Table of contents
November 2007 Vol 7 No 11
From the editors
p809 | doi:10.1038/nrc2269
Research Highlights
Ageing: Falling p53 function | PDF (343 KB)
p811 | doi:10.1038/nrc2265
Cancer stem cells: Underground movement | PDF (162 KB)
p812 | doi:10.1038/nrc2257
Genetics: Conserved by evolution, but altered in cancer | PDF (499 KB)
p812 | doi:10.1038/nrc2261
In the news
Dieting for the long term | PDF (74 KB)
p812 | doi:10.1038/nrc2268
Trial Watch
Trial and error | All or nothing? | PDF (85 KB)
p813 | doi:10.1038/nrc2266
Autophagy: Tumour or death? | PDF (122 KB)
p814 | doi:10.1038/nrc2259
Tumour suppressors: Sorting it out | PDF (403 KB)
p814 | doi:10.1038/nrc2260
In brief
Microenvironment | Inflammation | Cancer risk | Angiogenesis | PDF (92 KB)
p814 | doi:10.1038/nrc2267
Tumorigenesis: Size is everything | PDF (205 KB)
p815 | doi:10.1038/nrc2258
Genetics: Networks uncover new cancer susceptibility suspect | PDF (519 KB)
p816 | doi:10.1038/nrc2263
microRNA: Served with a TWIST | PDF (172 KB)
p816 | doi:10.1038/nrc2264
Tumorigenesis: A shocking enabler of tumour growth | PDF (188 KB)
p817 | doi:10.1038/nrc2262
Progress
microRNAs join the p53 network — another piece in the tumour-suppression puzzle
Lin He, Xingyue He, Scott W. Lowe & Gregory J. Hannon
p819 | doi:10.1038/nrc2232
Several recent papers have shown that the miR-34 family of microRNAs is directly involved in mediating the effects of p53, indicating that non-coding RNAs have an important role in tumorigenesis. This Progress article discusses these papers and their implications.
Reviews
MLL translocations, histone modifications and leukaemia stem-cell development
Andrei V. Krivtsov & Scott A. Armstrong
p823 | doi:10.1038/nrc2253
Mixed lineage leukaemia (MLL) has histone methyltransferase activity and regulates the expression of genes such as Hox genes. This activity is lost in MLL fusion proteins resulting from inter-chromosomal translocations, which are leukemogenic. How do MLL fusions function and what is their role in leukaemia stem cells?
Models, mechanisms and clinical evidence for cancer dormancy
Julio A. Aguirre-Ghiso
p834 | doi:10.1038/nrc2256
Cancer dormancy is a very important yet poorly understood phenomenon in cancer progression. What do we know about the mechanisms of cancer dormancy and can it be targeted therapeutically?
The emerging roles of forkhead box (Fox) proteins in cancer
Stephen S. Myatt & Eric W. -F. Lam
p847 | doi:10.1038/nrc2223
Fox proteins are transcriptional regulators of many biological processes. The authors discuss how these proteins are deregulated in cancer and the roles they have in both tumorigenesis and cancer progression.
See also: Correspondence by Radhakrishnan & Gartel
Perspectives
Opinion
The impact of a negligent G2/M checkpoint on genomic instability and cancer induction
Markus Löbrich & Penny A. Jeggo
p861 | doi:10.1038/nrc2248
How do DNA damage response pathways respond to low levels of DNA damage? Understanding this is essential when assessing environmental cancer risk. This Perspective considers the impact of a negligent G2/M checkpoint on genomic stability and cancer risk.
Opinion
Carboxypeptidase G2-based gene-directed enzyme–prodrug therapy: a new weapon in the GDEPT armoury
Douglas Hedley, Lesley Ogilvie & Caroline Springer
p870 | doi:10.1038/nrc2247
Gene-directed enzyme–prodrug therapy (GDEPT) aims to improve the therapeutic ratio by increasing tumour cell kill and decreasing systemic toxicity. How is this achieved and how close is this therapy to entering the clinic?
Opinion
Regulatory T-cell inhibition versus depletion: the right choice in cancer immunotherapy
Mario P. Colombo & Silvia Piconese
p880 | doi:10.1038/nrc2250
Tumour-induced expansion of regulatory T (TReg) cells is an obstacle to successful cancer immunotherapy. Does it make more sense to suppress the function of these cells rather than deplete them to improve the efficacy of cancer immunotherapy?
