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MYBL2 in blood cancer development and breast cancer

  • Full or part time
  • Application Deadline
    Applications accepted all year round
  • Self-Funded PhD Students Only
    Self-Funded PhD Students Only

About This PhD Project

Project Description

Our research interest is to understand the molecular mechanisms that maintain genome integrity in stem cells (both adult and embryonic stem cells) and how loss of genome stability leads to development of cancer specifically blood cancers and breast cancer. We have previously identified Mybl2 as a key regulator of chromosome stability and recently found that lower levels of the protein leads to defects in double strand break repair and promotes telomere fragility. We are now interested on defining the dual role of MYBL2 as oncogene and tumor suppessor in the different cancers.

References

* Bayley, R et al. MYBL2 supports DNA double strand break repair in Hematopoietic Stem Cells. Cancer Research 2018.

* Pfister, K et al. Identification of drivers of aneuploidy in breast tumors. Cell Reports 2018.

* Saldivar, J et al. An intrinsic S/G2 checkpoint enforced by ATR. Science 2018.
* Ward, C et al. Fine-tunning MYBL2 is required for proper Mesenchymal-to-Epithelial transition during somatic reprogramming. Cell Reports 2018.
* Skrypek et al. Epithelial-to-Mesenchymal transition: Epigenetic reprogramming driving cellular plasticity. Trends in Genetics 2017.

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