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  • Classifying the evolutionary and ecological features of neoplasms
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Carlo C. Maley, Athena Aktipis, Trevor A. Graham, Andrea Sottoriva, Amy M. Boddy, Michalina Janiszewska, Ariosto S. Silva, Marco Gerlinger, Yinyin Yuan, Kenneth J. Pienta, Karen S. Anderson, Robert Gatenby, Charles Swanton, David Posada, Chung-I Wu, Joshua D. Schiffman, E. Shelley Hwang, Kornelia Polyak, Alexander R. A. Anderson, Joel S. Brown, Mel Greaves, Darryl Shibata

    Classifying the evolutionary and ecological features of neoplasmsNature Reviews Cancer, Published online: 15 September 2017; doi:10.1038/nrc.2017.69Based on a consensus conference of experts in the evolution and ecology of cancer, this article proposes a framework for classifying tumours that includes four evolutionary and ecological processes: neoplastic cell diversity and changes over time in that diversity, hazards to cell survival and available resources.

    更新日期:2017-09-15
  • Tumour acidosis: from the passenger to the driver's seat
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Cyril Corbet, Olivier Feron

    The high metabolic demand of cancer cells leads to an accumulation of H+ ions in the tumour microenvironment. The disorganized tumour vasculature prevents an efficient wash-out of H+ ions released into the extracellular medium but also favours the development of tumour hypoxic regions associated with a shift towards glycolytic metabolism. Under hypoxia, the final balance of glycolysis, including breakdown of generated ATP, is the production of lactate and a stoichiometric amount of H+ ions. Another major source of H+ ions results from hydration of CO2 produced in the more oxidative tumour areas. All of these events occur at high rates in tumours to fulfil bioenergetic and biosynthetic needs. This Review summarizes the current understanding of how H+-generating metabolic processes segregate within tumours according to the distance from blood vessels and inversely how ambient acidosis influences tumour metabolism, reducing glycolysis while promoting mitochondrial activity. The Review also presents novel insights supporting the participation of acidosis in cancer progression via stimulation of autophagy and immunosuppression. Finally, recent advances in the different therapeutic modalities aiming to either block pH-regulatory systems or exploit acidosis will be discussed.

    更新日期:2017-09-15
  • Interrogating open issues in cancer medicine with patient-derived xenografts
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Annette T. Byrne, Denis G. Alférez, Frédéric Amant, Daniela Annibali, Joaquín Arribas, Andrew V. Biankin, Alejandra Bruna, Eva Budinská, Carlos Caldas, David K. Chang, Robert B. Clarke, Hans Clevers, George Coukos, Virginie Dangles-Marie, S. Gail Eckhardt, Eva Gonzalez-Suarez, Els Hermans, Manuel Hidalgo, Monika A. Jarzabek, Steven de Jong, Jos Jonkers, Kristel Kemper, Luisa Lanfrancone, Gunhild Mari Mælandsmo, Elisabetta Marangoni, Jean-Christophe Marine, Enzo Medico, Jens Henrik Norum, Héctor G. Palmer, Daniel S. Peeper, Pier Giuseppe Pelicci, Alejandro Piris-Gimenez, Sergio Roman-Roman, Oscar M. Rueda, Joan Seoane, Violeta Serra, Laura Soucek, Dominique Vanhecke, Alberto Villanueva, Emilie Vinolo, Andrea Bertotti, Livio Trusolino

    Interrogating open issues in cancer medicine with patient-derived xenograftsNature Reviews Cancer, Published online: 15 September 2017; doi:10.1038/nrc.2017.85

    更新日期:2017-09-15
  • Classifying the evolutionary and ecological features of neoplasms
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-09-15
    Carlo C. Maley, Athena Aktipis, Trevor A. Graham, Andrea Sottoriva, Amy M. Boddy, Michalina Janiszewska, Ariosto S. Silva, Marco Gerlinger, Yinyin Yuan, Kenneth J. Pienta, Karen S. Anderson, Robert Gatenby, Charles Swanton, David Posada, Chung-I Wu, Joshua D. Schiffman, E. Shelley Hwang, Kornelia Polyak, Alexander R. A. Anderson, Joel S. Brown, Mel Greaves, Darryl Shibata

    Classifying the evolutionary and ecological features of neoplasmsNature Reviews Cancer, Published online: 15 September 2017; doi:10.1038/nrc.2017.69Based on a consensus conference of experts in the evolution and ecology of cancer, this article proposes a framework for classifying tumours that includes four evolutionary and ecological processes: neoplastic cell diversity and changes over time in that diversity, hazards to cell survival and available resources.

