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The DNA damage response in cancer stem cells

Lammers, I.G. (2010) The DNA damage response in cancer stem cells. Bachelor's Thesis, Biology.

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Abstract In present day cancer therapy, patients are often treated with DNA damaging agents to induce excessive DNA damage in cancer cells in addition to other treatments such as surgery. The aim of these treatments is to induce apoptosis in cancer cells, nonetheless not all cancer cells die from such treatments. In recent years it has been described that there are subpopulations within tumor cell populations. In the cancer stem cell model, the structure of these subpopulations is described. It is assumed that so called cancer stem cells, or tumor-initiating cells form the foundations of tumors. In this model it is also described that cancer stem cells are the driving force of tumor growth and are highly resistant for therapy. Cancer stem cells were suggested to have a different response to DNA damage when compared to non-tumor-initiating cancer cells. This implicates that they need a different treatment than other cancer cells, before they acquire such an amount of DNA damage that they go into apoptosis. Not only inducing DNA damage is a way to eradicate cancer stem cells. Other ways of doing so for example is to destroy the niche the cancer stem cells need to keep their stem-like capacities, or sensitize them to DNA damaging agents. When these cells are not treated differently it is possible that they repair the damage that treatment has caused and may continue to divide and proliferate. It is important to know how these cancer stem cells react to DNA damage, because there is evidence that in a vast majority of tumors both solid and humoral, cancer stem cells are present. It is not yet known how exactly the DNA damage pathway of these cells differs from that of non-tumorigenic stem cells and other cancer cells.

Item Type: Thesis (Bachelor's Thesis)
Degree programme: Biology
Thesis type: Bachelor's Thesis
Language: English
Date Deposited: 15 Feb 2018 07:44
Last Modified: 15 Feb 2018 07:44

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