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Content archived on 2024-05-21

Interplay among mitochondria and p53 family proteins during apoptosis induced by dna damage - a new strategy for cancer therapy

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Innovative cancer therapies

Anticancer treatment is often dependent on the tumour's sensitivity to the administered therapy.

One of the key obstacles in the development of effective anticancer treatments is the resistance of certain tumours to apoptosis-promoting chemotherapeutic drugs. The EC-funded IMPALED project concentrated on a specific aspect of cancer therapy resistance, namely mitochondria and the p53 family of proteins. The p53 proteins are the main sensors of DNA damage in cells and their interplay with mitochondria can render cells susceptible to anticancer treatment. IMPALED project partners cooperated to identify new molecular targets to combat treatment resistance among certain tumour types. In doing so, the project was aiming to shed light on the mechanisms leading to therapy resistance in tumour cells. One of the observations made during the course of IMPALED linked apoptotic pathways in lung cancer cells to treatment resistance and overall prognosis. Specifically, the location (nulear or cytosolic) of Apaf-1, a key apoptotic protein was shown to be a reliable prognostic for overall survival. Further research can lead to new therapies with significant commercial potential.

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