Inga Reynisdóttir
Titill
About
Professor at Faculty of Medicine, School of Health Sciences, University of Iceland
Member of the European Molecular Biology Organization (EMBO)
Contact:
E-mail: eirikurs (at) hi.is
Telephone: +354-525-4270
Location:
Department of Biochemistry and Molecular Biology, BioMedical Center Sturlugata 8, 102 Reykjavik Iceland
RESEARCH PROFILE - PUBLICATION
(work in progress)
Inga completed her PhD from Columbia University in 1993. Her thesis centered on how the DNA tumor viruses SV40 and polyoma replicate in mammalian cells by inactivating the tumor suppressor proteins p53 and pRb resulting in loss of controlled cellular growth. Her post-doctoral studies, 1994–1997 at the Memorial-Sloan Kettering Cancer Center, focused on how cyclin-dependent kinases control cellular growth.
From 1997 to 2007, Inga worked at deCODE genetics in Reykjavik, Iceland. Until 2002 she led research on the genetics of metabolic diseases, mostly on type 2 diabetes, and for the subsequent 5 years she studied the functional effects of these genes on cellular pathways in cells originating from pancreas, muscle and adipose tissue. In 2007, Inga moved to the Department of Pathology at the Landspitali – University Hospital where she works on breast cancer.
Inga leads a research team, in collaboration with Dr. Rósa Björk Barkardóttir, at the Cell biology and molecular genetics unit at the Department of Pathology at the Landspitali – University Hospital. The focus is on understanding how alterations in the genome can play a role in disease generation andprogression, particularly in cancer. Not only can single nucleotide polymorphisms (SNP) increase the risk of cancer but genomic rearrangements such as amplifications can harbor genes that promote tumor initiation andgrowth. Our approach has been to identify genetic alterations in breast cancer patients and/or tumors, relating them to changes in gene expression and to pathological and clinical factors in addition to validating the effect in cell-based assays.
Our aim is to find changes in gene expression and/or genetic alterations that will be useful for future prognosis, diagnosis and as therapeutic targets. A well-known example is the HER2 gene, used for diagnosis of breast tumors and a drug target. Previously we reported the association of a SNP with a known risk to breast cancer with reduced survival in estrogen receptor positive patients. We also mapped copy number alterations on chromosome 8 in breast tumors, describing the correlation between amplification and high gene expression of ZNF703 with shorter survival in patients that carry luminal B breast tumors.