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| TABLE OF CONTENTS | |||||||||||||||||||||||||||||||||||||||||||||||
| August 2012 Volume 12 Number 8 | Advertisement | ||||||||||||||||||||||||||||||||||||||||||||||
| In this issue
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| Comment: Upper urinary tract urothelial cancers: where it is A:T Magali Olivier, Monica Hollstein, Heinz Hans Schmeiser, Kurt Straif & Christopher P. Wild p503 | doi:10.1038/nrc3311 Despite a ban on the use of plants of the Aristolochia genus in herbal medicine, as they contain known carcinogens, renal cancer attributable to the use of this plant seems to be more common than previously thought. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
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| REVIEWS | Top | ||||||||||||||||||||||||||||||||||||||||||||||
| Pushing the limits of targeted therapy in chronic myeloid leukaemia Thomas O'Hare, Matthew S. Zabriskie, Anna M. Eiring & Michael W. Deininger p513 | doi:10.1038/nrc3317 Although chronic myeloid leukaemia (CML) can be treated with tyrosine kinase inhibitors (TKIs) against BCR-ABL1, cure is not achieved in most cases. This Review provides an update on resistance to TKIs, and discusses strategies to target BCR-ABL1-independent resistance, which may be necessary to eliminate CML stem cells and advanced disease. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| Kinesins and cancer Oliver Rath & Frank Kozielski p527 | doi:10.1038/nrc3310 Kinesins — a family of molecular motors that travel unidirectionally along microtubule tracks — have emerged as potential targets for cancer drug development. As discussed in this Review, several compounds that inhibit mitotic kinesins have entered clinical trials and others are being developed, raising the possibility that the range of kinesin-based drug targets may expand in the future. Abstract | Full Text | PDF | Supplementary information | |||||||||||||||||||||||||||||||||||||||||||||||
| The rationale for targeting the LOX family in cancer Holly E. Barker, Thomas R. Cox & Janine T. Erler p540 | doi:10.1038/nrc3319 The family of lysyl oxidases (LOX) seem to have dichotomous roles in tumour progression: suppressing tumorigenesis and promoting metastasis. This Review discusses the functions of the LOX family and the rationale for targeting them. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| PERSPECTIVES | Top | ||||||||||||||||||||||||||||||||||||||||||||||
| TIMELINE The ERBB network: at last, cancer therapy meets systems biology Yosef Yarden & Gur Pines p553 | doi:10.1038/nrc3309 This Timeline article focuses on the ERBB network of receptor tyrosine kinases, which exemplifies how a constant dialogue between basic and clinical cancer research can lead to the development of both novel drugs and strategies to overcome acquired resistance. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| OPINION NRF2 and cancer: the good, the bad and the importance of context Michael B. Sporn & Karen T. Liby p564 | doi:10.1038/nrc3278 NFE2-related factor 2 (NRF2) has apparently contradictory roles in cancer. Activation of NRF2 contributes to the chemopreventive effects of various clinically used drugs against various diseases including cancer. However, NRF2 activity can also accelerate tumorigenesis in mouse models, thus highlighting a potential danger of NRF2 activation. This Opinion article discusses how these opposing roles might be reconciled. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| OPINION From cancer genomes to oncogenic drivers, tumour dependencies and therapeutic targets Cheryl Eifert & R. Scott Powers p572 | doi:10.1038/nrc3299 How many of the changes identified in human cancer by genome sequencing are meaningful? And how can we exploit these massive data sets to yield new therapeutic targets? This article outlines five approaches that aim to discover oncogenic drivers, tumour dependencies and, ultimately, new cancer therapies from cancer genome data. Abstract | Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
| Corrigendum: Developmental reprogramming of cancer susceptibility Cheryl Lyn Walker & Shuk-mei Ho p578 | doi:10.1038/nrc3334 Full Text | PDF | |||||||||||||||||||||||||||||||||||||||||||||||
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| *2011 Journal Citation Report (Thomson Reuters, 2012) |
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