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A paper inCell reports that breast cancer cells can transition between non-cancer stem cell (CSC)-like and CSC-like states; this is dependent on ZEB1, which can be readily activated by microenvironmental signals in non-CSCs that maintain the chromatin at the ZEB1promoter in a bivalent state.
A secreted translational variant of PTEN (PTEN-Long) can be taken up by neighbouring cells, where it can inhibit PI3K signalling, and administration of purified PTEN-Long to tumour-bearing mice induces tumour regression.
Two recent papers indicate that increasing the turnover of MYC proteins in tumours might promote the loss of an immature, self-renewing cell population and might, therefore, have a therapeutic impact.
Seluanov, Gorbunova and colleagues find that high-molecular-mass hyaluronan — a component of the extracellular matrix — activates early contact inhibition, which suppresses tumorigenesis in naked mole rats.
Offermanns and colleagues found that tumour cell-activated platelets induce endothelial opening — which promotes extravasation — through adenine nucleotide-mediated activation of P2Y2 on endothelial cells.
Adoptive T cell therapy using engineered T cells to improve antitumour responses is showing promise for the treatment of haematological malignancies in particular. This Review discusses the strategies to engineer T cells and the progress that has been made with using gene-modified T cells to treat cancer patients.
Several cancers and genetic disorders are linked to defects in helicases that have roles in genome maintenance and stability. This Review discusses helicase-dependent DNA repair pathways and how targeting these might improve cancer treatments based on DNA-damaging chemotherapy or radiation.
Although the ABL1 kinase is well known as the fusion partner with BCR in chronic myeloid leukaemia (CML), roles for the ABL family (ABL1 and ABL2) in solid tumours are beginning to be uncovered. Small-molecule ABL inhibitors are crucial in CML therapy, but can these kinases be targeted for therapeutic benefit in other cancer types?
This Review reminds us of all those pathways we longed to forget from first year biochemistry: deregulated one-carbon metabolism is a possible driver of oncogenesis. Given the wealth of clinically available agents that target one-carbon metabolism are there opportunities for translation into precision cancer medicine?
The DREAM complex provides a previously unsuspected unifying role in the cell cycle. This Opinion article explores the functions of the DREAM complex and how they might contribute to tumour development and progression.
Can novel materials, probes and tools, which represent an integration of traditional and new engineering approaches with cancer biology, help us to better understand tumour progression and invasion?
