Hot off the presses! Jun 01 Nat Rev Cancer

The Jun 01 issue of the Nat Rev Cancer is now up on Pubget (About Nat Rev Cancer): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

• From the editors
  - Nat Rev Cancer 9(6):379 (2009)
  
• Therapeutics: Selectively targeting turnover
  - Nat Rev Cancer 9(6):381 (2009)
  
• Proteomics: Biomarkers on a nanoscale
  - Nat Rev Cancer 9(6):382 (2009)
  
• Mouse Models: Closer than you think
  - Nat Rev Cancer 9(6):382 (2009)
  
• An ounce of prevention?
  - Nat Rev Cancer 9(6):382 (2009)
  
• In brief: Epigenetics, Metabolism, Biomarkers, Resistance
  - Nat Rev Cancer 9(6):383 (2009)
  
• Metastasis: Attack of the mutant p53
  - Nat Rev Cancer 9(6):384 (2009)
  
• Tumour Suppressors: Multi-tasking
  - Nat Rev Cancer 9(6):384 (2009)
  
• Melanoma: A more accurate diagnosis
  - Nat Rev Cancer 9(6):385 (2009)
  
• Prostate cancer: Resistance is (hopefully) futile
  - Nat Rev Cancer 9(6):386 (2009)
  
• Therapy: FGFR3 is key
  - Nat Rev Cancer 9(6):386 (2009)
  
• Personalized cocktails, Early warning
  - Nat Rev Cancer 9(6):386 (2009)
  
• Genomics: A modular approach to signalling
  - Nat Rev Cancer 9(6):387 (2009)
  
• High-throughput insertional mutagenesis screens in mice to identify oncogenic networks
  Kool J Berns A - Nat Rev Cancer 9(6):389-399 (2009)
  Retroviral insertional mutagenesis screens have been used for many years as a tool for cancer gene discovery. In recent years, completion of the mouse genome sequence as well as improved technologies for cloning and sequencing of retroviral insertions have greatly facilitated the retrieval of more complete data sets from these screens. The concomitant increase of the size of the screens allows researchers to address new questions about the genes and signalling networks involved in tumour development. In addition, the development of new insertional mutagenesis tools such as DNA transposons enables screens for cancer genes in tissues that previously could not be analysed by retroviral insertional mutagenesis.
• p21 in cancer: intricate networks and multiple activities
  - Nat Rev Cancer 9(6):400-414 (2009)
  One of the main engines that drives cellular transformation is the loss of proper control of the mammalian cell cycle. The cyclin-dependent kinase inhibitor p21 (also known as p21WAF1/Cip1) promotes cell cycle arrest in response to many stimuli. It is well positioned to function as both a sensor and an effector of multiple anti-proliferative signals. This Review focuses on recent advances in our understanding of the regulation of p21 and its biological functions with emphasis on its p53-independent tumour suppressor activities and paradoxical tumour-promoting activities, and their implications in cancer.
• The biology of ovarian cancer: new opportunities for translation
  Bast RC Hennessy B Mills GB - Nat Rev Cancer 9(6):415-428 (2009)
  Over the past two decades, the 5-year survival for ovarian cancer patients has substantially improved owing to more effective surgery and treatment with empirically optimized combinations of cytotoxic drugs, but the overall cure rate remains approximately 30%. Many investigators think that further empirical trials using combinations of conventional agents are likely to produce only modest incremental improvements in outcome. Given the heterogeneity of this disease, increases in long-term survival might be achieved by translating recent insights at the molecular and cellular levels to personalize individual strategies for treatment and to optimize early detection.
• Cancer prevention by tea: animal studies, molecular mechanisms and human relevance
  - Nat Rev Cancer 9(6):429-439 (2009)
  Extracts of tea, especially green tea, and tea polyphenols have been shown to inhibit the formation and development of tumours at different organ sites in animal models. There is considerable evidence that tea polyphenols, in particular (-)-epigallocatechin-3-gallate, inhibit enzyme activities and signal transduction pathways, resulting in the suppression of cell proliferation and enhancement of apoptosis, as well as the inhibition of cell invasion, angiogenesis and metastasis. Here, we review these biological activities and existing data relating tea consumption to human cancer risk in an attempt to understand the potential use of tea for cancer prevention.
• Facilitating replication under stress: an oncogenic function of MYC?
  Herold S Herkert B Eilers M - Nat Rev Cancer 9(6):441-444 (2009)
  Deregulated expression of MYC contributes to the genesis of multiple human tumours. The encoded protein, MYC, functions through the transcriptional regulation of large numbers of target genes. Recent publications show that MYC is closely involved in DNA replication and the checkpoint processes that monitor progress through the S phase, and suggest that limiting replication stress is a key function of this protein. These findings could have considerable implications for our understanding of how MYC transforms cells and which mechanisms protect normal cells from transformation by activated oncogenes.
• Inhibitors of indoleamine-2,3-dioxygenase for cancer therapy: can we see the wood for the trees?
  Löb S Königsrainer A Rammensee HG Opelz G Terness P - Nat Rev Cancer 9(6):445-452 (2009)
  Indoleamine-2,3-dioxygenase (IDO) is an immunosuppressive enzyme capable of inhibiting a destructive maternal T cell response against allogeneic fetuses. Expression of IDO is evident in tumours and is thought to enable escape from immunologically mediated rejection. Consequently, clinical trials using an inhibitor of IDO, 1-methyltryptophan (1MT), have been initiated. However, a review of the current literature indicates that we are far from understanding the biological relevance of IDO expression during tumorigenesis. A better understanding of IDO biology is needed to comprehend the effect of IDO inhibitors and to provide a rationale for their therapeutic application in cancer.