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Loss of the tumour suppressor APC in zebrafish embryos leads to upregulation of DNA demethylase components and promoter hypomethylation of key intestinal cell fate genes, leading to the maintenance of intestinal progenitor cells in an undifferentiated state.
This Review describes the evidence linking the renin–angiotensin system (RAS) to cancer, through its roles in processes such as apoptosis, angiogenesis and tissue remodelling. Could RAS inhibitors currently used in the clinic be retooled to treat cancer?
EGFRmutations define a subset of lung cancers associated with sensitivity to the kinase inhibitors gefitinib and erlotinib. However, primary and acquired resistance remains a major clinical problem. This article reviews recent advances towards biologically based rational treatment of this disease.
This Review discusses the new data that have revealed surprising insights into the pathogenesis of acute promyelocytic leukaemia (APL) and the mechanism by which retinoic acid plus arsenic trioxide combination therapy targets the oncogenic fusion protein promyelocytic leukaemia (PML)–retinoic acid receptor-α (RARα), curing most cases of APL.
Bacterial therapies have many advantages over standard cancer therapies — they specifically target tumours, induce controllable cytotoxicity and can be externally detected. This Innovation article proposes that synthetic biology can be applied to bacterial therapies and can tune their beneficial features, allowing the engineering of 'perfect' cancer therapies.
There are many similarities in tumour development between plants and animals, but fundamental differences prevent plants from developing cancer. In particular, cell division and proliferation are strictly regulated in plants, and plant tumours cannot metastasize owing to the rigid microenvironment surrounding plant cells (the cell wall). What can tumour development in plants tell us about cancer in animals?
This article proposes a new model outlining the early steps in the development of serous ovarian cancer. This model suggests that homologous recombination repair deficiency initiates a cascade of molecular events that sculpt the evolution of high-grade serous ovarian cancer and dictate its response to therapy.