    更新日期:2017-09-15
  • Tumour acidosis: from the passenger to the driver's seat
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-09-15
    Cyril Corbet, Olivier Feron

    The high metabolic demand of cancer cells leads to an accumulation of H+ ions in the tumour microenvironment. The disorganized tumour vasculature prevents an efficient wash-out of H+ ions released into the extracellular medium but also favours the development of tumour hypoxic regions associated with a shift towards glycolytic metabolism. Under hypoxia, the final balance of glycolysis, including breakdown of generated ATP, is the production of lactate and a stoichiometric amount of H+ ions. Another major source of H+ ions results from hydration of CO2 produced in the more oxidative tumour areas. All of these events occur at high rates in tumours to fulfil bioenergetic and biosynthetic needs. This Review summarizes the current understanding of how H+-generating metabolic processes segregate within tumours according to the distance from blood vessels and inversely how ambient acidosis influences tumour metabolism, reducing glycolysis while promoting mitochondrial activity. The Review also presents novel insights supporting the participation of acidosis in cancer progression via stimulation of autophagy and immunosuppression. Finally, recent advances in the different therapeutic modalities aiming to either block pH-regulatory systems or exploit acidosis will be discussed.

    更新日期:2017-09-15
  • Interrogating open issues in cancer medicine with patient-derived xenografts
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Annette T. Byrne, Denis G. Alférez, Frédéric Amant, Daniela Annibali, Joaquín Arribas, Andrew V. Biankin, Alejandra Bruna, Eva Budinská, Carlos Caldas, David K. Chang, Robert B. Clarke, Hans Clevers, George Coukos, Virginie Dangles-Marie, S. Gail Eckhardt, Eva Gonzalez-Suarez, Els Hermans, Manuel Hidalgo, Monika A. Jarzabek, Steven de Jong, Jos Jonkers, Kristel Kemper, Luisa Lanfrancone, Gunhild Mari Mælandsmo, Elisabetta Marangoni, Jean-Christophe Marine, Enzo Medico, Jens Henrik Norum, Héctor G. Palmer, Daniel S. Peeper, Pier Giuseppe Pelicci, Alejandro Piris-Gimenez, Sergio Roman-Roman, Oscar M. Rueda, Joan Seoane, Violeta Serra, Laura Soucek, Dominique Vanhecke, Alberto Villanueva, Emilie Vinolo, Andrea Bertotti, Livio Trusolino

    Interrogating open issues in cancer medicine with patient-derived xenograftsNature Reviews Cancer, Published online: 15 September 2017; doi:10.1038/nrc.2017.85

    更新日期:2017-09-15
  • Leukaemia: Beyond the C
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-09-08
    Ulrike Harjes

    Leukaemia: Beyond the CNature Reviews Cancer, Published online: 8 September 2017; doi:10.1038/nrc.2017.81Vitamin C supplementation has shown limited benefits in patients with solid tumours. Two studies report that vitamin C supplementation can reduce Tet-dependent leukaemia progression in mice, supporting the concept of high-dose vitamin C supplementation in certain patients with haematological malignancies.

    更新日期:2017-09-15
  • Prostate cancer: BET inhibitors — SPOP right there!
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-09-08
    Conor A. Bradley

    Prostate cancer: BET inhibitors — SPOP right there!Nature Reviews Cancer, Published online: 8 September 2017; doi:10.1038/nrc.2017.80Although speckle-type POZ protein (SPOP) is the most frequently mutated gene in primary prostate cancer, its therapeutic implications are incompletely understood. Now, three studies describe mechanisms of resistance to bromodomain and extraterminal (BET) protein inhibitors in SPOP-mutated prostate cancer.

