Table of contents
From the editors
p317 | doi:10.1038/nrc2138
Research Highlights
Metastasis: Inflammatory invasion
p319 | doi:10.1038/nrc2135
Expression profiling: Relative significance
p320 | doi:10.1038/nrc2132
Therapy: Crystal-clear targets?
p320 | doi:10.1038/nrc2133
Tumorigenisis: Branching defects
p321 | doi:10.1038/nrc2134
Tumour suppressor: Heads or tails? You lose!
p322 | doi:10.1038/nrc2137
In the news
Desperate patients turn to DCA
p322 | doi:10.1038/nrc2139
Immunotherapy: Beneficial loss
p322 | doi:10.1038/nrc2143
In brief
Genomic instability | Signalling | Innovation | Tumorigenesis
p323 | doi:10.1038/nrc2136
Metastasis: To grow and spread
p324 | doi:10.1038/nrc2140
Surprise, surprise | Hit and miss for cetuximab
p324 | doi:10.1038/nrc2142
Genetics: I am not a number...
p325 | doi:10.1038/nrc2141
Progress
The Delta paradox: DLL4 blockade leads to more tumour vessels but less tumour growth
Gavin Thurston, Irene Noguera-Troise & George D. Yancopoulos
p327 | doi:10.1038/nrc2130
Several recent papers have shown that the Delta-like ligand 4 (Dll4)-Notch system restrains angiogenesis but, paradoxically, Dll4 inhibition decreases tumour growth. Is too much angiogenesis actually a good thing?
Reviews
Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition
Thomas Force, Daniela S. Krause & Richard A. Van Etten
p332 | doi:10.1038/nrc2106
Although inhibition of tyrosine kinases has revolutionized cancer therapy, some of the inhibitors used have now been associated with cardiotoxicity. How does inhibition of cancer-relevant signalling pathways affect heart cells, and how can these effects be minimized?
Second generation inhibitors of BCR-ABL for the treatment of imatinib-resistant chronic myeloid leukaemia
Ellen Weisberg, Paul W. Manley, Sandra W. Cowan-Jacob, Andreas Hochhaus & James D. Griffin
p345 | doi:10.1038/nrc2126
Imatinib is a highly effective treatment for chronic myeloid leukaemia. However, patients often develop resistance to this ABL kinase inhibitor. This Review discusses second generation inhibitors of ABL and other signalling pathways that might help circumvent imatinib resistance.
Triterpenoids and rexinoids as multifunctional agents for the prevention and treatment of cancer
Karen T. Liby, Mark M. Yore & Michael B. Sporn
p357 | doi:10.1038/nrc2129
Synthetic oleanane triterpenoids and rexinoids are two new classes of multifunctional drugs. Both classes of agents can prevent and treat cancer in experimental animals. What promise do they hold for cancer prevention and treatment in humans?
Article series: Tumour Microenvironment
Laminin 332 in squamous-cell carcinoma
M. Peter Marinkovich
p370 | doi:10.1038/nrc2089
The basement membrane molecule laminin 332 (previously known as laminin 5) activates various signalling pathways and interacts with other basement membrane components to promote squamous-cell carcinoma (SCC) development. How does laminin 332 coordinate SCC tumorigenesis and can it be targeted therapeutically?
PIN1, the cell cycle and cancer
Elizabeth S. Yeh & Anthony R. Means
p381 | doi:10.1038/nrc2107
The peptidyl-prolyl isomerase PIN1 regulates a number of proteins important for cell-cycle progression, therefore it seems logical that alterations in PIN1 activity could be involved in tumorigenesis. But is loss or gain of function important?
Perspective
Timeline
Insights from transgenic mouse models of ERBB2-induced breast cancer
Josie Ursini-Siegel, Babette Schade, Robert D. Cardiff & William J. Muller
p389 | doi:10.1038/nrc2127
This Timeline article provides a historical perspective on the generation of mouse models of breast cancer induced by ERBB2 (also known as HER2). What have these models taught us and how similar are they to human breast cancer?
Erratum: Shaping the future of biomarker research
M. Carolina Hinestrosa, Kay Dickersin, Pamela Klein, Musa Mayer, Karin Noss, Dennis Slamon, George Sledge & Frances M. Visco
| doi:10.1038/nrc2144
