Biography
Dr. Annahita Sallmyr, received her B.S. in Biomedical Science from University of Malmo in Sweden November 1997 and a master?s degree in cell biology from University of Lund in Sweden in June 1999. Dr. Sallmyr earned her PhD in cell biology from University of Lund in Sweden November 2004. Following her PhD. degree completed a 2-year post-doctoral fellowship followed by promotion to research scientist at the University of Maryland, Baltimore USA. As research scientist she returned to University of Lund in Sweden for one year. Dr. Sallmyr, moved back to University of Maryland in Baltimore as Research Assistant professor 2010. One year later 2011, joined as Research Assistant professor in University of New Mexico and in 2017 was promoted to Research Associate professor at the university of New Mexico, comprehensive cancer center division of Molecular Medicine.
Personal Statement
My work is focused on the role of DNA repair and how the inaccurate repair of DNA double-strand breaks contributes to cancer. In journal of DNA Repair 2020 (Sallmyr A et al.) an overview of the roles of the DNA ligases encoded by the three human LIG genes in DNA replication and repair is provided. Also published in JBC 2018 (Sallmyr A, Tomkinson AE), reviewed the current understanding of the mechanisms and regulation of an alternative DNA end joining pathway in human disease and the potential utility of this pathway as a therapeutic target in cancer. I co-authored a review paper in the journal Gene (Tomkinson AE, Sallmyr A, gene.2013.08.061, 2013) on the structure and functions of mammalian DNA ligases, the major proteins involved in the final step of DNA damage repair. I co-authored a paper in the journal Molecular Cell (Ghezraoui et al, Mol. Cell 55 829-842, 2014) that shows how translocations, a type of genetic rearrangement that cause some childhood leukemia and are also frequently observed in other cancers, are formed.
In my recent work, I have been exploring the development of therapeutic approaches that target altered mitochondrial function in cancer cells. My work is published in Cancer Research entitled ?Inhibition of mitochondrial DNA ligaseIII alpha activates caspase1- dependent apoptosis in cancer cells? (Cancer Res. 15;76(18):5431-41, Sept 2016), there, I have shown that mitochondrial function is significantly altered in cancer cells and that this aberration can be exploited to selectively target cancer cells.
I have been teaching many students and mentees and my commitment to education and mentorship is clear from my efforts over the course of my career. I have expertise in guiding students in the theory and method of conducting laboratory work and research projects and teaching them theory and techniques in molecular and cell biology.
Complete List of Published Work in MyBibliography:
http://www.ncbi.nlm.nih.gov/sites/myncbi/1DAlAafHjnIkq/bibliography/50378218/public/?sort=date&direction=ascending
Areas of Specialty
My contributions to science are in three related research areas:
1) Mechanisms of DNA dependent protein kinase in human cells;
2) Mechanisms of non-homologous end-joining (NHEJ) and alternative end joining (Alt EJ) in cancer;
3) Targeting mitochondrial DNA repair pathways in cancer
Gender
Female
Languages
- English
- Swedish
Courses Taught
Tutoring students in BMS 507 advanced molecular biology for DNA replication, recombination and repair University of New Mexico Health Sciences Center, USA
Research and Scholarship
1) Sallmyr A, Rashid I, Bhandari SK, Naila T, Tomkinson AE. Human DNA ligases in replication and repair. DNA Repair (Amst). 2020 Sept;93:102908. doi: 10.1016/j.dnarep.2020.102908
2) Sallmyr A, Tomkinson AE. Repair of DNA double-strand breaks by mammalian alternative end-joining pathways. J Biol Chem. 2018 Jul 6;293(27):10536-10546. doi: 10.1074/jbc.TM117.000375. Epub 2018 Mar 12. Review
3) Sallmyr A, Tomkinson AE, Rassool FV. Up-regulation of WRN and DNA ligase III-alpha in chronic myeloid leukemia: consequences for the repair of DNA double-strand breaks. Blood. 2008 Aug 15; 112(4): 1413-23. Epub 2008 Jun 4.
4) Sallmyr A, Fan J, Rassool FV. Genomic instability in myeloid malignancies: increased reactive oxygen species (ROS), DNA double strand breaks (DSBs) and error-prone repair. Cancer Lett. 2008 Oct 18; 270(1): 1-9. Epub 2008 May 7. Review. 5) Sallmyr A, Fan J, Datta K, Kim KT, Grosu D, Shapiro P, Small D, Rassool F. Internal tandem duplication of FLT3 (FLT3/ITD) induces increased ROS production, DNA damage, and misrepair: implications for poor prognosis in AML. Blood. 2008 Mar 15; 111(6): 3173-82. Epub 2008 Jan 11.