Tarik Regad

Tarik Regad

Senior Research Fellow

School of Science & Technology

Staff Group(s)


Dr Tarik Regad is a Senior Research Fellow in Molecular and Cellular Tumour Biology and his research focuses on investigating the role of cancer stem cells in cancer initiation, invasion and metastasis. He is also involved in delivering lectures and practical sessions on cancer and cancer stem cells for post-graduate level students within the module Biology of Disease.

Career overview

Dr Regad is a Doctor of Veterinary Medicine (DvetMed). He undertook his MSc, MRes and PhD at the University Paris VII (Denis Diderot) before joining the Gurdon Institute at the University of Cambridge (UK) as a Research Associate. In 2006, he moved to the MRC Toxicology Unit (University of Leicester) to undertake a position as a Career Development Fellow. He joined NTU in 2010 as a Lecturer/Senior Lecturer in Biosciences and he is now working as a Senior Research Fellow at the John van Geest Cancer Research Centre.

Research areas

Cancer stem cells (CSCs) are responsible for cancer initiation, invasion and metastasis in patients who were subjected to cancer therapies such as chemotherapy or radiotherapy. Therefore, the major challenges facing the cancer scientific community reside in identifying those malignant cells and develop therapies to target them. His projects are carried out at the John van Geest Cancer Research Centre and focus on:

  • Identifying tissue specific CSCs
  • Identifying CSCs specific biomarkers
  • Developing CSCs targeting strategies (Chemical therapy, antibody therapy and immunotherapy)
  • Investigating the molecular and cellular processes involved in cancer invasion and metastasis.

Opportunities to carry out postgraduate research towards an MPhil/PhD exist and further information may be obtained from the NTU Graduate School.

Sponsors and collaborators

Recent research has been funded by:

His collaborations involve several clinicians and scientists at national and international levels.


Selected Publications:

A promyelocytic leukemia protein-thrombospondin 2 axis and the risk of relapse in neuroblastoma. Dvorkina M, Nieddu V, Chakelam S, Pezzolo A, Cantilena S, Leite AP, Chayka O, Regad T, Pistorio A, Sementa AR, Virasami A, Barton J, Montano X, Lechertier T, Brindle N, Morgenstern D, Le Bras M, Burns A, Saunders N, Hodivala-Dilke K, Bagella L, De The H, Anderson J, Sebire N, Pistoia V, Sala A and Salomoni P, Clinical Cancer Research, 2016, 22 (15)

Cytoplasmic PML promotes TGF-β-associated epithelial–mesenchymal transition and invasion in prostate cancer. Buczek ME, Miles AK, Green W, Johnson C, Boocock DJ, Pockley AG, Rees RC, Hulman G, Van Schalkwyk G, Parkinson R, Hulman J, Powe DG and Regad T, Oncogene, 2015

Targeting RTK signaling pathways in cancer., Cancers. Regad, T, Cancers, 2015, 7 (3), 1758-1784

The helicase HAGE prevents interferon-a-induced PML expression in ABCB5+ malignant melanoma-initiating cells by promoting the expression of SOCS1. Mathieu MG, Miles AK, Ahmad M, Buczek ME, Pockley AG, Rees RC and Regad T, Cell Death and Disease, 2014, 5 (2)

Molecular and cellular pathogenesis of melanoma initiation and progression. Regad T, Cellular and Molecular Life Sciences 2013, 70 (21), 4055-4065

The helicase HAGE expressed by malignant melanoma-initiating cells is required for tumor cell proliferation in vivo. Linley AJ, Mathieu MG, Miles AK, Rees RC, McArdle SEB, Regad T, Journal of Biological Chemistry, 2012, 287 (17), 13633-13643

SUMOylation promotes PML degradation during EMCV infection. Regad T *, El Mchichi B *, Maroui MA*, Rodriguez MS, Aminev A, Gerbaud S, Escriou N, Dianoux L and Chelbi-Alix MK, Journal of Virology, 2010, 84 (22), 11634-45 *Equal first authors

The tumour suppressor Pml regulates cell fate in the developing neocortex. Regad T, Bellodi C, Nicotera P and Salomoni P, Nature Neuroscience, 2009, 2 (2), 132-40

See all of Tarik Regad's publications...

Press expertise

  • Stem cells
  • Cancer stem cells
  • Cancer therapies (chemical and monoclonal antibody targeting)
  • Cancer initiation and progression (invasion and metastasis)