I am an experienced cancer biologist investigating innovative cancer therapeutics targeting the DNA damage response. My goal is to develop effective therapeutic approaches to target relapsed ovarian cancer and the blood cancer multiple myeloma, diseases with limited treatment options and poor survival outcomes.
My team investigates a novel approach to cancer therapy, which is currently showing promising results in early phase clinical trials, in both blood and solid cancers. Our pre-clinical studies have shown that this therapy has real potential in treatment-resistant ovarian cancer and multiple myeloma models.
My team is also investigating new vulnerabilities that could stop ovarian cancer cells from being able to repair the DNA damage caused by chemotherapy. This has the potential to be extended to a wider range of cancers, including multiple myeloma, breast, prostate and pancreatic cancers.
2018 Peter Mac Lea Medal, for research excellence; Cancer research exchange program with Dana Farber Cancer Institute (USA) (inaugural participant); Invited to attend Victorian Government Medical Research Trade Mission delegation to Japan (supported by Victorian Cancer Agency)
2022 Monash University, School of Biomedical Sciences; Adjunct Associate Professor (Research)
2021 The University of Melbourne / St Vincent’s Hospital Melbourne; Honorary Principal Fellow (Associate Professor)
2020-2023 Victorian Cancer Agency Mid-Career Research Fellow
Yan S., Xuan J., Brajanovski N., Tancock M., Madhamshettiwar P., Simpson K., Ellis S., Kang J., Cullinane C., Sheppard K. E., Hannan K. M, Hannan R. D., Sanij E. *, Pearson R. B. * and Chan K*. The RNA polymerase I transcription inhibitor CX-5461 cooperates with topoisomerase 1 inhibition by enhancing the DNA damage response in homologous recombination-proficient high-grade serous ovarian cancer. British Journal of Cancer (2021); Feb;124(3):616-627. *co-senior author
Sanij E.*,#, Hannan K. M.*, Xuan J., Brajanovski N., Ahern J., Yan S., Chan K. T., Son J., Kondrashova O., Lieschke E., Wakefield M., Trigos A., Frank D., Cullinane C., Poortinga G., Khanna K., Andrew J. Deans, Mileshkin L., McArthur G. A., Soong J., Berns E., Hannan R. D., Scott C., Sheppard K. E. and Pearson R. B#. CX-5461 activates the DNA damage response and demonstrates therapeutic efficacy in high-grade serous ovarian cancer. Nature Communications (2020) May 11(1):2641. *co-first author, # co-corresponding authors
Significance: This study shows the Pol I transcription inhibitor CX-5461 is a promising therapy in ovarian cancer utilizing high-grade serous ovarian cancer-PDX models
Khot A., Brajanovski N., Cameron D.P., Hein N., Maclachlan K.H., Sanij E., Lim J., Soong J., Link E., Blombery P., Thompson ER., Fellowes a., Sheppard KE., McArthur GA., Pearson RB., Hannan RD., Porrtinga G and Harrison SJ. First-in-Human RNA Polymerase I Transcription Inhibitor CX-5461 in Patients with Advanced Hematological Cancers: Results of a Phase I Dose Escalation Study. Cancer Discovery (2019) 9 (8), 1036-1049.
Significance: Critical paper describing the first-in-human clinical trial of the first-in-class Pol I inhibitor CX-5461, demonstrating CX-5461 has single-agent anti-tumour activity against advanced hematological cancers.
Quin J., Chan T.K, Devlin J.R, Cameron D.P, Diesch J, Cullinane C, Ahern J, Khot A, Hein N, George A.J, Hannan K.M, Poortinga G, Sheppard E, Khanna K, Johnstone R.W, Drygin D, McArthur G.A, Pearson R.B, Sanij E*. Hannan R.D*. Inhibition of RNA Polymerase I transcription initiation activates non-canonical ATM/ATR Signalling. Oncotarget (2016) 7(31): 49800-49818. *co-senior author
Significance: In this paper, we showed that CX-5461 activates DNA damage signalling pathways within the nucleoli and sensitizes cells to DNA damaging agents. We demonstrated that the combination of CX-5461 and a drug targeting ATM/ATR signalling improved therapeutic efficacy in vivo thus extending the utility of both classes of drugs.
Sanij E.*, Diesch J., Lesmana A., Poortinga G., Hein N., Lidgerwood G., Cameron D.P., Ellul J., Goodall G.J., Wong L.H., Dhillon A.S., Hamdane N., Rothblum L.I., Pearson R.B., Haviv. I., Moss T. and Hannan, R.D*. A novel role for the Pol I transcription factor UBTF in maintaining genome stability through the regulation of highly transcribed Pol II genes. Genome Research (2015); 5(2):201-212. *Corresponding author
Significance: In this paper, we reported a novel role the Pol I-transcription factor UBTF in regulating the expression of highly transcribed Pol II genes critical for chromatin packaging and DNA repair. The coordinated regulation of these processes emphasizes the therapeutic opportunities of targeting Pol I transcription for cancer therapy.
Bywater M., Poortinga G., Sanij E., Hein N., Peck a., Cullinane C., Wall M., Cluse L., Drygin D., Anderes K., Huser N., Proffitt C., Bliesath J., Haddach M., Schwaebe M., Ryckman D.M. Rice W.G., Lowe S.W., Johnstone R.W., Pearson R.B., McArthur G.A., Hannan R. Inhibition of RNA Polymerase I as a therapeutic strategy to promote cancer-specific activation of p53. Cancer Cell (2012); 22(1):51-65.
Significance: Critical and high-profile paper demonstrating that dysregulated Pol I transcription can be targeted in vivo to selectively kill cancer cells. Resulted in the initiation of clinical trial of CX-5461 targeting patients with haematological malignancies at Peter Mac.
ORCID profile: https://orcid.org/0000-0002-2063-7813
Google Scholar profile: https://scholar.google.com.au/citations?user=d6ANt4kAAAAJ&hl=en