Subscribe: Nature Reviews Cancer - Issue - science feeds
Preview: Nature Reviews Cancer - Issue - science feeds

Nature Reviews Cancer - Issue - science feeds


The current state of cancer metabolism


The study of cancer metabolism has grown exponentially over the past decade. Although the initial observations by Otto Warburg and his contemporaries during the early twentieth century strongly suggested that core cellular metabolism was altered during the process of malignant transformation, the oncogene revolution and

Tumour metabolism: The sugar-free, full-fat diet


Acidosis reprograms the metabolism of cancer cells toward fatty acid oxidation by downregulating acetyl-CoA carboxylase ACC2 through histone deacetylation

Tumour metabolism: Feeding your friends


Sousa et al. demonstrate a reciprocal metabolic cross-talk between pancreatic stellate cells (PSCs) and pancreatic tumour cells whereby secreted autophagic alanine from PSCs is taken up by tumour cells and used as an alternative carbon source to support tumour growth.

Tumour metabolism: Adapting to harsh conditions


Chae et al. show that mitochondrially-localized AKT phosphorylates pyruvate dehydrogenase kinase 1 (PDK1) to promote tumour cell growth and survival in hypoxic conditions.

Tumour metabolism: Metabolic flexibility


Glutamine supports cancer cell growth, yet cancer cells can survive glutamine depletion. Reid et al. reveal a novel pathway exploited by tumours to adapt to glutamine starvation through the activation of inhibitor of nuclear factor-κB (NF-κB) kinase subunit-β (IKKβ). Independently of inducing NF-κB transcriptional

Tumour metabolism: Functions of fumarate


Sciacovelli et al. find that the higher levels of intracellular fumarate that result from loss of fumarate hydratase (FH), which causes hereditary leiomyomatosis and renal cell carcinoma (HLRCC), promotes epithelial-to-mesenchymal transition (EMT). Fumarate inhibits tet methylcytosine dioxygenase (TET) family enzymes, and the

Tumour evolution: Evolving resistance in Tasmanian devils


Devil facial tumour disease (DFTD) is a transmissable cancer that affects Tasmanian devils and has substantially depleted their population, rasing concern that the species faces extinction. However, a new study offers some hope. Epstein et al. report that three populations of Tasmanian devil are

Genetics: Transcribing for the enemy


Clark et al. carried out genomic analyses of 775 meningiomas and found recurrent mutations in POLR2A, which encodes the catalytic subunit of RNA polymerase II, an essential enzyme that mediates the transcription of all protein-coding genes in eukaryotic cells. Mutant POLR2A allows

From Krebs to clinic: glutamine metabolism to cancer therapy


The resurgence of research into cancer metabolism has recently broadened interests beyond glucose and the Warburg effect to other nutrients, including glutamine. Because oncogenic alterations of metabolism render cancer cells addicted to nutrients, pathways involved in glycolysis or glutaminolysis could be exploited for therapeutic purposes.

Reprogramming glucose metabolism in cancer: can it be exploited for cancer therapy?


In recent years there has been a growing interest among cancer biologists in cancer metabolism. This Review summarizes past and recent advances in our understanding of the reprogramming of glucose metabolism in cancer cells, which is mediated by oncogenic drivers and by the undifferentiated character

Serine and one-carbon metabolism in cancer


The non-essential amino acid serine supports several metabolic processes that are crucial for the growth and survival of proliferating cells, including protein, amino acid and glutathione synthesis. As an important one-carbon donor to the folate cycle, serine contributes to nucleotide synthesis, methylation reactions and the

Oxygen availability and metabolic adaptations


Oxygen availability, along with the abundance of nutrients (such as glucose, glutamine, lipids and albumin), fluctuates significantly during tumour evolution and the recruitment of blood vessels, leukocytes and reactive fibroblasts to complex tumour microenvironments. As such, hypoxia and concomitant nutrient scarcity affect large gene expression