Tuesday, January 24, 2012

Hot off the presses! Feb 01 Nat Rev Cancer

The Feb 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:

  • Breast cancer: Reprogramming ERα | PDF (274 KB)
    - Nat Rev Cancer 12(2):79 (2012)
    The transcription factor oestrogen receptor-α (ERα) is expressed in most breast cancers, and the expression of its target genes, which vary between tumours, drives tumour growth and invasion and determines the response to endocrine therapy. Understanding what determines ERα binding to chromatin and what determines target gene selection and expression is therefore important for improving the treatment of patients with breast cancer.
  • Angiogenesis: What's the alternative? | PDF (295 KB)
    - Nat Rev Cancer 12(2):80 (2012)
    Alternative splicing of vascular endothelial growth factor A (VEGFA) leads to the formation of pro-angiogenic or anti-angiogenic isoforms. The anti-angiogenic isoform VEGFA165b is suppressed in patients with Denys–Drash Syndrome (DDS), which is caused by mutation in the Wilms' tumour suppressor gene (WT1) and that predisposes to highly vascularized kidney tumours (Wilms' tumours).
  • Signalling: SRC and survival | PDF (143 KB)
    - Nat Rev Cancer 12(2):80 (2012)
    When deregulated, the tyrosine kinase SRC can cause havoc in cells in which it is overexpressed. Recent results from Margaret Frame, Simon Wilkinson, Emma Sandilands and colleagues have shown that, in cancer cells in which the SRC pathway is hyperactive, active SRC is subject to autophagy as a route to enable cancer cell survival.
  • Retinoblastoma: Epigenetic outcome | PDF (272 KB)
    - Nat Rev Cancer 12(2):80 (2012)
    Retinoblastoma is a childhood cancer that arises owing to the inactivation of both copies of the tumour suppressor RB1. A recent paper published in Nature shows that, aside from this genetic change, few genetic alterations are evident and instead epigenetic changes are paramount.
  • Cancer stem cells: TAZ takes centre stage | PDF (238 KB)
    - Nat Rev Cancer 12(2):82 (2012)
    Epithelial to mesenchymal transition (EMT) is a process in which cells lose epithelial-like characteristics, such as cell–cell adhesion and polarity, and acquire mesenchymal properties that include increased motility. Most carcinomas exhibit a partial EMT, which is thought to promote the formation of cell populations that are enriched in cancer stem cells (CSCs).
  • Therapeutics: Keeping one step ahead | PDF (170 KB)
    - Nat Rev Cancer 12(2):82 (2012)
    Inhibiting the oncogenic kinase BCR–ABL1, which causes chronic myeloid leukaemia (CML), is a paradigm for clinically successful targeted therapy. However, drug-resistant mutations frequently emerge during clinical treatment.
  • Bevacizumab in ovarian cancer | PDF (88 KB)
    - Nat Rev Cancer 12(2):83 (2012)
    Expression of vascular endothelial growth factor (VEGF) and angiogenesis correlate with ovarian cancer progression, and the VEGF-neutralizing monoclonal antibody bevacizumab has shown activity in Phase II trials in ovarian cancer. Two Phase III trials have now shown that bevacizumab may be beneficial when added to standard chemotherapy in the first-line treatment of ovarian cancer.
  • Therapeutics: Mosaic glioblastoma | PDF (156 KB)
    - Nat Rev Cancer 12(2):81 (2012)
    Snuderl et al. analysed receptor tyrosine kinase (RTK) mutations in glioblastoma and found that around 5% of samples had co-amplification of RTKs, including epidermal growth factor receptor (EGFR), MET and platelet-derived growth factor receptor-α.

  • - Nat Rev Cancer 12(2):81 (2012)

  • - Nat Rev Cancer 12(2):81 (2012)

