Thursday, March 24, 2011

Hot off the presses! Apr 01 Nat Rev Cancer

The Apr 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:

  • - Nat Rev Cancer 11(4):229 (2011)
  • Therapy: Trimming the excess | PDF (141 KB)
    - Nat Rev Cancer 11(4):231 (2011)
    Like seasoned travellers, cells do their best to avoid excess baggage, such as supernumerary chromosomes. But it is not easy being aneuploid: most cells collapse under the pressure of carrying an abnormal chromosome number.
  • Stem cells: The same, but different | PDF (190 KB)
    - Nat Rev Cancer 11(4):232 (2011)
    The development of human induced pluripotent stem cells (HiPSCs) has been hailed as a great ethical step forwards in regenerative medicine, because in principle these cells reduce the need to obtain and study human embryonic stem cells (HESCs). However, three papers published in Nature indicate that these cell types are not the same at the genomic and the epigenomic levels.
  • Tumour microenvironment: T cell opposition | PDF (163 KB)
    - Nat Rev Cancer 11(4):232 (2011)
    The types of T cells infiltrating the tumour microenvironment can correlate with different clinical outcomes, which reflect their diverse roles in tumour progression. Galon and colleagues investigated the influence of different T cell subsets on the outcome of patients with colorectal cancer.
  • DNA damage: Wrap-around care | PDF (126 KB)
    - Nat Rev Cancer 11(4):233 (2011)
    The existence of regions of DNA that are difficult to replicate is exemplified by chromosome fragile sites. These sites are overtly sensitive to small changes in the rate of DNA synthesis and can result in breaks in mitotic chromosomes.
  • Chromosome Instability: Chaos from within | PDF (155 KB)
    - Nat Rev Cancer 11(4):234 (2011)
    Aneuploidy, the gain or loss of chromosomes, is thought to primarily arise from mutations that disrupt mitosis or that alter centrosome numbers. However, routes to aneuploidy might actually be more varied.
  • Immunology: Pro-metastatic TReg cells get RANKed | PDF (115 KB)
    - Nat Rev Cancer 11(4):234 (2011)
    The presence of regulatory T (TReg) cells in breast cancer tumours marks an invasive phenotype and poor prognosis. A study published in Nature shows that, in addition to their immunosuppressive role in antitumoural responses, CD4+TReg cells contribute to mammary tumour metastasis through the expression of receptor activator of nuclear factor-κB ligand (RANKL; also known as TNFSF11).
  • Tumorigenesis: Wound-up tumours | PDF (149 KB)
    - Nat Rev Cancer 11(4):235 (2011)
    Cancer development and wound healing share common features that have led to the view that tumours are wounds that do not heal. Indeed, an increased risk of basal cell carcinoma (BCC) has been associated with both chronic and acute wounds, but the mechanisms underlying this association are unknown.

