Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Despite a ban on the use of plants of theAristolochiagenus in herbal medicine, as they contain known carcinogens, urothelial carcinoma attributable to the use of this plant seems to be more common than previously thought.
Three papers show that hepatocyte growth factor (HGF)–MET signalling is an important determinant of therapeutic responses and can be induced through paracrine, autocrine and endocrine production of HGF.
Joan Massagué and colleagues have identified a paracrine signalling network between tumour and stromal cells in breast cancer that seems to drive both metastasis and resistance to chemotherapy.
Knockout of the Notch effectorRbpjkin mesenchymal fibroblasts enhances the formation of squamous cell carcinomas of the skin in mice, and similar changes can be induced by exposure of human skin to ultraviolet A irradiation.
A paper published inNature Physicshas experimentally and mathematically modelled epithelial cell migration and identified mechanically generated waves that are important for cellular motility.
Wigard Kloosterman, Edwin Cuppen and colleagues have evidence that chromothripsis might arise owing to clustered DNA double-strand breaks (DSBs) and nonhomologous repair mechanisms.
Two papers show that KRAS-G12D-transformed pancreatic tumour cells produce GM-CSF, which recruits MDSCs to promote an immunosuppressive microenvironment.
Although chronic myeloid leukaemia (CML) can be treated with tyrosine kinase inhibitors (TKIs) against BCR-ABL1, cure is not achieved in most cases. This Review provides an update on resistance to TKIs, and discusses strategies to target BCR-ABL1-independent resistance, which may be necessary to eliminate CML stem cells and advanced disease.
Kinesins — a family of molecular motors that travel unidirectionally along microtubule tracks — have emerged as potential targets for cancer drug development. As discussed in this Review, several compounds that inhibit mitotic kinesins have entered clinical trials and others are being developed, raising the possibility that the range of kinesin-based drug targets may expand in the future.
The family of lysyl oxidases (LOX) seem to have dichotomous roles in tumour progression: suppressing tumorigenesis and promoting metastasis. This Review discusses the functions of the LOX family and the rationale for targeting them.
This Timeline article focuses on the ERBB network of receptor tyrosine kinases, which exemplifies how a constant dialogue between basic and clinical cancer research can lead to the development of both novel drugs and strategies to overcome acquired resistance.
NFE2-related factor 2 (NRF2) has apparently contradictory roles in cancer. Activation of NRF2 contributes to the chemopreventive effects of various clinically used drugs against various diseases including cancer. However, NRF2 activity can also accelerate tumorigenesis in mouse models, thus highlighting a potential danger of NRF2 activation. This Opinion article discusses how these opposing roles might be reconciled.
How many of the changes identified in human cancer by genome sequencing are meaningful? And how can we exploit these massive data sets to yield new therapeutic targets? This article outlines five approaches that aim to discover oncogenic drivers, tumour dependencies and, ultimately, new cancer therapies from cancer genome data.
