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.
The semaphorins and their receptors, the neuropilins and the plexins, originally characterized as proteins involved in the guidance of axons, can either promote or inhibit tumour progression. This Review documents their effects on tumour angiogenesis, as well as on metastasis and cell survival.
Gene fusions have long been known to have an important role in leukaemias, but they have recently been identified in a majority of prostate cancers. Understanding their role in this disease could lead to better targeted therapies.
Using recent evidence from mouse models, this Review discusses whether p53-dependent senescence induced by dysfunctional telomeres is as potent as apoptosis in suppressing tumorigenesisin vivo.
Hypoxia and free radicals, such as reactive oxygen and nitrogen species, alter the activity of the transcription factor HIF1, which can regulate tumour cell survival and angiogenesis. Intratumoural heterogeneity of these factors significantly affects HIF1 and consequently the response to cytotoxic therapy.
Cell cycle progression is regulated by phosphorylation and protein degradation, which is mediated by ubiquitin ligases. This Review explores the relevance of two ubiquitin ligase specificity factors (F-box proteins) that are emerging as important players in tumour development.
Angiogenesis and lymphangiogenesis are regulated by integrins, which are cell surface receptors whose ligands are extracellular matrix proteins and immunoglobulin superfamily molecules. Here, the evidence implicating integrins as regulators of angiogenesis and lymphangiogenesis and the current state of therapeutic strategies to target them are discussed.
Recent advances in our understanding of intestinal crypt biology, including how mutations in stem cells become fixed and expand within the epithelium, has led to new theories on the origins of colonic adenomas and cancers.
Imatinib has been an extremely successful treatment for chronic myeloid leukaemia. However, we need to know about the stem cells involved in the disease to understand why relapse is so common when imatinib is stopped.
Changes in the levels of the second messenger Ca2+ can result in the activation of broadly proliferative or cytotoxic responses. As reviewed here, to tip the balance in their favour, cancer cells often remodel the expression or activity of their Ca2+signalling apparatus.
This Review discusses the recent progress in the treatment of established (pre)malignant disease of viral or non-viral origin with synthetic long peptide vaccines that are capable of inducing robust T-cell responses.
Most cancer deaths are caused by metastatic spread and subsequent growth of tumour cells at distant organs. How are disseminating tumour cells relevant to the biology of early metastatic spread and how might they be used to improve cancer treatment?
This Review examines whether GATA1-related leukaemias in both human and mouse can provide important insights into the mechanism of multi-step leukaemogenesis.
The cyclin-dependent kinase (Cdk) inhibitor p27 regulates cell proliferation, cell motility and apoptosis, and is inactivated through various means in many types of human cancer. Recent studies in several tumour types indicate that p27 expression levels have both prognostic and therapeutic implications.
Testing for prostate-specific antigen is a powerful tool in the detection of prostate cancer, but how should it be used and how can testing be improved to ensure against overdiagnosis?
One explanation for the relative lack of progress in treating cancer in adolescents and young adults is that the biology of malignant diseases in this age group is different. Do molecular, epidemiological and therapeutic outcome comparisons support this?
Adoptive cell therapy (ACT), using either autologous tumour-infiltrating lymphocytes or donor lymphocytes, has proved an effective treatment for some patients with advanced cancers. Can the ability to genetically engineer human lymphocytes for ACT further expand the use of this treatment?
Metastatic dissemination and growth at distant sites are influenced by cells of the tumour microenvironment. What roles do these cells have in the underlying processes that determine metastatic growth?
Can we exploit the DNA repair pathways in cancer cells to increase the efficacy of existing and future cancer treatments? This Review discusses the current state of play.
Intratumoural hypoxia is a negative prognostic indicator and can underlie therapeutic resistance for many patients. This Review explores the differential biological effects of acute hypoxia versus longer-term, chronic hypoxia on genomic instability and DNA damage repair pathways. What does this mean for therapeutic strategies?
A specific telomerase inhibitor and several telomerase therapeutic vaccines are in clinical trials, and other telomerase-based therapies are in preclinical development. What are the advantages and disadvantages of these approaches and which cancer patients might benefit most?
