תפריט ראשי עליון

תפריט עמוד

Dr. Efrat Dvash Riesenfeld

 

Efrat Dvash Riesenfeld
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Education

​

2009-2015- PhD. In Molecular Genetics. Weizmann Institute of Science, Rehovot, Israel.

2005-2008- M. Sc. In Genetics and Breeding. summa cum laude. The Hebrew University of Jerusalem, Israel.

2001-2005- B. Sc. In Biotechnology and Food Engineering. Major: Biotechnology Engineering. Technion–Israel Institute of Technology, Israel.


​Continuing education

09/2016-06/2018 Post-doctoral fellow at Harvard Medical School, USA.

04/2016-08/2016 Intern at the Weizmann Institute of Science, Israel.

2015-04/2016 Post-doctoral fellow at the Weizmann Institute of Science, Israel.


​2018-present – Senior researcher and director of the breast cancer translational research lab at Tel Aviv Sourasky Medical center

​Dvash E, Katov A, Rubinstein M (2016) MGST2-generated LTC4 is the major mediator of stresstriggered DNA damage. The Weizmann Institute of Science. Lipid Mediators in Health and Disease II: From the Cutting Edge. La Jolla, California.

 

Dvash E, Har-Tal M, Barak S, Meir O, Rubinstein M (2016) LTC4 is the major trigger of oxidative DNA damage elicited by ER stress and by cytotoxic agents. The Weizmann Institute of Science. LIPID MAPS Annual Meeting 2016: Lipidomics Impact on Metabolic, Cancer, Cardiovascular and Inflammatory Diseases. La Jolla, California.

 

Dvash E, Katov A, Rubinstein M (2016) LTC4 antagonists may serve as practical NOX4 inhibitors.The Weizmann Institute of Science. NOX Family NADPH Oxidases, Gordon Research Conference. Waterville Valley, NH.

 

Dvash E, Katov A, Rubinstein M (2016) Programmed DNA damage: Potential clinical Implications. DNA Damage, Mutation & Cancer, Gordon Research Conference. Ventura, California.

 

Rubinstein M, Meir O, Dvash E (2012) C/EBPbeta Attenuates ER Stress- Triggered Cell Death By Inducing Microsomal Glutathione S Transferase 1 (MGST1). The Weizmann Institute of Science. EMBO Conference Series. The Physiology of the endoplasmic reticulum (ER): Function and Dysfunction. Caldes de Malavella, Spain.




  • Rubinstein M and Dvash E (2018) Leukotrienes and kidney diseases. Curr Opin Nephrol Hypertens 27(1):42-48.

  • Dvash E and Rubinstein M (2016) Leukotriene C4 is the major mediator of endoplasmic reticulum stress-triggered oxidative stress. Free Radic Biol Med 100:S68. 

  • Dvash E and Rubinstein M (2016) A surprising mediator of oxidative DNA damage. Cell Cycle, doi: 10.1080/15384101.2016.1144989.

  • Dvash E, Har-Tal M, Barak S, Meir O and Rubinstein M (2015) Leukotriene C4 is the major trigger of stress-induced oxidative DNA damage. Nat. Commun., 6:10112 doi:10.1038/ncomms10112.
This work was recommended by the Faculty of 1000 (2016)
This work was highlighted by Larochelle, Nature Chemical Biology (2016)

  • Meir O, Dvash E, Werman A and Rubinstein M (2010) C/EBPb regulates endoplasmic reticulum stress triggered cell death in mouse and human models. PLoS One 5: e9516-. Dvash E, Kra-Oz G, Ziv C, Carmeli S and Yarden O (2010) The NDR Kinase DBF-2 Is Involved in Regulation of Mitosis, Conidial Development, and Glycogen Metabolism in Neurospora crassa. Eukaryotic Cell, 9(4), 502–513. 

​Grants/Awards

January 2018 American Diabetes Association Postdoctoral Fellowship

June 2008 Summa cum laude: M. Sc. In Genetics and Breeding.

June 2000 Outstanding chief of staff

May 2000 Outstanding main officer soldier

 

Patents

(i)  Inhibitors of Leukotriene-Mediated Activity for Treating Side Effects of Statin Therapy. Patent application: WO/2015/125138A1 (27.08.2015).

(ii)  Inhibitors of Leukotriene-Mediated Activity for Alleviating Chemotherapy Side Effects and Stress Induced Cell Death. Patent application: WO/2015/125137 (27.08.2015).

(iii) Method for delaying the onset of insulin dependence in diabetic subjects. Patent application: IL 248491 (31.01.2017).


​Breast cancer translational research, mechanisms involved in breast cancer progression and resistance development to anti-cancer drugs, personalized medicine

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