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Targeting the DNA damage response pathway has a great potential for the treatment of cancer.
Pancreatic cancer has a poor prognosis, where 90% of pancreatic cancer patient die within 5 years of diagnosis, thus, new therapies are urgently required. ATMIN is an essential Zn2+ finger ATM-binding protein that regulates ATM signalling and DNA damage responses. A recent study had shown that multiple transcript variants of the DNA repair gene ATMIN are expressed in pancreatic cancer. The aim of this project is to investigate the ability of truncated and full length variants of ATMIN to activate DNA damage responses and maintain genome stability, and to determine their effect on pancreatic cell growth, apoptosis and sensitivity to cytotoxic drug.
This project will use a wide range of cell and molecular biology techniques, including confocal microscopy, quantitative PCR, cell culture and DNA repair assays. We will knockout endogenous ATMIN expression using CRISPR/Cas 9 in three different pancreatic cancer cell lines (AsPC-1, Capan-1, Hpaf-1) and determine cell growth/survival using Incucyte and BrdU incorporation in response to a range of DNA damaging agents.
Both degrees in Cancer Biology and Biomedical Science at Kingston University have given me the opportunity to gain an in depth understanding of the complexity and fragility of the human body.
I undertook my undergrad dissertation project with Dr Natasha Hill in the field of pancreatic cancer where I researched the use of retinoic acid as a treatment strategy to inhibit pancreatic cancer progression. I obtained a first class mark and my results will be incorporated into a manuscript, titled ‘Context-dependent effects of SPARC on pancreatic cancer cell proliferation are determined by fibronectin' by authors Dandagama Mudiyanselage A., Mohamedi F., Moaraf S., Jones L., Kocher H. and Hill N, currently in preparation for publishing later this year. I also achieved a distinction for my Master's degree project, which was completed with Dr Athina-Myrto Chioni in the field of cervical cancer where I investigated fibroblast growth factor receptor (FGFR) signaling in different cervical cancer cell lines using FGF-7 stimulation in the presence or absence of SU5402 inhibitor drug.
I have great theoretical and practical skills, all achieved through the projects and in combination with frequent practical sessions held throughout the duration of my degree and a year working within the histopathology laboratory at Hammersmith Hospital. I have gained valuable hands on laboratory experience in a wide range of laboratory techniques including, but not limited to fluorescent and confocal microscopy, ELISA, cell/tissue culture, immunohistochemistry, western blotting and gel electrophoresis.
Fibronectin acts as a molecular switch to convert SPARC from tumour- promoter to tumour suppressor protein. Amanda Munasinghe, Fatemia Mohamedi, Stan Moaraf, Hemant Kocher and Natasha J Hill* Manuscript in preparation (June 2019).