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Cancer Metabolism: A driver of tumour progression and drug resistance?

Cancer cells frequently hijack the metabolic processes hardwired in normal cells to support their enhanced growth, proliferation and spread.

Importantly, we've shown that changes in tumour cell metabolism can present novel vulnerabilities, that when targeted pharmacologically can limit tumour growth; and also alter the sensitivity of these tumour cells to standard-of-care chemotherapies and targeted therapies.

Defining the impact of metabolic reprogramming on dictating therapeutic susceptibilities and driving resistance mechanisms is imperative to improving treatment response for cancer patients.

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Leveraging imposed metabolic vulnerabilities to improve therapeutic response

As tumours progress, the metabolic demands become more complex, resulting in heterogeneity in metabolic networks within the one tumour mass, and altering how cells respond to treatment.

Response to many anti-cancer therapies are impacted by metabolic programs present within the tumour, and so this heterogeneity can limit the success of anticancer treatment and promote relapse.

Importantly, cancer cells often mount a metabolic response to standard chemotherapy or targeted therapy in an effort to survive, resulting in an imposed metabolic vulnerability.

By identifying these imposed vulnerabilities, we can suggest novel therapeutic combinations with chemotherapy/targeted therapy to enhance anti-cancer responses.

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Our aim is to integrate state-of-the-art cancer models, metabolic analyses and multi-omics platforms to comprehensively map metabolic reprogramming, uncover induced vulnerabilities, mechanisms of drug resistance and novel therapeutic opportunities in KRAS driven cancers,  leading to better patient stratification, and suggesting novel therapeutic combinations to improve patient outcome.

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