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.
Misregulation of cyclin-dependent kinases (CDKs) can induce unscheduled proliferation and genomic and chromosomal instability. How has recent genetic evidence changed our understanding of the roles of CDKs in the cell cycle of normal and tumour cells?
Relapse remains almost inevitable for patients with advanced ovarian cancer. can the introduction of novel targeted therapies affect the management of this disease?
Metastasis suppressors inhibit metastasis but not the development of a primary tumour. Many of these genes have now been identified, and the therapeutic potential of restoring metastasis suppressor function is beginning to be examined.
Gene amplification is an essential process in several organisms including the ciliateTetrahymena thermophila. What can amplification in this model system teach us about mechanisms of amplification in cancer cells?
Neurotransmitters released through the activation of nicotinic acetylcholine receptors (nAChRs) regulate the synthesis and release of growth, angiogenic and neurotrophic factors. Evidence suggests that smoking and possibly other factors increase the activity of certain nAChRs, and might therefore contribute to tumour development.
Thrombospondin 1, an endogenous angiogenesis inhibitor, affects nitric oxide signalling and therefore haemostasis and blood flow. What is the role of thrombospondin 1 in cancer and what can it teach us about therapeutic inhibition of angiogenesis?