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Oncogenic alteration of the endocytic machinery is a hallmark of cancer. As reviewed here, these alterations can lead to changes in morphology, polarity, motility, adhesion and growth factor-activated signalling pathways.
Responses to hypoxia are orchestrated not only through activation of the hypoxia–inducible factor family of transcription factors (HIFs), but also through HIF–independent signalling pathways. How are these pathways integrated?
Deregulation of hypoxia-inducible factor (HIF) is an established feature of tumours that develop in patients with von Hippel–Lindau disease, caused by inactivating germline mutations of theVHLtumour suppressor gene. However, HIF-independent activities of VHL also seem to be important for the pathogenesis of the disease.
Ageing is thought to be associated with increased oxidative stress and increased cancer risk. However, recent evidence that breast cancers arising in older women are not associated with oxidative stress questions the link between age and increasing oxidative stress. Does ageing cause or simply permit cancer development?
Recent data indicates an anti-angiogenic function for a new class of VEGF-A isoforms. In this Opinion article, Steven Harper and David Bates discuss the emerging role of these proteins in tumourigenesis and anti-angiogenic therapeutic strategies.
In patients with advanced cancer, pro-inflammatory cytokines are associated with anorexia and cachexia, pain, fatigue, depression, toxicity of treatment and resistance to treatment. What is our current understanding of the pathways that mediate these effects and how can we prevent them?
