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Found 13 matching student topics

Displaying 1–12 of 13 results

Characterisation of a novel protein co-amplified with the n-MYC oncogene

The MYCN oncogene is amplified in a number of tumour types, including Neuroblastoma (NB) and Neuroendocrine Prostate Cancer (NEPC), where it is associated with worse patient prognosis, as compared to non-amplified tumours. However, the high expression of MYCN (encoding the n-MYC protein) alone in non-amplified tumours is associated with better patient prognosis and less aggressive disease. This suggests that other genes co-expressed in MYCN amplified tumours may be responsible for mediating the aggressive traits of n-MYC. Our team has identified …

Study level
PhD, Master of Philosophy, Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences
Research centre(s)
Centre for Genomics and Personalised Health

Engineering Chimeric Antigen Receptor (CAR) T cell for the treatment of cancer

Chimeric Antigen Receptor (CAR) T cells are genetically modified immune cells that can recognise and kill cancer cells. They do so through the CAR, which recognises specific antigens expressed on cancer cells. CAR T cell therapy has emerged as an effective form of cancer immunotherapy in certain types of blood cancers and are now approved for use in patients. However, CAR T cell therapy can only benefit a very small proportion of cancer patients at present because it is very …

Study level
Master of Philosophy, Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences

Determining the theapeutic efficiency of epigenetic drugs in ovarian cancer

Because cancer and many diseases arise from a combination of genetic propensity and the response of cells to external factors mediated through changes to the expression of key genes, it is important to understand epigenetic regulation. The epigenome is crucial to the changes of gene expression and there is now strong evidence that epigenetic alterations are key drivers of cancer progression. However, very few drugs targeting epigenetic modifiers have been successful, in part due to the lack of effective means …

Study level
Master of Philosophy, Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences

Investigating immunosuppression downstream of activated FGFR2 in endometrial cancer

FGFR2 encodes two alternatively spliced isoforms that differ in their ligand binding domain and the combination of tissue specific expression of these isoforms and tissue specific expression of the FGF ligands is the foundation of normal paracrine signalling. Isoform switching from FGFR2b (inclusion of exon 8) to FGFR2c (inclusion of exon 9) occurs in tumorigenesis as it establishes an autocrine loop in epithelial cancer cells. Our lab has reported that FGFR2 activation by mutations or isoform switching is associated with …

Study level
PhD
Faculty
Faculty of Health
School
School of Biomedical Sciences

Epigenetic regulation of non-coding RNAs in hypoxic tumours

In solid tumours, hypoxia occurs as a result of limitation on oxygen diffusion in avascular primary tumours or their metastases. Persistent hypoxia, significantly reduces the efficacy of radiation and chemotherapy and lead to poor outcomes. This is mainly due to increase in pro-survival genes that suppress apoptosis, enhance tumour angiogenesis, the epithelial-to-mesenchymal transition, invasiveness and metastasis. Much of tumour hypoxia research has been centred on examining the transcriptional targets of hypoxia inducible factors (HIFs).HypothesisEpigenetic changes mediate the effect of hypoxia …

Study level
Master of Philosophy, Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences

Therapeutic opportunities targeting epigenetic-metabolism crosswalks in cancer

Epigenetic and metabolic pathways in cancer cells are highly interconnected. Epigenetic landscape in cancer cells is modified by oncogene-driven metabolic changes. Metabolites modulate the activities of epigenetic modifying enzymes to regulate the expression of specific genes. Conversely, epigenetic deregulation that occurs in cancer affect the expression of metabolic genes, thereby altering the metabolome. These changes all coordinately enhance cancer cell proliferation, metastasis and therapy resistance.The overall aim of the project is to understand the link between the activity of epigenetic …

Study level
Master of Philosophy, Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences

Characterise a novel DNA repair protein as a target for cancer therapies

Data generated in the lab has identified a novel DNA repair protein previously described as a key protein in HSP70/90 complexes. Many pathways of tumourigenesis are mediated by Heat Shock Proteins and HSP70/90 are found significantly upregulated in ovarian cancers. The targeting of HSP70/90 are an emerging therapeutic avenue for the treatment of ovarian cancer. Supporting this, an inhibitor of HSP90 has been shown to sensitise breast cancer cells to PARP inhibitors and paclitaxel.Our preliminary data indicates that this new …

Study level
Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences

A novel molecular targeted therapy for anaplastic prostate cancer

In advanced PCa, where the cancer has spread into the bone and other organs, the emergence of treatment resistance remains inevitable. For decades the primary form of treatment in advanced PCa has been to target the production and actions of male sex hormones, androgens, the primary developmental and survival factor of prostate tissue. While these therapies result in tumour regression and cancer control, this is temporary and treatment resistance occurs, referred to as castrate resistant prostate cancer (CRPC). In the …

Study level
Master of Philosophy, Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences

Characterising the role of PARPs in DNA repair and cancer therapy

The genome of our cells is damaged multiple times each day, by various factors including sunlight and reactive oxygen species. In order for the DNA damage response to be efficient, our cells utilise highly coordinated repair pathways that function accurately and rapidly throughout the damaged cell. Cells that do not repair DNA damage correctly will accumulate damage and display increased genomic instability, which is a key hallmark of cancer cells, promoting their survival and rapid growth. DNA repair pathways are …

Study level
Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences

Improving platinum-based chemotherapy by targeting drug metabolism in lung cancer

Lung cancer is the deadliest cancer accounting for 18.4% of all cancer-related deaths. Platinum-based chemotherapy remains a key treatment option for most people living with this disease, either as adjuvant therapy or in combination with immunotherapy. However, resistance to therapy is a significant issue in the treatment of lung cancer. Novel therapeutic strategies combined with predictive biomarkers chemotherapy response are needed to transform the clinical management of NSCLC.Our published work has identified novel biomarkers and druggable proteins from deregulated protein …

Study level
Master of Philosophy, Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences
Research centre(s)
Centre for Genomics and Personalised Health

Characterising a DNA repair protein as an anti-cancer therapeutic target and diagnostic marker in brain cancer

Cancer is the single biggest clinical problem facing the world and will account for half of all global deaths by 2030. Even though there have been significant advances in immunotherapy, we are still unable to cure most cancers. New therapeutic targets, individualised to patient needs, must be identified and validated in order to improve cancer outcomes.Brain cancer causes more deaths in people under the age of 40 than any other cancer and more deaths in children than any other disease. …

Study level
PhD, Master of Philosophy, Honours
Faculty
Faculty of Health
School
School of Biomedical Sciences
Research centre(s)
Centre for Genomics and Personalised Health

Testing a promising targeted therapeutic for triple-negative breast cancer

Triple-negative breast cancers (TNBC) are negative for Estrogen Receptor, Progesterone Receptor and HER2 expression, are clinically aggressive and cannot be treated with the available hormonal or targeted drugs used for other breast cancer subtypes. TNBC accounts for 15-20% of all invasive breast cancer and patients have increased risk of recurrence, mortality and metastases early during disease progression. There is an urgent clinical need to develop improved treatment strategies for these women since the median survival of patients with metastatic TNBC …

Study level
PhD, Master of Philosophy
Faculty
Faculty of Health
School
School of Biomedical Sciences

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