Table of contents
June 2007 Vol 7 No 6
From the editors
p399 | doi:10.1038/nrc2164
Research Highlights
Senescence: Arrest me!
p401 | doi:10.1038/nrc2159
Hypoxia: Opposing effects
p402 | doi:10.1038/nrc2151
Therapy: Addicted to repair
p402 | doi:10.1038/nrc2155
Trial Watch
Combining the risk?
p402 | doi:10.1038/nrc2163
In brief
Innovation | Microrna | Therapy | Leukaemia
p403 | doi:10.1038/nrc2165
Tumour suppressors: Detaining division
p404 | doi:10.1038/nrc2156
Tumorigenesis: Taking the hallmark?
p404 | doi:10.1038/nrc2161
Drug resistance: Alternative routes
p405 | doi:10.1038/nrc2158
Therapy: Synergy
p406 | doi:10.1038/nrc2160
In the news
You snus you lose?
p406 | doi:10.1038/nrc2162
Metabolism: A subtle role for HIF1
p407 | doi:10.1038/nrc2150
Breast cancer: AKT1 wears many hats
p407 | doi:10.1038/nrc2157
Progress
Changing venues for tumour suppression: balancing destruction and localization by monoubiquitylation
Leonardo Salmena & Pier Paolo Pandolfi
p409 | doi:10.1038/nrc2145
Three major tumour-suppressor proteins have recently been shown to undergo monoubiquitylation-mediated nuclear–cytoplasmic shuttling. Can our increasing knowledge of this mechanism be used to treat cancer?
Reviews
Snail, Zeb and bHLH factors in tumour progression: an alliance against the epithelial phenotype?
Héctor Peinado, David Olmeda & Amparo Cano
p415 | doi:10.1038/nrc2131
This article reviews how the identification of Snail, ZEB and some basic helix–loop–helix (bHLH) factors as inducers of epithelial–mesenchymal transition (EMT) and potent repressors of E cadherin expression has opened new avenues for cancer research with potential clinical implications.
The cofilin pathway in breast cancer invasion and metastasis
Weigang Wang, Robert Eddy & John Condeelis
p429 | doi:10.1038/nrc2148
Metastatic capacity appears to be an inherent feature of breast tumours. In this context, the cofilin pathway has been identified as a major determinant of metastasis and, as discussed in this Review, studies indicate that the overall activity of the cofilin pathway determines the invasive and metastatic phenotype of tumour cells.
Chronic myeloid leukaemia as a model of disease evolution in human cancer
Junia V. Melo & David J. Barnes
p441 | doi:10.1038/nrc2147
What leads to the incurable advanced phase of chronic myeloid leukaemia (CML)? This Review explores the mechanisms that underlie differentiation arrest, genomic instability and loss of tumour-suppressor function, which seem to drive the progression to blast crisis in CML and might help to identify new therapeutic targets. These findings can potentially be translated to other tumours that progress through similar mechanisms.
Nuclear microenvironments in biological control and cancer
Sayyed K. Zaidi, Daniel W. Young, Amjad Javed, Jitesh Pratap, Martin Montecino, Andre van Wijnen, Jane B. Lian, Janet L. Stein & Gary S. Stein
p454 | doi:10.1038/nrc2149
Nucleic acids and regulatory proteins are compartmentalized in microenvironments within the nucleus. These precise arrangements can be distrupted in cancer cells. How can we measure these changes and what might they tell us about cancer development and treatment?
Morphogens, morphostats, microarchitecture and malignancy
John D. Potter
p464 | doi:10.1038/nrc2146
We are all familiar with the concept of morphogens instructing tissue architecture during development, but how are tissue form and function maintained in the adult, and does this have a bearing on tumorigenesis?
Perspective
Opinion
Possible molecular mechanisms involved in the toxicity of angiogenesis inhibition
Henk. M. W. Verheul & Herbert M. Pinedo
p475 | doi:10.1038/nrc2152
Angiogenesis inhibitors are now being used in the treatment of patients with cancer. However, these agents can lead to toxicities. This Perspective discusses these toxicities and the possible molecular mechanisms behind them.
Erratum: HCLK2 is essential for the mammalian S-phase checkpoint and impacts on Chk1 stability
| doi:10.1038/nrc2166