This review article analyses how cancer cells exploit metabolic pathways and how mannose—being the C-2 epimer of glucose—can counteract the “Warburg effect” by entering the glycolytic pathway inefficiently, thereby slowing tumour cell proliferation. When mannose catabolism is compromised in cancer cells (e.g., low MPI activity), mannose leads to a metabolic bottleneck, making tumour cells more chemosensitive and less capable of sustaining growth. The review outlines mechanisms and therapeutic opportunities for targeting mannose metabolism in oncology.


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