Hot off the presses! Sep 01 Nat Rev Cancer

The Sep 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(9):607 (2009)
  
• Metastasis: Influencing bad behaviour
  - Nat Rev Cancer 9(9):609 (2009)
  
• Tumour suppressors: Different roads to inactivation
  - Nat Rev Cancer 9(9):610 (2009)
  
• Metastasis: Route master
  - Nat Rev Cancer 9(9):610 (2009)
  
• In brief: Apoptosis, Prostate cancer
  - Nat Rev Cancer 9(9):611 (2009)
  
• Small RNAs: p53 makes microRNAs mature
  - Nat Rev Cancer 9(9):612 (2009)
  
• Tumour suppression: Full on
  - Nat Rev Cancer 9(9):612 (2009)
  
• In brief: Breast cancer, Oncogenes, Metabolism, Hypoxia
  - Nat Rev Cancer 9(9):612 (2009)
  
• Tumorigenesis: Replicating recurrence
  - Nat Rev Cancer 9(9):613 (2009)
  
• Normal and cancer-related functions of the p160 steroid receptor co-activator (SRC) family
  - Nat Rev Cancer 9(9):615-630 (2009)
  The three homologous members of the p160 SRC family (SRC1, SRC2 and SRC3) mediate the transcriptional functions of nuclear receptors and other transcription factors, and are the most studied of all the transcriptional co-activators. Recent work has indicated that the SRCgenes are subject to amplification and overexpression in various human cancers. Some of the molecular mechanisms responsible for SRC overexpression, along with the mechanisms by which SRCs promote breast and prostate cancer cell proliferation and survival, have been identified, as have the specific contributions of individual SRC family members to spontaneous breast and prostate carcinogenesis in genetically manipulated mouse models. These studies have identified new challenges for cancer research and therapy.
• Biological determinants of endocrine resistance in breast cancer
  - Nat Rev Cancer 9(9):631-643 (2009)
  Endocrine therapies targeting oestrogen action (anti-oestrogens, such as tamoxifen, and aromatase inhibitors) decrease mortality from breast cancer, but their efficacy is limited by intrinsic and acquired therapeutic resistance. Candidate molecular biomarkers and gene expression signatures of tamoxifen response emphasize the importance of deregulation of proliferation and survival signalling in endocrine resistance. However, definition of the specific genetic lesions and molecular processes that determine clinical endocrine resistance is incomplete. The development of large-scale computational and genetic approaches offers the promise of identifying the mediators of endocrine resistance that may be exploited as potential therapeutic targets and biomarkers of response in the clinic.
• RecQ helicases: multifunctional genome caretakers
  Chu WK Hickson ID - Nat Rev Cancer 9(9):644-654 (2009)
  Around 1% of the open reading frames in the human genome encode predicted DNA and RNA helicases. One highly conserved group of DNA helicases is the RecQ family. Genetic defects in three of the five human RecQ helicases, BLM, WRN and RECQ4, give rise to defined syndromes associated with cancer predisposition, some features of premature ageing and chromosomal instability. In recent years, there has been a tremendous advance in our understanding of the cellular functions of individual RecQ helicases. In this Review, we discuss how these proteins might suppress genomic rearrangements, and therefore function as 'caretaker' tumour suppressors.
• Avoidable global cancer deaths and total deaths from smoking
  - Nat Rev Cancer 9(9):655-664 (2009)
  On the basis of current consumption patterns, approximately 450 million adults will be killed by smoking between 2000 and 2050. At least half of these adults will die between 30 and 69 years of age, losing decades of productive life. Cancer and the total deaths due to smoking have fallen sharply in men in high-income countries but will rise globally unless current smokers, most of whom live in low- and middle-income countries, stop smoking before or during middle age. Tripling the taxes on tobacco could rapidly raise cessation rates and deter the initiation of smoking. Higher taxes, regulations on smoking and information for consumers could avoid at least 115 million smoking-associated deaths in the next few decades, including around 25 million cancer deaths.
• Environment-mediated drug resistance: a major contributor to minimal residual disease
  - Nat Rev Cancer 9(9):665-674 (2009)
  Environment-mediated drug resistance is a form of de novo drug resistance that protects tumour cells from the initial effects of diverse therapies. Surviving foci of residual disease can then develop complex and permanent acquired resistance in response to the selective pressure of therapy. Recent evidence indicates that environment-mediated drug resistance arises from an adaptive, reciprocal signalling dialogue between tumour cells and the surrounding microenvironment. We propose that new therapeutic strategies targeting this interaction should be applied during initial treatment to prevent the emergence of acquired resistance.
• Idiotype vaccines for lymphoma: proof-of-principles and clinical trial failures
  - Nat Rev Cancer 9(9):675-681 (2009)
  The clonal immunoglobulin idiotype displayed on the surface of most malignant B cells is a patient- and tumour-specific antigen that can be used for therapeutic vaccination. Several studies have confirmed the biological efficacy of soluble protein idiotypic vaccination and two clinical trials have shown the clinical efficacy of this procedure. One study has demonstrated clinical benefit associated with idiotypic vaccination. However, three randomized clinical trials have recently failed to achieve their main end points for reasons that are probably unrelated to the vaccine. While scepticism towards this type of non-toxic medical intervention is mounting, such patient-specific treatments might yet see the light of day through better designed clinical trials.