Latest Articles Include:
- From the editors
- Nature Reviews Cancer 10(2):77 (2010)
As our knowledge of tumour development grows, our interpretations of the best methods for treating this heterogeneous disease also evolve. This is undoubtedly true for the diagnosis and treatment of oesophageal adenocarcinoma. - Wildlife cancer: The details are not so devilish
- Nature Reviews Cancer 10(2):79 (2010)
Devil facial tumour disease (DFTD) is a fatal cancer that affects the Tasmanian devil (Sarcophilus harrisii), an endangered species that is predicted to be extinct in 25–35 years as a result of DFTD. DFTD is thought to be a transmissible allograft tumour of neuroendocrine origin, but little is known about its biology. - Systems biology: Network spreading
- Nature Reviews Cancer 10(2):80 (2010)
High-grade gliomas, such as glioblastoma, are incurable partly because the tumour cells are widely disseminated throughout the brain. This capacity for invasive growth has been associated with the expression of genes more commonly transcribed in mesenchymal cells. - Metastasis: Motion capture
- Nature Reviews Cancer 10(2):80 (2010)
The ever more complex story of p53 and its relations took an interesting turn as the decade drew to a close. The function of mutant p53 proteins during tumour development is a hotly debated topic and a recent publication in Cell indicates that invasion, integrins and receptor recycling are all important to the tale. - Cancer code cracked?
- Nature Reviews Cancer 10(2):80 (2010)
The entire genome sequences of two individual cancers — one small-cell lung cancer and one melanoma — have revealed the staggering number of mutations present in tumour cells compared with normal cells from the same patient.The research, published in Nature, was led by Peter Campbell, Michael Stratton and Andrew Futreal at the Wellcome Trust Sanger Institute, UK. - In brief: Therapy, Genomic instability, Lymphoma, Tumorigenesis
- Nature Reviews Cancer 10(2):81 (2010)
Novel mutant-selective EGFR kinase inhibitors against EGFR T790M Zhou, W.et al. Nature 462, 1070–1074 (2009)Strategies to inhibit mutant epidermal growth factor receptor (EGFR) in non-small-cell lung cancer have been limited by the development of drug-resistant mutations, including the T790M mutation, and toxicity caused by inhibition of wild-type EGFR. - Computational biology: Mutual ties
- Nature Reviews Cancer 10(2):82 (2010)
Advances in sequencing and microarray technologies are providinga wealth of cancer genome and gene expression data. However, discovering the perturbed underlying networks remains a formidable challenge for cancer biology. - DNA damage response: DNA takes a break with SUMO
- Nature Reviews Cancer 10(2):82 (2010)
During the DNA damage response (DDR), repair proteins such as the E3 ubiquitin ligase BRCA1 accumulate at DNA double-stranded breaks (DSBs), and ubiquitylation at these sites helps recruit further repair proteins. Small ubiquitin-related modifier (SUMO) — which is attached to proteins by a pathway involving the E1 enzyme SAE1, the E2 enzyme UBC9 (also known as UBE21) and an E3 ligase (such as PIAS1 and PIAS4) — has also been implicated in the DDR, but its role was unclear. - Lymphomagenesis: Far, far away
- Nature Reviews Cancer 10(2):83 (2010)
Translocations involving the immunoglobulin heavy chain (Igh) locus and Myc are oncogenic, but the elements that are involved in activating the transcription of these fusion genes have not been resolved. Fred Alt, Monica Gostissa and colleagues have used mouse models to show that the Igh 3′ regulatory region (Igh3′ RR) can function over long distances to activate the transcription of translocated Myc. - Genome architecture: Reliable repositioning in cancer
- Nature Reviews Cancer 10(2):84 (2010)
One of the biggest challenges in cancer is proper diagnosis in the smallest possible amounts of tissue, such as that from a core needle biopsy in potential breast cancer cases. Routine protocols now in place generally rely on the opinion of a trained cytopathologist and have not been automated with any quantifiable assay. - Senescence: A key role for CDK2
- Nature Reviews Cancer 10(2):84 (2010)
Oncogenes such as KRAS and MYC promote growth, but their expression can also induce apoptosis or cellular senescence. Two papers reveal that cyclin-dependent kinase 2 (CDK2) both suppresses the induction of senescence by MYC and phosphorylates MYC to bypass Ras-induced senescence. - Angiogenesis: Regulating vessel size
- Nature Reviews Cancer 10(2):85 (2010)
Angiogenesis is a crucial step in tumour progression and is therefore an attractive target for therapeutic intervention. However, dissecting the role of angiogenesis genes in disease in vivo can be challenging as knockouts of many of these genes are embryonic lethal. - Barrett's oesophagus and oesophageal adenocarcinoma: time for a new synthesis