  • - Nat Rev Cancer 12(2):81 (2012)
  • Metabolism: Catabolic effects
    - Nat Rev Cancer 12(2):83 (2012)
    Nature Reviews Cancer11, 757 (2011) 10.1038/nrc3161 In the above Research Highlight, the sentence "Infiltration of immune cells into TDO-expressing tumours was attenuated in Ahr-/- host mice, underscoring the importance of AHR in the recruitment of immune cells." is incorrect. This has been corrected online to "Infiltration of immune cells into TDO-expressing tumours was attenuated in Ahr-proficient, but not Ahr-/- host mice, underscoring the importance of AHR in suppressing immune cell recruitment."
  • Are snoRNAs and snoRNA host genes new players in cancer?
    - Nat Rev Cancer 12(2):84 (2012)
    Small nucleolar RNAs (snoRNAs) have long been considered important but unglamorous elements in the production of the protein synthesis machinery of the cell. Recently, however, several independent lines of evidence have indicated that these non-coding RNAs might have crucial roles in controlling cell behaviour, and snoRNA dysfunction could consequently contribute to oncogenesis in previously unsuspected ways.
  • Targeting MET in cancer: rationale and progress
    - Nat Rev Cancer 12(2):89 (2012)
    Uncontrolled cell survival, growth, angiogenesis and metastasis are essential hallmarks of cancer. Genetic and biochemical data have demonstrated that the growth and motility factor hepatocyte growth factor/scatter factor (HGF/SF) and its receptor, the tyrosine kinase MET, have a causal role in all of these processes, thus providing a strong rationale for targeting these molecules in cancer. Parallel progress in understanding the structure and function of HGF/SF, MET and associated signalling components has led to the successful development of blocking antibodies and a large number of small-molecule MET kinase inhibitors. In this Review, we discuss these advances, as well as results from recent clinical studies that demonstrate that inhibiting MET signalling in several types of solid human tumours has major therapeutic value.
  • Balancing repair and tolerance of DNA damage caused by alkylating agents
    - Nat Rev Cancer 12(2):104 (2012)
    Alkylating agents constitute a major class of frontline chemotherapeutic drugs that inflict cytotoxic DNA damage as their main mode of action, in addition to collateral mutagenic damage. Numerous cellular pathways, including direct DNA damage reversal, base excision repair (BER) and mismatch repair (MMR), respond to alkylation damage to defend against alkylation-induced cell death or mutation. However, maintaining a proper balance of activity both within and between these pathways is crucial for a favourable response of an organism to alkylating agents. Furthermore, the response of an individual to alkylating agents can vary considerably from tissue to tissue and from person to person, pointing to genetic and epigenetic mechanisms that modulate alkylating agent toxicity.
  • The diverse and complex roles of NF-κB subunits in cancer
    - Nat Rev Cancer 12(2):121 (2012)
    It is only recently that the full importance of nuclear factor-κB (NF-κB) signalling to cancer development has been understood. Although much attention has focused on the upstream pathways leading to NF-κB activation, it is now becoming clear that the inhibitor of NF-κB kinases (IKKs), which regulate NF-κB activation, have many independent functions in tissue homeostasis and normal immune function that could compromise the clinical utility of IKK inhibitors. Therefore, if the NF-κB pathway is to be properly exploited as a target for both anticancer and anti-inflammatory drugs, it is appropriate to reconsider the complex roles of the individual NF-κB subunits.
  • Cancer stem cells: an evolving concept
    - Nat Rev Cancer 12(2):133 (2012)
    The cancer stem cell (CSC) concept derives from the fact that cancers are dysregulated tissue clones whose continued propagation is vested in a biologically distinct subset of cells that are typically rare. This idea is not new, but has recently gained prominence because of advances in defining normal tissue hierarchies, a greater appreciation of the multistep nature of oncogenesis and improved methods to propagate primary human cancers in immunodeficient mice. As a result we have obtained new insights into why the CSC concept is not universally applicable, as well as a new basis for understanding the complex evolution, phenotypic heterogeneity and therapeutic challenges of many human cancers.
  • Mouse models of cancer: does the strain matter?
    - Nat Rev Cancer 12(2):144 (2012)
    Mouse models are indispensible tools for understanding the molecular basis of cancer. However, despite the invaluable data provided regarding tumour biology, owing to inbreeding, current mouse models fail to accurately model human populations. Polymorphism is the essential characteristic that makes each of us unique humans, with different disease susceptibility, presentation and progression. Therefore, as we move closer towards designing clinical treatment that is based on an individual's unique biological makeup, it is imperative that we understand how inherited variability influences cancer phenotypes, how it can confound experiments and how it can be exploited to reveal new truths about cancer biology.
  • Correspondence: On the evidence for ESR1 amplification in breast cancer
    - Nat Rev Cancer 12(2):149 (2012)
    We read the correspondence regarding the recent Review (The different roles of ER subtypes in cancer biology and therapy. Nature Rev. Cancer, 597–608 (2011)

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