Genomics: Beyond the usual suspects

p225 | doi:10.1038/nrc2117

Therapy: Implementing interference

p226 | doi:10.1038/nrc2114

Signalling: DNA damage is stressful

p226 | doi:10.1038/nrc2116

Tumorigenesis: Alternative view

p228 | doi:10.1038/nrc2119

Epigenetics: Patterns of inheritance

p229 | doi:10.1038/nrc2115

MicroRNA: Let's suppress tumours

p229 | doi:10.1038/nrc2120

Radiation sensitivity: Tolerance is not a virtue

p230 | doi:10.1038/nrc2118

Virology: Inducing instability

p230 | doi:10.1038/nrc2121

Tumour suppressors: You're the one

p231 | doi:10.1038/nrc1221

The impact of translocations and gene fusions on cancer causation

Felix Mitelman, Bertil Johansson & Fredrik Mertens

p233 | doi:10.1038/nrc2091

Gene fusions are generally thought to be causally associated with sarcomas and haematological cancers, but recent evidence has shown that they occur in all malignancies, and account for 20% of human cancer morbidity. This Review discusses the implications of this for cancer research.

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Reprogramming metastatic tumour cells with embryonic microenvironments

Mary J. C. Hendrix, Elisabeth A. Seftor, Richard E. B. Seftor, Jennifer Kasemeier-Kulesa, Paul M. Kulesa & Lynne-Marie Postovit

p246 | doi:10.1038/nrc2108

Aggressive tumour cells share many characteristics with embryonic stem cells, contributing to the conundrum of tumour cell plasticity. This review discusses the evidence for the convergence of embryonic and tumorigenic signalling pathways, highlighting the most prominent targets that could be therapeutically beneficial.

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Inflammation in prostate carcinogenesis

Angelo M. De Marzo, Elizabeth A. Platz, Siobhan Sutcliffe, Jianfeng Xu, Henrik Grönberg, Charles G. Drake, Yasutomo Nakai, William B. Isaacs & William G. Nelson

p256 | doi:10.1038/nrc2090

Recent evidence indicates that both endogenous and environmental factors induce prostate inflammatory lesions that are proposed to increase the risk of cancer development. This Review explores different approaches aimed at clarifying whether inflammation drives prostate cancer and could be used to develop new prevention strategies.

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Human T-cell leukaemia virus type 1 (HTLV-1) infectivity and cellular transformation

Masao Matsuoka & Kuan-Teh Jeang

p270 | doi:10.1038/nrc2111

HTLV-1 causes adult T-cell leukaemia (ATL). The HTLV-1 Tax protein, which affects multiple cellular pathways, is required to transform cells. What are the molecular mechanisms of leukaemogenesis by Tax and other HTLV-1 genes?

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Protein kinase C and other diacylglycerol effectors in cancer

Erin M. Griner & Marcelo G. Kazanietz

p281 | doi:10.1038/nrc2110

Since the discovery of protein kinase C (PKC) in the 1980s, we still have only a partial understanding of how this family of serine/threonine kinases is involved in tumour promotion. What do we still need to learn and what about the other proteins known to respond downstream of the PKC activator diacylglycerol?

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Hyperactive Ras in developmental disorders and cancer

Suzanne Schubbert, Kevin Shannon & Gideon Bollag

p295 | doi:10.1038/nrc2109

Ras genes are the most common targets for somatic gain-of-function mutations in human cancer. Germline mutations that affect components of the Ras signalling pathway were shown to cause several developmental disorders. What are the implications of germline mutations in the Ras pathway for our understanding of normal developmental processes and cancer pathogenesis?

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