    更新日期:2017-09-15
  • Metaplasia: tissue injury adaptation and a precursor to the dysplasia–cancer sequence
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-09-01
    Veronique Giroux, Anil K. Rustgi

    Metaplasia is the replacement of one differentiated somatic cell type with another differentiated somatic cell type in the same tissue. Typically, metaplasia is triggered by environmental stimuli, which may act in concert with the deleterious effects of microorganisms and inflammation. The cell of origin for intestinal metaplasia in the oesophagus and stomach and for pancreatic acinar–ductal metaplasia has been posited through genetic mouse models and lineage tracing but has not been identified in other types of metaplasia, such as squamous metaplasia. A hallmark of metaplasia is a change in cellular identity, and this process can be regulated by transcription factors that initiate and/or maintain cellular identity, perhaps in concert with epigenetic reprogramming. Universally, metaplasia is a precursor to low-grade dysplasia, which can culminate in high-grade dysplasia and carcinoma. Improved clinical screening for and surveillance of metaplasia might lead to better prevention or early detection of dysplasia and cancer.

    更新日期:2017-09-15
  • Targeting neoantigens to augment antitumour immunity
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Mark Yarchoan, Burles A. Johnson III, Eric R. Lutz, Daniel A. Laheru, Elizabeth M. Jaffee

    Targeting neoantigens to augment antitumour immunityNature Reviews Cancer, Published online: 24 August 2017; doi:10.1038/nrc.2017.74

    更新日期:2017-09-15
  • Metastasis: Throwing oil into the flames
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Ulrike Harjes

    Metastasis: Throwing oil into the flamesNature Reviews Cancer, Published online: 24 August 2017; doi:10.1038/nrc.2017.76Both obesity and systemic inflammation promote cancer progression, although how obesity-associated inflammation affects cancer metastasis is poorly understood. Quail et al. now show that obesity induces cytokines that stimulate lung neutrophilia in mice, thereby promoting breast cancer metastasis.

    更新日期:2017-09-15
  • Leukaemia: Beyond the C
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Ulrike Harjes

    Leukaemia: Beyond the C Nature Reviews Cancer, Published online: 8 September 2017; doi:10.1038/nrc.2017.81 Vitamin C supplementation has shown limited benefits in patients with solid tumours. Two studies report that vitamin C supplementation can reduce Tet-dependent leukaemia progression in mice, supporting the concept of high-dose vitamin C supplementation in certain patients with haematological malignancies.

    更新日期:2017-09-14
  • Prostate cancer: BET inhibitors — SPOP right there!
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Conor A. Bradley

    Prostate cancer: BET inhibitors — SPOP right there! Nature Reviews Cancer, Published online: 8 September 2017; doi:10.1038/nrc.2017.80 Although speckle-type POZ protein (SPOP) is the most frequently mutated gene in primary prostate cancer, its therapeutic implications are incompletely understood. Now, three studies describe mechanisms of resistance to bromodomain and extraterminal (BET) protein inhibitors in SPOP-mutated prostate cancer.

    更新日期:2017-09-14
  • Metaplasia: tissue injury adaptation and a precursor to the dysplasia–cancer sequence
    Nat. Rev. Cancer (IF 37.147) Pub Date : 
    Veronique Giroux, Anil K. Rustgi

    Metaplasia is the replacement of one differentiated somatic cell type with another differentiated somatic cell type in the same tissue. Typically, metaplasia is triggered by environmental stimuli, which may act in concert with the deleterious effects of microorganisms and inflammation. The cell of origin for intestinal metaplasia in the oesophagus and stomach and for pancreatic acinar–ductal metaplasia has been posited through genetic mouse models and lineage tracing but has not been identified in other types of metaplasia, such as squamous metaplasia. A hallmark of metaplasia is a change in cellular identity, and this process can be regulated by transcription factors that initiate and/or maintain cellular identity, perhaps in concert with epigenetic reprogramming. Universally, metaplasia is a precursor to low-grade dysplasia, which can culminate in high-grade dysplasia and carcinoma. Improved clinical screening for and surveillance of metaplasia might lead to better prevention or early detection of dysplasia and cancer.

