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Mechanisms of apoptosis resistance in chemotherapy-resistant cancer cells

Most chemotherapy drugs work through the induction of apoptosis in tumour cells. Mutations in apoptotic pathways, notably p53 and Bcl-2, are common in cancer and associated with increased resistance to apoptosis and therefore to chemotherapy. The sensitivity of two types of cells have been compared, A 172 human glioblastoma cells and MDA-MB-23l human breast cancer cells, for their sensitivity to the chemotherapy drugs cisplatin, doxorubicin, gemcitabine, vincristine and temozolomide. Data shows that there were differences in the sensitivity of breast cancer and glioma cells to a variety of chemotherapy drugs. There were differences in nitric oxide synthase (NOS) expression between the two different types of cancer cells and yet a role was not observed for nitric oxide in changing the expression of the Bcl-2 family of proteins (both pro- or antiapoptotic). Additionally, NOS expression changed following treatment with chemotherapy drugs, suggesting that this may be the mechanism by which the cells become resistant.

Identiferoai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:627931
Date January 2014
CreatorsBarnawi, Ibrahim
PublisherUniversity of Reading
Source SetsEthos UK
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation

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