Special Lecture hosted by the IRIC and IRICoR

Promoting Tumor Dormancy of Breast Cancer Cells by ‘Normalizing’ their Microenvironment and their Malignant Phenotype


In May of 2017 and October of 2018, IRICoR took part in both economic missions in Israel in the Life Sciences sector organized by the Ministère de l’Économie, de la Science et de l’Innovation. During the course of the missions, IRICoR was able to exchange and forge links in view of collaborations with research centres, biotechnology companies and renowned investigators.

Following these initiatives, IRICoR is pleased to announce that Dalit Barkan, Head, Laboratory of Tumor Dormancy and Metastasis, Department of Human Biology and Medical Sciences, Faculty of Natural Sciences, University of Haifa, in Israel, will be presenting her research work as part of a special lecture hosted by the IRIC and IRICoR, on Tuesday, February 5, at 11:30 am.

Dalit Barkan received her Ph.D. in Molecular Endocrinology at the Weizmann Institute of Science, in Israel. She completed her Postdoctoral studies at the National Cancer Institute (USA) in Dr. Jeffrey Green’s lab. During her Postdoctoral studies, she established the first in vitro model system enabling the study of the biology of cancer dormancy and the transition from dormancy to proliferative growth. By using this system, she went on to discover the role of extracellular matrix remodeling in mediating the reactivation of disseminated dormant tumor cells. Furthermore, the generation of a fibrotic-like milieu at the site of metastasis was shown, for the first time, to be required for the switch of dormant tumor cells to metastatic growth via activation of beta1-integrin and its downstream-signaling.

In 2010, Dr. Barkan joined the Department of Human Biology at the University of Haifa, in Israel. Her research currently involves potential strategies to prevent and/or treat recurrent metastatic cancer.

Two main approaches are being used in her lab:

1) Maintaining residual disease in a dormant state by targeting either the metastatic niche by promoting resolution of inflammation, or the out-breaking dormant tumor cells by inhibiting their acquisition of stem cell-like properties; and,

2) Promoting tumor dormancy of proliferating metastases by ”normalizing” their malignant phenotype.

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