    更新日期:2017-09-14
  • Targeting neoantigens to augment antitumour immunity
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-24
    Mark Yarchoan, Burles A. Johnson, Eric R. Lutz, Daniel A. Laheru, Elizabeth M. Jaffee

    Targeting neoantigens to augment antitumour immunity Nature Reviews Cancer, Published online: 24 August 2017; doi:10.1038/nrc.2017.74

    更新日期:2017-09-14
  • Metastasis: Throwing oil into the flames
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-24
    Ulrike Harjes

    Metastasis: Throwing oil into the flames Nature Reviews Cancer, Published online: 24 August 2017; doi:10.1038/nrc.2017.76 Both obesity and systemic inflammation promote cancer progression, although how obesity-associated inflammation affects cancer metastasis is poorly understood. Quail et al. now show that obesity induces cytokines that stimulate lung neutrophilia in mice, thereby promoting breast cancer metastasis.

    更新日期:2017-09-14
  • Evolutionary biology of high-risk multiple myeloma
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-24
    Charlotte Pawlyn, Gareth J. Morgan

    The outcomes for the majority of patients with myeloma have improved over recent decades, driven by treatment advances. However, there is a subset of patients considered to have high-risk disease who have not benefited. Understanding how high-risk disease evolves from more therapeutically tractable stages is crucial if we are to improve outcomes. This can be accomplished by identifying the genetic mechanisms and mutations driving the transition of a normal plasma cell to one with the features of the following disease stages: monoclonal gammopathy of undetermined significance, smouldering myeloma, myeloma and plasma cell leukaemia. Although myeloma initiating events are clonal, subsequent driver lesions often occur in a subclone of cells, facilitating progression by Darwinian selection processes. Understanding the co-evolution of the clones within their microenvironment will be crucial for therapeutically manipulating the process. The end stage of progression is the generation of a state associated with treatment resistance, increased proliferation, evasion of apoptosis and an ability to grow independently of the bone marrow microenvironment. In this Review, we discuss these end-stage high-risk disease states and how new information is improving our understanding of their evolutionary trajectories, how they may be diagnosed and the biological behaviour that must be addressed if they are to be treated effectively.

    更新日期:2017-09-14
  • Immunotherapy: Searching in the immune checkpoint black box
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-24
    M. Teresa Villanueva

    Immunotherapy: Searching in the immune checkpoint black box Nature Reviews Cancer, Published online: 24 August 2017; doi:10.1038/nrc.2017.75 Reporting in Nature, the team led by Haining has identified that deletion of Ptpn2, among other genes, in tumour cells makes them more susceptible to PD1 inhibitors.

    更新日期:2017-09-14
  • Therapy-related myeloid neoplasms: when genetics and environment collide
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-24
    Megan E. McNerney, Lucy A. Godley, Michelle M. Le Beau

    Therapy-related myeloid neoplasms (t-MN) arise as a late effect of chemotherapy and/or radiation administered for a primary condition, typically a malignant disease, solid organ transplant or autoimmune disease. Survival is measured in months, not years, making t-MN one of the most aggressive and lethal cancers. In this Review, we discuss recent developments that reframe our understanding of the genetic and environmental aetiology of t-MN. Emerging data are illuminating who is at highest risk of developing t-MN, why t-MN are chemoresistant and how we may use this information to treat and ultimately prevent this lethal disease.

    更新日期:2017-09-14
  • Therapeutic resistance: Ironing it out
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-11
    Ulrike Harjes

    Since mesenchymal-like properties in cancer cells are often associated with therapy resistance, Viswanathan et al. explored vulnerabilities of these cells. They identified an enzyme of the lipid peroxidase pathway, inhibition of which caused ferroptosis in a range of cancer types.

    更新日期:2017-08-24
  • Tumour evolution: Metastasis takes a different route
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-11
    Anna Dart

    A new study has looked at the evolutionary origins of lymphatic and distant metastases in human colorectal cancer and found that, in most cases, cancer spread to lymph nodes is not a precursor for seeding of cancer cells to other organs.

    更新日期:2017-08-24
  • Targeting autophagy in cancer
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-28
    Jean M. Mulcahy Levy, Christina G. Towers, Andrew Thorburn

    Autophagy is a mechanism by which cellular material is delivered to lysosomes for degradation, leading to the basal turnover of cell components and providing energy and macromolecular precursors. Autophagy has opposing, context-dependent roles in cancer, and interventions to both stimulate and inhibit autophagy have been proposed as cancer therapies. This has led to the therapeutic targeting of autophagy in cancer to be sometimes viewed as controversial. In this Review, we suggest a way forwards for the effective targeting of autophagy by understanding the context-dependent roles of autophagy and by capitalizing on modern approaches to clinical trial design.

