Hot off the presses! Aug 01 Nat Rev Cancer

The Aug 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:

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  - Nat Rev Cancer 11(8):533 (2011)
  
• Leukaemia and lymphoma: The expansive reach of TET2 | PDF (232 KB)
  - Nat Rev Cancer 11(8):535 (2011)
  The gene encoding the methyl cytosine dioxygenase TET2 is often targeted by monoallelic or biallelic loss-of-function mutations and genomic alterations in myeloid malignancies. To investigate the role of TET2 directly, two papers report mouse models of Tet2 deficiency.
• Cachexia: Putting the brakes on lipid loss | PDF (192 KB)
  - Nat Rev Cancer 11(8):536 (2011)
  Cancer-associated cachexia (CAC), a multifactorial wasting syndrome that is characterized by the loss of adipose tissue and muscle, occurs in many cancer patients, and about 15% of cancer-associated deaths can be attributed to CAC. Evidence suggests that fat breakdown in CAC is a result of the increased degradation of triglyceride lipids; so, Das, Zechner, Hoefler and colleagues examined the role of two enzymes that are crucial for triglyceride lipolysis in CAC.
• Disease mechanisms: Out with the old, in with the new | PDF (289 KB)
  - Nat Rev Cancer 11(8):536 (2011)
  Barrett's oesophagus, a precursor of oesophageal adenocarcinoma, is thought to be induced by acid reflux. One hallmark of this disease is a change from the stratified (layered) squamous oesophageal epithelium to a columnar, intestinal-like epithelium, a process known as metaplasia.
• Nanotechnology: Tag teams | PDF (225 KB)
  - Nat Rev Cancer 11(8):537 (2011)
  Nanoparticles are being used to address the long-standing problem of delivering and activating a cytotoxic drug specifically in tumours. Two recent papers have exploited some of the properties of nanoparticles to efficiently kill tumour cells in vivo.
• Systems biology: Lethal weaknesses | PDF (188 KB)
  - Nat Rev Cancer 11(8):538 (2011)
  We often tend to think of metabolic changes in isolation. However, what is important in metabolomics is the flux through the reaction cycles, as the dynamics of the system show both its strengths and its weaknesses.
• Ovarian cancer: Driving force | PDF (259 KB)
  - Nat Rev Cancer 11(8):538 (2011)
  In order to metastasize, ovarian cancer cells form clusters (spheroids) that travel through the ascites fluid and attach to organs within the peritoneal cavity, a process that requires invasion of the mesothelial cell layer covering these organs. A lack of mesothelial cells directly under ovarian tumour spheroids has been observed in electron micrographs, but how this mesothelial clearance occurs is unknown.
• Immunotherapy: A vaccine for prostate cancer? | PDF (225 KB)
  - Nat Rev Cancer 11(8):539 (2011)
  Virus-based anticancer strategies have attracted increasing interest in recent years, and oncolytic virus-based vaccine therapies have reached late-stage clinical trials. Now, reporting in Nature Medicine, the group of Richard Vile present a virus-based anticancer strategy that works predominantly by an immune-enhancing rather than an oncolytic mechanism.
• Advances in sarcoma genomics and new therapeutic targets
  - Nat Rev Cancer 11(8):541 (2011)
  Increasingly, human mesenchymal malignancies are being classified by the abnormalities that drive their pathogenesis. Although many of these aberrations are highly prevalent within particular sarcoma subtypes, few are currently targeted therapeutically. Indeed, most subtypes of sarcoma are still treated with traditional therapeutic modalities, and in many cases sarcomas are resistant to adjuvant therapies. In this Review, we discuss the core molecular determinants of sarcomagenesis and emphasize the emerging genomic and functional genetic approaches that, coupled with novel therapeutic strategies, have the potential to transform the care of patients with sarcoma.
• Cyclin D as a therapeutic target in cancer
  - Nat Rev Cancer 11(8):558 (2011)
