsOpen access<p>PDF file 80K, Cases with deleterious germline mutations, somatic HR mutations, and somatic PTEN mutations</p>
2023-03-31
supplementary-materialsOpen access<p>PDF file 48K, Genomic regions for targeted capture</p>
2023
- Biology
- Molecular biology
- Cancer research
<div>Abstract<p><b>Purpose:</b> Hallmarks of germline <i>BRCA1/2</i>-associated ovarian carcinomas include chemosensitivity and improved survival. The therapeutic impact of somatic <i>BRCA1/2</i> mutations and mutations in other homologous recombination DNA repair genes is uncertain.</p><p><b>Experimental Design:</b> Using targeted capture and massively parallel genomic sequencing, we assessed 390 ovarian carcinomas for germline and somatic loss-of-function mutations in 30 genes, including <i>BRCA1</i>, <i>BRCA2</i>, and 11 other genes in the homologous recombination pathway.</p><p><b>Results:</b> Thirty-one percent of ovarian carcinomas had a deleterious germline (24%) and/or somatic (9%) mutation in one or more of the 13 homologous recombination genes: <i>BRCA1</i>, <i>BRCA2</i>, <i>ATM</i>, <i>BARD1</i>, <i>BRIP1</i>, <i>CHEK1</i>, <i>CHEK2</i>, <i>FAM175A</i>, <i>MRE11A</i>, <i>NBN, PALB2</i>, <i>RAD51C</i>, and <i>RAD51D</i>. Nonserous ovarian carcinomas had similar rates of homologous recombination mutations to serous carcinomas (28% vs. 31%, <i>P</i> = 0.6), including clear cell, endometrioid, and carcinosarcoma. The presence of germline and somatic homologous recombination mutations was highly predictive of primary platinum sensitivity (<i>P</i> = 0.0002) and improved overall survival (<i>P</i> = 0.0006), with a median overall survival of 66 months in germline homologous recombination mutation carriers, 59 months in cases with a somatic homologous recombination mutation, and 41 months for cases without a homologous recombination mutation.</p><p><b>Conclusions:</b> Germline or somatic mutations in homologous recombination genes are present in almost one third of ovarian carcinomas, including both serous and nonserous histologies. Somatic <i>BRCA1/2</i> mutations and mutations in other homologous recombination genes have a similar positive impact on overall survival and platinum responsiveness as germline <i>BRCA1/2</i> mutations. The similar rate of homologous recombination mutations in nonserous carcinomas supports their inclusion in PARP inhibitor clinical trials. <i>Clin Cancer Res; 20(3); 764–75. ©2013 AACR</i>.</p></div>
2023-03-31
supplementary-materialsOpen access<p>PDF file 51K, Cases with both germline and somatic HR mutations</p>
2023-03-31
supplementary-materialsOpen access<p>PDF file 69K, Paired primary and recurrent carcinomas</p>
2023
- Biology
- Molecular biology
- Cancer research
<div>Abstract<p><b>Purpose:</b> Hallmarks of germline <i>BRCA1/2</i>-associated ovarian carcinomas include chemosensitivity and improved survival. The therapeutic impact of somatic <i>BRCA1/2</i> mutations and mutations in other homologous recombination DNA repair genes is uncertain.</p><p><b>Experimental Design:</b> Using targeted capture and massively parallel genomic sequencing, we assessed 390 ovarian carcinomas for germline and somatic loss-of-function mutations in 30 genes, including <i>BRCA1</i>, <i>BRCA2</i>, and 11 other genes in the homologous recombination pathway.</p><p><b>Results:</b> Thirty-one percent of ovarian carcinomas had a deleterious germline (24%) and/or somatic (9%) mutation in one or more of the 13 homologous recombination genes: <i>BRCA1</i>, <i>BRCA2</i>, <i>ATM</i>, <i>BARD1</i>, <i>BRIP1</i>, <i>CHEK1</i>, <i>CHEK2</i>, <i>FAM175A</i>, <i>MRE11A</i>, <i>NBN, PALB2</i>, <i>RAD51C</i>, and <i>RAD51D</i>. Nonserous ovarian carcinomas had similar rates of homologous recombination mutations to serous carcinomas (28% vs. 31%, <i>P</i> = 0.6), including clear cell, endometrioid, and carcinosarcoma. The presence of germline and somatic homologous recombination mutations was highly predictive of primary platinum sensitivity (<i>P</i> = 0.0002) and improved overall survival (<i>P</i> = 0.0006), with a median overall survival of 66 months in germline homologous recombination mutation carriers, 59 months in cases with a somatic homologous recombination mutation, and 41 months for cases without a homologous recombination mutation.</p><p><b>Conclusions:</b> Germline or somatic mutations in homologous recombination genes are present in almost one third of ovarian carcinomas, including both serous and nonserous histologies. Somatic <i>BRCA1/2</i> mutations and mutations in other homologous recombination genes have a similar positive impact on overall survival and platinum responsiveness as germline <i>BRCA1/2</i> mutations. The similar rate of homologous recombination mutations in nonserous carcinomas supports their inclusion in PARP inhibitor clinical trials. <i>Clin Cancer Res; 20(3); 764–75. ©2013 AACR</i>.</p></div>
2023-03-31
supplementary-materialsOpen access<p>PDF file 48K, Genomic regions for targeted capture</p>
2023-03-31
supplementary-materialsOpen access<p>PDF file 51K, Cases with both germline and somatic HR mutations</p>
2023-03-31
supplementary-materialsOpen access<p>PDF file 80K, Cases with deleterious germline mutations, somatic HR mutations, and somatic PTEN mutations</p>
Frequent coauthors
- 2 shared
Colin C. Pritchard
University of Washington
- 2 shared
Anne Thornton
- 2 shared
Silvia Casadei
- 2 shared
Christopher C. Pennil
University of Washington
- 2 shared
Kathy Agnew
- 2 shared
Barbara M. Norquist
- 2 shared
Sheena Scroggins
- 2 shared
Rochelle L. Garcia
Washington DC VA Medical Center
Labs
Education
- 2014
Postdoctoral Scholar, Genomics Division
Lawrence Berkeley National Laboratory
- 2011
PhD, Genome Sciences
University of Washington
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