Reviews & Analysis

Stress does not cause cancer per se, but depression and a lack of social support might influence cancer progression and clinical outcome. Can identification of the molecular and biological mechanisms involved be used to improve patient treatment?

Integrins contribute to squamous cell carcinoma as well as invasion and metastasis. Mutation or upregulation of integrins in tumour cells can inhibit differentiation and apoptosis, and integrins that are expressed by differentiated cells can alter the proliferation of neighbouring tumour stem cells.

This review examines whether the ASPP family of p53-interacting proteins are a missing link in the regulation of p53-induced cell-cycle arrest and apoptosis.

Despite the success in treating childhood leukaemia, its causes remain enigmatic. A plethora of candidate environmental exposures have been proposed but, as this review discusses, an abnormal immune response to common infection(s) has emerged as the most plausible aetiological mechanism.

Mutation or deletion of PTEN is found in many cancers — however, in others, deregulation of the PI3K–PTEN network occurs in the absence of PTEN mutation. This review examines whether 'crosstalk' with other tumorigenic signalling pathways contributes to PI3K–PTEN deregulation.

Recent evidence implies that germline polymorphisms might significantly influence the metastatic capacity of tumours. This article discusses whether, in the future, inherited, prospective metastatic biomarkers might be in common use for cancer prognosis and the selection of tailored tumour treatment.

Carney complex is a genetic condition in which affected individuals develop benign tumours in various tissues, including the heart. This review examines the genes implicated in the development of cardiac myxomas.

Aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) show promise in colorectal cancer prevention, but there have been concerns about potential toxicity. Pharmacogenetic studies to establish an individual's risk– benefit ratio might allow tailoring of chemoprevention.

Germline polymorphisms and gene-expression profiles in acute lymphoblastic leukaemia (ALL) cells are emerging as useful clinical diagnostics for this disease. Lessons learnt from development of polygenic models for ALL might inform the optimization of treatment for other cancers.

Epigenetically mediated transcriptional-silencing events occur at key genes during the earliest stages of tumorigenesis. Understanding how these events alter cell signal transduction and function can provide useful clues to improve cancer detection, prevention and therapy.

When normal cells are compared to cancer cells by microarray analysis, the most obvious differences occur in the expression levels of genes that control cell proliferation. Can this 'proliferation signature' be used as a biomarker for cancer research and therapy?

Flow cytometry can be used to map signalling networks in individual cancer cells. This form of 'single-cell proteomics' can reveal important new information about the pathways that are activated in therapy-resistant cells and provide biomarkers for use in diagnosis and determining prognosis.

How have the data from the initial clinical trials of histone deacetylase inhibitors (HDACi) improved our understanding of how these drugs work? And what key facts do we still need to understand about the biology of HDACi?

The transcription factors of the Pax gene family are important in growth regulation and, therefore, the prevention of malignant growth. This review examines their roles in embryogenesis and how these can be subverted to contribute to tumorigenesis.

This review examines how recent insights, gained from mouse models, have improved our understanding of the contradictory role of adaptive and innate leukocytes in cancer development.