Sébastien Tabariès

Abstract Patients with colorectal cancer (CRC) frequently develop liver metastases1,2,3. The prognosis of these patients is skewed by the histopathological heterogeneity of their liver metastases4,5. Patients with ‘replacement’ metastases have a 5-year overall survival of less than 44.2%, compared with 73.4% in patients with ‘encapsulated’ (previously known as desmoplastic) metastases5; yet there are currently no approved therapies targeting replacement liver metastases.

Abstract Mitochondrial electron transport flavoprotein (ETF) insufficiency causes metabolic diseases known as a multiple acyl-CoA dehydrogenase deficiency (MADD). Although essential in muscle, we identified ETF dehydrogenase (ETFDH) as one of the most dispensable metabolic genes in neoplasia, and its expression is reduced across human cancers.

Abstract Cancer cells reprogram their metabolism to meet the energy demands of neoplasia. We observed that the level of expression of mitochondrial enzyme electron transfer flavoprotein dehydrogenase (ETFDH) is unexpectedly decreased in most human malignancies relative to that in tissue-of-origin. Reduced ETFDH expression increases proliferation and neoplastic growth.