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TABLE OF CONTENTS
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November 2018 Volume 18, Issue 11 |
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| Research Highlights Reviews Perspectives Amendments & Corrections | |
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Research Highlights | |
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BETting on YAP–TAZ Ulrike Harjes p663 | doi:10.1038/s41568-018-0065-9 Two papers recently published in Nature Medicine and Science Signaling highlight the various interdependent or independent ways by which YAP and TAZ can affect tumour growth. PDF
| mRNA alterations mimic genetic mutations Sarah Seton-Rogers pp664 - 665 | doi:10.1038/s41568-018-0059-7 Lee, Singh et al. find that cancer-specific intronic polyadenylation events occur frequently in tumour suppressor genes in chronic lymphocytic leukaemia (CLL) and generate truncated proteins that could act as CLL drivers. PDF
| STAT3's true colours Maria Giuseppina Baratta pp664 - 665 | doi:10.1038/s41568-018-0062-z D'Amico et al. show that, in the presence of oncogenic RAS mutations, STAT3 acts as a tumour modifier by regulating the epithelial differentiation of pancreatic and lung cancer cells via p63. PDF
| Neighbourly deaths dictate fate Anna Dart p665 | doi:10.1038/s41568-018-0064-x Seehawer, Heinzmann et al. show that lineage commitment in liver cancer is independent of oncogenic driver expression and is instead dictated by the type of cell death occurring in the nearby liver microenvironment. PDF
| A multiplexed view of immune infiltration Sarah Seton-Rogers pp666 - 667 | doi:10.1038/s41568-018-0063-y Keren et al. have used multiplexed imaging in intact samples from breast cancer patients to gain insights into the architecture of the tumour immune microenvironment. PDF
| Back to the beginning to understand metastasis Sarah Seton-Rogers pp666 - 667 | doi:10.1038/s41568-018-0069-5 Yang et al. have used genetically engineered mouse models of small cell lung cancer to show that the same genomic alterations in different cells of origin lead to the formation of tumours that follow distinct evolutionary paths to metastasis. PDF
| SPOP mutations disrupt phase separation Sarah Seton-Rogers p667 | doi:10.1038/s41568-018-0066-8 PDF
| New targets for cancer immunotherapy Anna Dart p667 | doi:10.1038/s41568-018-0067-7 PDF
| Oncogenic mRNA modification explained Ulrike Harjes p667 | doi:10.1038/s41568-018-0068-6 PDF
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Reviews | |
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Stem cell fate in cancer growth, progression and therapy resistance Nikki K. Lytle, Alison G. Barber & Tannishtha Reya pp669 - 680 | doi:10.1038/s41568-018-0056-x This Review discusses how cells with stem cell characteristics often serve as the tumour cell of origin, as they are preferentially primed for transformation. Furthermore, the activation of stem cell programmes can be crucial for promoting cancer progression and therapy resistance. Full Text | PDF
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Polyamine metabolism and cancer: treatments, challenges and opportunities Robert A. Casero Jr, Tracy Murray Stewart & Anthony E. Pegg pp681 - 695 | doi:10.1038/s41568-018-0050-3 This Review discusses new insights into molecular mechanisms that link the dysregulation of polyamine metabolism with carcinogenesis and strategies for targeting this pathway for cancer therapy. Full Text | PDF
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The COSMIC Cancer Gene Census: describing genetic dysfunction across all human cancers Zbyslaw Sondka, Sally Bamford, Charlotte G. Cole, Sari A. Ward, Ian Dunham et al. pp696 - 705 | doi:10.1038/s41568-018-0060-1 This Review discusses the 2018 Catalogue of Somatic Mutations in Cancer (COSMIC) Cancer Gene Census (CGC), an expert-curated description of human cancer genes, which has recently been expanded to include functional descriptions of how each gene contributes to cancer. Full Text | PDF
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SPOTLIGHT ON KANAZAWA
An alternative Japan experience - Meet the sides of Japanese cities that most international researchers never see | | |
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Perspectives | |
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Fasting and cancer: molecular mechanisms and clinical application Alessio Nencioni, Irene Caffa, Salvatore Cortellino & Valter D. Longo pp707 - 719 | doi:10.1038/s41568-018-0061-0 This Opinion discusses the potential of fasting and fasting-mimicking diets to help overcome toxicities induced by anticancer therapy. The differential response of normal and cancer cells undergoing starvation is argued to make normal cells less sensitive to therapy-induced toxicity, while cancer cells become more sensitive to therapy-induced cell death. Full Text | PDF Collection: Cancer at Nature Research
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Nature Outlook: Brain cancer
The uncontrolled growth of a tumour inside the brain creates an extraordinarily potent threat to our being. A diagnosis of brain cancer still carries the high likelihood of death within five years. But efforts to prolong survival are advancing on several fronts.
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Produced with support from Novocure | |
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Amendments & Corrections | |
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Publisher Correction: Engineering and physical sciences in oncology: challenges and opportunities Michael J. Mitchell, Rakesh K. Jain & Robert Langer p720 | doi:10.1038/s41568-018-0072-x Full Text | PDF
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