    更新日期:2017-08-24
  • Unravelling biology and shifting paradigms in cancer with single-cell sequencing
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-24
    Timour Baslan, James Hicks

    The fundamental operative unit of a cancer is the genetically and epigenetically innovative single cell. Whether proliferating or quiescent, in the primary tumour mass or disseminated elsewhere, single cells govern the parameters that dictate all facets of the biology of cancer. Thus, single-cell analyses provide

    更新日期:2017-08-24
  • Tumour evolution: Metastasis takes a different route
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-11
    Anna Dart

    A new study has looked at the evolutionary origins of lymphatic and distant metastases in human colorectal cancer and found that, in most cases, cancer spread to lymph nodes is not a precursor for seeding of cancer cells to other organs.

    更新日期:2017-08-11
  • Therapeutic resistance: Ironing it out
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-08-11
    Ulrike Harjes

    Since mesenchymal-like properties in cancer cells are often associated with therapy resistance, Viswanathan et al. explored vulnerabilities of these cells. They identified an enzyme of the lipid peroxidase pathway, inhibition of which caused ferroptosis in a range of cancer types.

    更新日期:2017-08-11
  • Therapeutic resistance: Transcribing patterns of resistance
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Sarah Seton-Rogers

    Shaffer et al. analysed resistance in melanoma at the single-cell level and found that non-genetic, transcriptional variability in rare cells can predict the eventual emergence of drug resistance.

    更新日期:2017-08-10
  • Pancreatic cancer: iExosomes target the 'undruggable'
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-06-30
    Conor A. Bradley

    Kamerkar et al. have engineered exosomes that target KRASG12D (iExosomes) and have demonstrated the specificity and efficacy of iExosomes in targeting oncogenic KRAS in mouse models of pancreatic cancer.

    更新日期:2017-08-10
  • Tumour vaccines: Personal training by vaccination
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Ulrike Harjes

    Two groups have shown that personalized, neoantigen-based tumour vaccines elicit effective T cell responses in patients with advanced melanoma, leading to favourable clinical outcomes. Combination with checkpoint blockade can be of additional benefit.

    更新日期:2017-08-10
  • Tumour immunology: Feeding frenzy
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Anna Dart

    Tumour cells are thought to avoid being phagocytosed through expression of the 'self' marker CD47, which ligates the macrophage receptor SIRPα. Alvey et al. investigated the potential of SIRPα-inhibited bone marrow-derived macrophages, primed with tumour-targeting antibodies, to clear tumours in vivo. Systemic injection

    更新日期:2017-08-10
  • Epigenetics: Tumour suppressive HIF2α
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Anna Dart

    Westerlund et al. found that combining the DNA demethylating drug 5-aza-deoxycytidine with the differentiation-promoting therapy retinoic acid inhibited tumour growth and prolonged survival in mouse xenograft models of high-risk neuroblastoma. This treatment resulted in high hypoxia-inducible factor 2α (HIF2α) levels but not HIF1α, and

    更新日期:2017-08-10
  • Immunotherapy: Keeping breast cancer in check
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-07
    Liesbet Lieben

    Nolan et al. show that triple-negative breast cancers with BRCA1 mutations are immunogenic and susceptible to treatment with a combination of two checkpoint inhibitors and chemotherapy.

    更新日期:2017-08-10
  • Leukaemia: Multiple origins of relapse
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Ulrike Harjes

    The origin of relapse in acute myeloid leukaemia (AML) is thought to be due to drug-promoted mutagenesis or to the selection of drug-resistant cells. Shlush et al. provide evidence for the latter and propose at least two distinct patterns of relapse in AML. In

    更新日期:2017-08-10
  • Tumour immunology: Tumours copy to escape
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Ulrike Harjes

    How tumours escape the immune system is not well defined. Nirschl et al. show that immune phagocytes in human melanoma share a physiological gene signature, which co-enriches and correlates with interferon-γ (IFNγ)-directed gene transcripts, and which is induced across multiple human cancers. Suppressor of

    更新日期:2017-08-10
  • Neuroblastoma: Tumours get super-enhanced
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Conor A. Bradley

    Van Groningen et al. unravel the epigenetic nature of intratumoural heterogeneity in neuroblastoma, which comprises both lineage-committed adrenergic cells and undifferentiated mesenchymal cells that are defined by unique super-enhancer transcriptional networks and gene expression signatures.

