Research Strand 1:
Novel Targeted Therapies for Triple Negative Breast Cancer
Strand leader: Prof Michael J Duffy, email: (JavaScript must be enabled to view this email address)
Triple negative breast cancers lack expression of estrogen receptor, progesterone receptor and do not exhibit overexpression or amplificatio of HER2. Consquently, targeted therapy is currently unavailable to this subgroup of patients. Triple negative cancers represent approximately 15-20% of invasive breast cancers and are responsible for a disproportionate number of breast cancer deaths. There is thus an urgent need to develop novel therapeutic strategies, and associated biomarkers to improve the prognosis for this sub-group of breast cancer patients.
(Research Strand 1 Programme Overview »)
Research Strand 2:
Response and Resistance to HER2 Targeted Therapies in Breast Cancer (Under construction)
Strand leader: Prof John Crown, email: (JavaScript must be enabled to view this email address)
Research Strand 3:
Targeting IGF Signalling in Breast Cancer (Under construction)
Strand leader: Dr Judith Harmey, email: (JavaScript must be enabled to view this email address)
Research Strand 4:
Molecular Determinants of Resistance to Endocrine-directed Therapies
Strand leaders: Prof William Gallagher/Prof William Watson, email: (JavaScript must be enabled to view this email address) / (JavaScript must be enabled to view this email address)
- Molecular determinants of endocrine resistance and tumour progression in breast cancer
Hormonal therapy is focussed on modulating the activity of steroid hormone receptors, by down-regulating the levels of the receptors themselves, blocking the production of steroid hormones, or inhibiting the action of those hormones. However, when used either as adjuvant therapy following surgery or as a first line treatment in advanced disease, significant numbers of patients do not respond and eventually succumb to their disease.
- Molecular determinants of apoptotic resistance in androgen resistant prostate cancer
Unfortunately, there are no effective treatment options for androgen-independent prostate cancer. Defining the precise mechanisms of resistance represents a key challenge facing clinicians and scientists. In collaboration with international collaborators, we have derived and started to characterise the anti-apoptotic phenotype of androgen-independent sublines.
