Current Issue
From the editors
p763 | doi:10.1038/nrc2762
Research Highlights
Genetics: An unanticipated role | PDF (257 KB)
p765 | doi:10.1038/nrc2749
Genetics: Becoming mobile | PDF (195 KB)
p766 | doi:10.1038/nrc2750
MicroRNA: Stage-specific signatures | PDF (172 KB)
p766 | doi:10.1038/nrc2752
In brief
Therapy | Senescence | Genetics | PDF (105 KB)
p766 | doi:10.1038/nrc2758
Trial Watch
A double hit | Ligands could be key | PDF (123 KB)
p767 | doi:10.1038/nrc2759
Therapeutic resistance: Smoothing the way | PDF (193 KB)
p768 | doi:10.1038/nrc2751
Cancer stem cells: Symmetry is key | PDF (136 KB)
p768 | doi:10.1038/nrc2757
Hypoxia: HIF1 in opposition | PDF (223 KB)
p769 | doi:10.1038/nrc2755
Therapy: Swings and roundabouts | PDF (221 KB)
p770 | doi:10.1038/nrc2754
Genomics: We are individuals | PDF (157 KB)
p770 | doi:10.1038/nrc2756
In the news
Emotionally stressed | PDF (94 KB)
p770 | doi:10.1038/nrc2760
Nanotechnology: Take a deep breath | PDF (124 KB)
p771 | doi:10.1038/nrc2753
Focus on: p53 - 30 years on
Review
p53 — a Jack of all trades but master of none
Melissa R. Junttila & Gerard I. Evan
p821 | doi:10.1038/nrc2728
p53 is an evolutionarily ancient coordinator of metazoan stress responses and its role in tumour suppression is likely to be a relatively recent adaptation. This Review discusses how such evolutionary retooling of this venerable transcription factor entails compromises that restrict its efficacy as a tumour suppressor.
Perspectives
Timeline
20 years studying p53 functions in genetically engineered mice
Lawrence A. Donehower & Guillermina Lozano
p831 | doi:10.1038/nrc2731
Understanding the activities of p53 in tumour suppression and in other processes has been substantially aided by the use of mouse models. How have these models evolved and what have they taught us about p53 and tumour suppression?
Reviews
Article series: Epigenetics and genetics
Polycomb group proteins: navigators of lineage pathways led astray in cancer
Adrian P. Bracken & Kristian Helin
p773 | doi:10.1038/nrc2736
The Polycomb group (PcG) proteins are transcriptional repressors that regulate lineage choices during development and differentiation and are often deregulated in cancer. How might they become deregulated and how does this contribute to tumorigenesis?
Article series: RB and E2F
Emerging roles of E2Fs in cancer: an exit from cell cycle control
Hui-Zi Chen, Shih-Yin Tsai & Gustavo Leone
p785 | doi:10.1038/nrc2696
The E2F transcription factors function in cell cycle control and are intimately regulated by RB. However, some tumours have concurrent RB1 inactivation and E2F overexpression. Are there alternative tumour-promoting activities for the E2F family that are independent of cell cycle regulation?
STATs in cancer inflammation and immunity: a leading role for STAT3
Hua Yu, Drew Pardoll & Richard Jove
p798 | doi:10.1038/nrc2734
Signal transducer and activator of transcription (STAT) proteins help determine whether immune responses promote or inhibit tumours. Specifically, STAT3 increases tumour cell proliferation, survival and invasion and activates tumour-promoting inflammation, but also suppresses anti-tumour immune responses. STAT3 is therefore a promising target for cancer therapy.
NFAT proteins: emerging roles in cancer progression
Maria Mancini & Alex Toker
p810 | doi:10.1038/nrc2735
Although the nuclear factor of activated T cells (NFAT) transcription factors have been studied predominantly in the immune system, they are expressed in all tissues. This Review discusses the emerging roles of NFATs in cells that comprise the tumour and tumour microenvironment, and how this pathway might be targeted therapeutically.
Correspondence
Correspondence: Increase of wildlife cancer: an echo of plastic pollution?
Thomas Erren,
Dominique Zeu
,
Frank Steffany
&
Benno Meyer-Rochow
p842 | doi:10.1038/nrc2665-c1
Correspondence: Wildlife cancer and plastic pollution
Denise McAloose & Alisa L. Newton
p842 | doi:10.1038/nrc2665-c2
Correspondence: Genetic matters of CYP2D6 in breast cancer: copy number variations and nucleotide polymorphisms
Ke-Da Yu & Zhi-Ming Shao
p842 | doi:10.1038/nrc2683-c1