  Cyclin D1, and to a lesser extent the other D-type cyclins, is frequently deregulated in cancer and is a biomarker of cancer phenotype and disease progression. The ability of these cyclins to activate the cyclin-dependent kinases (CDKs) CDK4 and CDK6 is the most extensively documented mechanism for their oncogenic actions and provides an attractive therapeutic target. Is this an effective means of targeting the cyclin D oncogenes, and how might the patient subgroups that are most likely to benefit be identified?
• Chemotaxis in cancer
  - Nat Rev Cancer 11(8):573 (2011)
  Chemotaxis of tumour cells and stromal cells in the surrounding microenvironment is an essential component of tumour dissemination during progression and metastasis. This Review summarizes how chemotaxis directs the different behaviours of tumour cells and stromal cells in vivo, how molecular pathways regulate chemotaxis in tumour cells and how chemotaxis choreographs cell behaviour to shape the tumour microenvironment and to determine metastatic spread. The central importance of chemotaxis in cancer progression is highlighted by discussion of the use of chemotaxis as a prognostic marker, a treatment end point and a target of therapeutic intervention.
• Cancer biology and NuRD: a multifaceted chromatin remodelling complex
  - Nat Rev Cancer 11(8):588 (2011)
  The nucleosome remodelling and histone deacetylase (NuRD; also known as Mi-2) complex regulates gene expression at the level of chromatin. The NuRD complex has been identified — using both genetic and molecular analyses — as a key determinant of differentiation in mouse embryonic stem cells and during development in various model systems. Similar to other chromatin remodellers, such as SWI/SNF and Polycomb complexes, NuRD has also been implicated in the regulation of transcriptional events that are integral to oncogenesis and cancer progression. Emerging molecular details regarding the recruitment of NuRD to specific loci during development, and the modulation of these events in cancer, are used to illustrate how the inappropriate localization of the complex could contribute to tumour biology.
• The different roles of ER subtypes in cancer biology and therapy
  - Nat Rev Cancer 11(8):597 (2011)
  By eliciting distinct transcriptional responses, the oestrogen receptors (ERs) ERα and ERβ exert opposite effects on cellular processes that include proliferation, apoptosis and migration and that differentially influence the development and the progression of cancer. Perturbation of ER subtype-specific expression has been detected in various types of cancer, and the differences in the expression of ERs are correlated with the clinical outcome. The changes in the bioavailability of ERs in tumours, together with their specific biological functions, promote the selective restoration of their activity as one of the major therapeutic approaches for hormone-dependent cancers.
• Calcium in tumour metastasis: new roles for known actors
  - Nat Rev Cancer 11(8):609 (2011)
  In most cases, metastasis, not the primary tumour per se, is the main cause of mortality in cancer patients. In order to effectively escape the tumour, enter the circulation and establish secondary growth in distant organs cancer cells must develop an enhanced propensity to migrate. The ubiquitous second messenger Ca2+ is a crucial regulator of cell migration. Recently, a number of known molecular players in cellular Ca2+ homeostasis, including calcium release-activated calcium channel protein 1 (ORAI1), stromal interaction molecule 1 (STIM1) and transient receptor potential (TRP) channels, have been implicated in tumour cell migration and the metastatic cell phenotype. We discuss how these developments have increased our understanding of the Ca2+ dependence of pro-metastatic behaviours.
• Correspondence: The two faces of autophagy and the pathological underestimation of DCIS
  - Nat Rev Cancer 11(8):618 (2011)
  We read with great interest the Opinion article (What is the malignant nature of human ductal carcinoma in situ?Nature Rev. Cancer 11, 68–75 (2011)
• Otto Warburg's contributions to current concepts of cancer metabolism
  - Nat Rev Cancer 11(8):618 (2011)
  The acknowledgement for the source of Figure 1 on page 327 of this article was incorrect and has now been corrected online.