Table of contents
From the editors
p167 | doi:10.1038/nrc1834
Research Highlights
Angiogenesis: Initiation
p168 | doi:10.1038/nrc1822
Immunotherapy: Armed for action
p169 | doi:10.1038/nrc1825
Tumorigenesis: Disruptive influence
p169 | doi:10.1038/nrc1831
In the news
Poor devils
p170 | doi:10.1038/nrc1827
Tumorigenesis: Culpable kinase
p170 | doi:10.1038/nrc1830
Signalling pathways: A flying start
p171 | doi:10.1038/nrc1824
In brief
Targeted therapy | Metastasis | Immunology | Chromosomal translocations
p171 | doi:10.1038/nrc1826
DNA methylation: Methylation gastronomy
p172 | doi:10.1038/nrc1828
Hypoxia: A breath of fresh air
p172 | doi:10.1038/nrc1832
Genomics: Complete coverage?
p173 | doi:10.1038/nrc1823
Immunology: Early warning
p174 | doi:10.1038/nrc1829
Trial Watch
Assessing radiation exposure
p174 | doi:10.1038/nrc1833
Reviews
New roles for integrins in squamous-cell carcinoma
Sam M. Janes & Fiona M. Watt
p175 | doi:10.1038/nrc1817
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.
Beyond PTEN mutations: the PI3K pathway as an integrator of multiple inputs during tumorigenesis
Megan Cully, Han You, Arnold J. Levine & Tak W. Mak
p184 | doi:10.1038/nrc1819
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.
Infection, immune responses and the aetiology of childhood leukaemia
Mel Greaves
p193 | doi:10.1038/nrc1816
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.
Vaccines for tumour prevention
Pier-Luigi Lollini, Federica Cavallo, Patrizia Nanni & Guido Forni
p204 | doi:10.1038/nrc1815
Why should vaccines be particularly effective in cancer prevention? Guido Forni and colleagues discuss the rationale for, and the challenges involved in, developing such preventive vaccines.
ASPPs and cancer
Giuseppe Trigiante & Xin Lu
p217 | doi:10.1038/nrc1818
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.
Perspectives
Article series: Tumour Microenvironment
Validating matrix metalloproteinases as drug targets and anti-targets for cancer therapy
Christopher M. Overall & Oded Kleifeld
p227 | doi:10.1038/nrc1821
Clinical trial results with matrix metalloproteinase (MMP) inhibitors have been poor. So, which MMPs are validated drug targets with a crucial role in disease pathogenesis and which MMPs are actually proteins that have unacceptable deleterious effects when inhibited (anti-targets)?
Opinion
The influence of bio-behavioural factors on tumour biology: pathways and mechanisms
Michael H. Antoni, Susan K. Lutgendorf, Steven W. Cole, Firdaus S. Dhabhar, Sandra E. Sephton, Paige Green McDonald, Michael Stefanek & Anil K. Sood
p240 | doi:10.1038/nrc1820
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?
Corrigendum: Acute lymphoblastic leukaemia: a model for the pharmacogenomics of cancer therapy
Meyling H. Cheok & William E. Evans
p249 | doi:10.1038/nrc1835
and ARD1: enemies, friends or neither?