The Cancer Cell Biology research area aims to improve our understanding of the cellular mechanisms that lead to the development and treatment of cancer.
Our team work with clinicians, clinical scientists, radiologists, pathologists, and collaborators from both academia and the pharmaceutical industry to investigate the mechanisms of tumour development, progression and metastasis, in order to develop novel treatments and diagnostic techniques.
Our specialist research interests span a range of areas including ovarian, prostate, liver and breast cancer. In particular we study alterations in DNA repair (the repairome) in human disease, the role of transglutaminase enzymes in chemotheraputic drug resistance, and by investigating the effects of naturally occurring compounds from sources such as herbs and red wine on the molecular basis of programmed cell death (apoptosis) in cancer cells. These projects typically involve experimental aspects of cell and molecular biology, tissue culture, cellular imaging, (using specialist flow cytometry techniques and confocal microscopy), high throughput immunohistological analysis of human tissue samples, epidemiology and bioinformatics.
Our academic interests in the underlying basic biology of cancer provide a focus for our inter-disciplinary research, which aims to deliver positive translational impact in order to improve the treatment and quality of life for cancer patients.
Our research is focused into three main themes:
The Cancer Cell Biology research area is part of the Biomedical Research Group.
Find out more about our members by exploring their staff profiles.
PhD researcher, Dipak Meshram and his supervisors Dr Claire Pike and Dr Peter Coussons, have published a paper with a new approach to overcoming drug resistance in cancer cells to chemotherapy.
Cisplatin is an effective chemotherapeutic drug used in the treatment of several types of cancer that works by being selectively toxic to the rapidly dividing cells that characterises many cancers. However, it is also toxic to normally-dividing healthy cells, so its use has side-effects that can cause damage to vital organs. This means cisplatin can’t be used at high doses.
The problem is compounded during repeated drug treatments, as cancer cells that are able to evade cisplatin cytotoxicity become resistant to the concentrations of cisplatin that are normally used for chemotherapy. The high concentrations of the drug that would then be required to have an anti-cancer effect are intolerable to the patient.
Transglutaminases are a family of calcium-dependent enzymes that are more highly expressed in cancer cells than in normal cells, an effect that is further amplified in drug-resistant cancers.
The paper is entitled 'Inhibition of Transglutaminase 2 activity increases cisplatin cytotoxicity in a model of human hepatocarcinoma chemotherapy' and can be found referenced below under key publications.
This article originally appeared in the October 2017 issue of 'First', our Faculty Research Newsletter.
Bourton, E.C., Ahorner, P.A., Plowman, P.N., Zahir, S.A., Al-Ali, H. and Parris, C.N., 2017. The PARP-1 inhibitor Olaparib suppresses BRCA1 protein levels, increases apoptosis and causes radiation hypersensitivity in BRCA1 lymphoblastoid cells. Journal of Cancer, 19(8), pp.4048-4056.
Meshram, D.D., Pike, C.V.S. and Coussons, PJ., 2017. Inhibition of Transglutaminase 2 activity increases cisplatin cytotoxicity in a model of human hepatocarcinoma chemotherapy. European Journal of Pharmacology, (815), pp.332-342.