    更新日期:2017-08-10
  • Chemotherapy: Neutrophils deliver the goods
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    M. Teresa Villanueva

    Neutrophils carrying liposomes that contain the antimitotic drug paclitaxel can penetrate the brain and suppress the recurrence of glioma in mice, thereby significantly improving survival.

    更新日期:2017-08-10
  • Microenvironmental regulation of tumour angiogenesis
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-14
    Michele De Palma, Daniela Biziato, Tatiana V. Petrova

    Tumours display considerable variation in the patterning and properties of angiogenic blood vessels, as well as in their responses to anti-angiogenic therapy. Angiogenic programming of neoplastic tissue is a multidimensional process regulated by cancer cells in concert with a variety of tumour-associated stromal cells and their bioactive products, which encompass cytokines and growth factors, the extracellular matrix and secreted microvesicles. In this Review, we discuss the extrinsic regulation of angiogenesis by the tumour microenvironment, highlighting potential vulnerabilities that could be targeted to improve the applicability and reach of anti-angiogenic cancer therapies.

    更新日期:2017-08-10
  • Epigenetics: Therapy-induced transcription is cryptically widespread
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-14
    Darren J. Burgess

    A new study demonstrates that DNA methyltransferase inhibitors and histone deacetylase inhibitors induce widespread cryptic transcription from transposable elements that may contribute to cancer immunogenicity.

    更新日期:2017-08-10
  • Novel insights into mesothelioma biology and implications for therapy
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Timothy A. Yap, Joachim G. Aerts, Sanjay Popat, Dean A. Fennell

    Malignant mesothelioma is a universally lethal cancer that is increasing in incidence worldwide. There is a dearth of effective therapies, with only one treatment (pemetrexed and cisplatin combination chemotherapy) approved in the past 13 years. However, the past 5 years have witnessed an exponential growth in our understanding of mesothelioma pathobiology, which is set to revolutionize therapeutic strategies. From a genomic standpoint, mesothelioma is characterized by a preponderance of tumour suppressor alterations, for which novel therapies are currently in development. Other promising antitumour agents include inhibitors against angiogenesis, mesothelin and immune checkpoints, which are at various phases of clinical trial testing.

    更新日期:2017-08-10
  • Fragile sites in cancer: more than meets the eye
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-25
    Thomas W. Glover, Thomas E. Wilson, Martin F. Arlt

    Ever since initial suggestions that instability at common fragile sites (CFSs) could be responsible for chromosome rearrangements in cancers, CFSs and associated genes have been the subject of numerous studies, leading to questions and controversies about their role and importance in cancer. It is now

    更新日期:2017-08-10
  • Drugging the 'undruggable' cancer targets
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-06-23
    Chi V. Dang, E. Premkumar Reddy, Kevan M. Shokat, Laura Soucek

    The term 'undruggable' was coined to describe proteins that could not be targeted pharmacologically. However, progress is being made to 'drug' many of these targets, and therefore more appropriate terms might be 'difficult to drug' or 'yet to be drugged'. Many desirable targets in cancer

    更新日期:2017-08-10
  • Targeting autophagy in cancer
    Nat. Rev. Cancer (IF 37.147) Pub Date : 2017-07-28
    Jean M. Mulcahy Levy, Christina G. Towers, Andrew Thorburn

    Autophagy is a mechanism by which cellular material is delivered to lysosomes for degradation, leading to the basal turnover of cell components and providing energy and macromolecular precursors. Autophagy has opposing, context-dependent roles in cancer, and interventions to both stimulate and inhibit autophagy have been proposed as cancer therapies. This has led to the therapeutic targeting of autophagy in cancer to be sometimes viewed as controversial. In this Review, we suggest a way forwards for the effective targeting of autophagy by understanding the context-dependent roles of autophagy and by capitalizing on modern approaches to clinical trial design.

    更新日期:2017-08-10
Some contents have been Reproduced with permission of the American Chemical Society.
Some contents have been Reproduced by permission of The Royal Society of Chemistry.
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