  • - Nat Rev Cancer 11(4):237 (2011)
  • Strategies to improve radiotherapy with targeted drugs
    - Nat Rev Cancer 11(4):239 (2011)
    Radiotherapy is used to treat approximately 50% of all cancer patients, with varying success. The dose of ionizing radiation that can be given to the tumour is determined by the sensitivity of the surrounding normal tissues. Strategies to improve radiotherapy therefore aim to increase the effect on the tumour or to decrease the effects on normal tissues. These aims must be achieved without sensitizing the normal tissues in the first approach and without protecting the tumour in the second approach. Two factors have made such approaches feasible: namely, an improved understanding of the molecular response of cells and tissues to ionizing radiation and a new appreciation of the exploitable genetic alterations in tumours. These have led to the development of treatments combining pharmacological interventions with ionizing radiation that more specifically target either tumour or normal tissue, leading to improvements in efficacy.
  • CD44: can a cancer-initiating cell profit from an abundantly expressed molecule?
    - Nat Rev Cancer 11(4):254 (2011)
    Can an abundantly expressed molecule be a reliable marker for the cancer-initiating cells (CICs; also known as cancer stem cells), which constitute the minority of cells within the mass of a tumour? CD44 has been implicated as a CIC marker in several malignancies of haematopoietic and epithelial origin. Is this a fortuitous coincidence owing to the widespread expression of the molecule or is CD44 expression advantageous as it fulfils some of the special properties that are displayed by CICs, such as self-renewal, niche preparation, epithelial–mesenchymal transition and resistance to apoptosis?
  • The tumorigenicity of human embryonic and induced pluripotent stem cells
    - Nat Rev Cancer 11(4):268 (2011)
    The unique abilities of human pluripotent stem cells to self-renew and to differentiate into cells of the three germ layers make them an invaluable tool for the future of regenerative medicine. However, the same properties also make them tumorigenic, and therefore hinder their clinical application. Hence, the tumorigenicity of human embryonic stem cells (HESCs) has been extensively studied. Until recently, it was assumed that human induced pluripotent stem cells (HiPSCs) would behave like their embryonic counterparts in respect to their tumorigenicity. However, a rapidly accumulating body of evidence suggests that there are important genetic and epigenetic differences between these two cell types, which seem to influence their tumorigenicity.
  • Testicular germ cell tumours: predisposition genes and the male germ cell niche
    - Nat Rev Cancer 11(4):278 (2011)
    Testicular germ cell tumours (TGCTs) of adults and adolescents are putatively derived from primordial germ cells or gonocytes. Recently reported genome-wide association studies implicate six gene loci that predispose to TGCT development. Remarkably, the functions of proteins encoded by genes within these regions bridge our understanding between the pathways involved in primordial germ cell physiology, male germ cell development and the molecular pathology of TGCTs. Furthermore, this improved understanding of the mechanisms underlying TGCT development and dissemination has clinical relevance for the management of patients with these tumours.
  • PTEN loss in the continuum of common cancers, rare syndromes and mouse models
    - Nat Rev Cancer 11(4):289 (2011)
    PTEN is among the most frequently inactivated tumour suppressor genes in sporadic cancer. PTEN has dual protein and lipid phosphatase activity, and its tumour suppressor activity is dependent on its lipid phosphatase activity, which negatively regulates the PI3K–AKT–mTOR pathway1, 2. Germline mutations in PTEN have been described in a variety of rare syndromes that are collectively known as the PTEN hamartoma tumour syndromes (PHTS). Cowden syndrome is the best-described syndrome within PHTS, with approximately 80% of patients having germline PTEN mutations3. Patients with Cowden syndrome have an increased incidence of cancers of the breast, thyroid and endometrium, which correspond to sporadic tumour types that commonly exhibit somatic PTEN inactivation. Pten deletion in mice leads to Cowden syndrome-like phenotypes, and tissue-specific Pten deletion has provided clues to the role of PTEN mutation and loss in specific tumour types. Studying PTEN in the continuum o! f rare syndromes, common cancers and mouse models provides insight into the role of PTEN in tumorigenesis and will inform targeted drug development.
  • The Bio-PIN: a concept to improve biobanking
    - Nat Rev Cancer 11(4):303 (2011)
    A new biobanking method is proposed, wherein samples and associated data would be deposited anonymously and labelled using a PIN code that is produced on the basis of personal biological characteristics, such as single nucleotide polymorphisms. The code would be the 'Bio-PIN' to uniquely distinguish the sample depositors, plus their samples and data. This method could help to diminish several long-discussed ethical, legal and societal problems in biobanking regarding privacy, informed consent, autonomy, data security and public trust.
  • Can corruption of chromosome cohesion create a conduit to cancer?
    - Nat Rev Cancer 11(4):309 (2011)
    In Figure 4 on page 205 of this article, the REC8 locus on chromosome 14 was labelled as 12q11.2, but it should have been 14q11.2.
  • Cell lineage and cell death: Caenorhabditis elegans and cancer research
    - Nat Rev Cancer 11(4):309 (2011)
    On page 51 of this article, it was stated that "The identification of CED-9 as a homologue of BCL-2 (REF. 16) has been cited as the 'Aha!' moment of discovery in the work on programmed cell death20, as it suggested that the mechanism was evolutionarily conserved in animals. The conservation of this crucial function in cell death was supported by experiments in which human BCL-2 expression rescued the cell death phenotype that is evident in ced 9 mutants17,21." The citation of reference 16 in the first sentence is incorrect and should have been reference 17. In addition, the references at the end of the second sentence should have been references 16 and 21 and not 17 and 21.
  • Genetic prognostic and predictive markers in colorectal cancer
    - Nat Rev Cancer 11(4):309 (2011)
    In the Acknowledgements section of this article on page 499 the following information was missing: I.T. was funded by the Oxford Comprehensive Biomedical Research Centre.

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