- Nature Reviews Cancer 10(2):87 (2010)
The public health importance of Barrett's oesophagus lies in its association with oesophageal adenocarcinoma. The incidence of oesophageal adenocarcinoma has risen at an alarming rate over the past four decades in many regions of the Western world, and there are indications that the incidence of this disease is on the rise in Asian populations in which it has been rare. Much has been learned of host and environmental risk factors that affect the incidence of oesophageal adenocarcinoma, and data indicate that patients with Barrett's oesophagus rarely develop oesophageal adenocarcinoma. Given that 95% of oesophageal adenocarcinomas arise in individuals without a prior diagnosis of Barrett's oesophagus, what strategies can be used to reduce late diagnosis of oesophageal adenocarcinoma? - Mitotic chromosomal instability and cancer: mouse modelling of the human disease
- Nature Reviews Cancer 10(2):102 (2010)
The stepwise progression from an early dysplastic lesion to full-blown metastatic malignancy is associated with increases in genomic instability. Mitotic chromosomal instability — the inability to faithfully segregate equal chromosome complements to two daughter cells during mitosis — is a widespread phenomenon in solid tumours that is thought to serve as the fuel for tumorigenic progression. How chromosome instability (CIN) arises in tumours and what consequences it has are still, however, hotly debated issues. Here we review the recent literature with an emphasis on models that recapitulate observations from human disease. - Fibroblast growth factor signalling: from development to cancer
- Nature Reviews Cancer 10(2):116 (2010)
Fibroblast growth factors (FGFs) and their receptors control a wide range of biological functions, regulating cellular proliferation, survival, migration and differentiation. Although targeting FGF signalling as a cancer therapeutic target has lagged behind that of other receptor tyrosine kinases, there is now substantial evidence for the importance of FGF signalling in the pathogenesis of diverse tumour types, and clinical reagents that specifically target the FGFs or FGF receptors are being developed. Although FGF signalling can drive tumorigenesis, in different contexts FGF signalling can mediate tumour protective functions; the identification of the mechanisms that underlie these differential effects will be important to understand how FGF signalling can be most appropriately therapeutically targeted. - Targeting the cancer kinome through polypharmacology
- Nature Reviews Cancer 10(2):130 (2010)
Kinase inhibitors are the largest class of new cancer drugs. However, it is already apparent that most tumours can escape from the inhibition of any single kinase. If it is necessary to inhibit multiple kinases, how do we choose which ones? In this Opinion article, we discuss some of the strategies that are currently being used to identify new therapeutic combinations of kinase targets. - Instructive role of the vascular niche in promoting tumour growth and tissue repair by angiocrine factors
- Nature Reviews Cancer 10(2):138 (2010)
The precise mechanisms whereby anti-angiogenesis therapy blocks tumour growth or causes vascular toxicity are unknown. We propose that endothelial cells establish a vascular niche that promotes tumour growth and tissue repair not only by delivering nutrients and O2 but also through an 'angiocrine' mechanism by producing stem and progenitor cell-active trophogens. Identification of endothelial-derived instructive angiocrine factors will allow direct tumour targeting, while diminishing the unwanted side effects associated with the use of anti-angiogenic agents. - ABC transporters in cancer: more than just drug efflux pumps
- Nature Reviews Cancer 10(2):147 (2010)
Multidrug transporter proteins are best known for their contributions to chemoresistance through the efflux of anticancer drugs from cancer cells. However, a considerable body of evidence also points to their importance in cancer extending beyond drug transport to fundamental roles in tumour biology. Currently, much of the evidence for these additional roles is correlative and definitive studies are needed to confirm causality. We propose that delineating the precise roles of these transporters in tumorigenesis and treatment response will be important for the development of more effective targeted therapies. - Correspondence: Parallel progression of tumour and metastases
- Nature Reviews Cancer 10(2):156 (2010)
The Opinion article (Parallel progression of primary tumours and metastases. Nature Rev. Cancer. 9, 302–312 (2009) - Correspondence: Tumour cell dissemination and growth of metastasis
- Nature Reviews Cancer 10(2):156 (2010)
I am grateful for the letter of S. Koscielny and M.
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