A report submitted in part fulfilment of the examination requirements for the award of a B.Sc. (Hons) degree title awarded by the University of Lincoln, June 2014, supervised by Issam Hussain.
Samuel Good
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CERTIFICATE OF ORIGINALITY
This is to certify that I am responsible for the work submitted in this thesis, that the original work is my own, except as specified in the acknowledgements and in references, and that neither the thesis nor the original work contained therein has been previously submitted to any institution for a degree.
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Word count excluding references approx. 9000
Abstract
Breast cancer is one of the leading causes of death in women in western countries (Cancer Research, 2009). There are a number of risk factors which include, gender, age and familial susceptibility. Estrogens are integral regulators in the development of normal breast tissue, however it also plays a role in cancer development and progression (Martin et al, 2000). Tamoxifen is known as a selective estrogen receptor modulator (SERM), it has been the “mainstay of endocrine therapy in breast cancer” (Martin et al, 2000). Tamoxifen is effective when used against estrogen receptor positive (ER+) breast cancers, problems arise when the breast cancer is estrogen receptor negative (ER-). We took two cell lines, MDA MB 231 (ER-) and MCF7/WT (ER+), and tested the ability of Tamoxifen on both. As hypothesised, we discovered that estrogen had a better response when used with the ER+ cell line. To take the research further, we calculated the ED50 for both lines, and found that the ER- negative cell line had a much higher value, again due to its ER status.
The second part of the thesis was aimed at investigating the idea of cancer stem cells (CSC’s) and its cell surface marker CD44 and CSC’s transcription factors OCT4 and NANOG.
CSC’s are a “subpopulation of tumour cells” that
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