Impact of the transcription factor Nrf2 on the metabolic state of colorectal cells during inflammation associated carcinogenesis. The transcription factor Nrf2 plays a key role in oxidative stress response and mediates profound cy­toprotection. Contrary to the previous view, it was recently found that deregulated Nrf2 activity contributes to car­cinogenesis. Deregulated Nrf2 activity can result from persistent oxidative stress, which is often seen in the permanent presence of e.g. macro­phages during the course of a chronic inflammation such as inflammatory bowel disease (IBD) or in the context of colorectal cancer (CRC). Under such conditions, epithelial cells adapt to oxidative stress through the enhanced and durable activation of Nrf2. One conse­quence is an increased resistance to apoptosis, manifesting in chemo­resistance, but several other growth advantages are conferred by an enhanced Nrf2 activation, too. Recent data indicates that Nrf2 is involved in metabolic reprogramming, as well. In fact, the altered condition not only covers the high energy demand, but also ensures masses of glucose as intermediate metabolite for biomass production along with cell proliferation and tumor growth. Recently, it was shown that oxidative stress modulates the expression of monocarboxylate transporters (MCT) - these are involved in the cellular balance of lactate -, thus pointing to a possible contribution of Nrf2 in cancer metabolism. This would particularly apply to inflammation associated cancers (IAC) initiated and promoted by persistent oxidative stress and Nrf2 dependent adaptation processes.