2,058 results match your criteria Nature Reviews Cancer [Journal]


Extrachromosomal oncogene amplification in tumour pathogenesis and evolution.

Nat Rev Cancer 2019 Mar 14. Epub 2019 Mar 14.

Ludwig Institute for Cancer Research, San Diego, La Jolla, CA, USA.

Recent reports have demonstrated that oncogene amplification on extrachromosomal DNA (ecDNA) is a frequent event in cancer, providing new momentum to explore a phenomenon first discovered several decades ago. The direct consequence of ecDNA gains in these cases is an increase in DNA copy number of the oncogenes residing on the extrachromosomal element. A secondary effect, perhaps even more important, is that the unequal segregation of ecDNA from a parental tumour cell to offspring cells rapidly increases tumour heterogeneity, thus providing the tumour with an additional array of responses to microenvironment-induced and therapy-induced stress factors and perhaps providing an evolutionary advantage. Read More

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http://www.nature.com/articles/s41568-019-0128-6
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http://dx.doi.org/10.1038/s41568-019-0128-6DOI Listing
March 2019
1 Read

To be (immunosuppressive) or not to be.

Nat Rev Cancer 2019 Mar 12. Epub 2019 Mar 12.

Senior Editor, Nature Communications, .

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http://dx.doi.org/10.1038/s41568-019-0130-zDOI Listing

Host tissue determinants of tumour immunity.

Nat Rev Cancer 2019 Mar 12. Epub 2019 Mar 12.

Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Although common evolutionary principles drive the growth of cancer cells regardless of the tissue of origin, the microenvironment in which tumours arise substantially differs across various organ sites. Recent studies have established that, in addition to cell-intrinsic effects, tumour growth regulation also depends on local cues driven by tissue environmental factors. In this Review, we discuss how tissue-specific determinants might influence tumour development and argue that unravelling the tissue-specific contribution to tumour immunity should help the development of precise immunotherapeutic strategies for patients with cancer. Read More

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http://dx.doi.org/10.1038/s41568-019-0125-9DOI Listing

States of exhaustion.

Authors:
Ulrike Harjes

Nat Rev Cancer 2019 Mar 7. Epub 2019 Mar 7.

Nature Reviews Cancer, .

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http://www.nature.com/articles/s41568-019-0129-5
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http://dx.doi.org/10.1038/s41568-019-0129-5DOI Listing
March 2019
6 Reads

Diverging inflammasome signals in tumorigenesis and potential targeting.

Nat Rev Cancer 2019 Mar 6. Epub 2019 Mar 6.

Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN, USA.

Inflammasomes are molecular platforms that assemble upon sensing various intracellular stimuli. Inflammasome assembly leads to activation of caspase 1, thereby promoting the secretion of bioactive interleukin-1β (IL-1β) and IL-18 and inducing an inflammatory cell death called pyroptosis. Effectors of the inflammasome efficiently drive an immune response, primarily providing protection against microbial infections and mediating control over sterile insults. Read More

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http://www.nature.com/articles/s41568-019-0123-y
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March 2019
1 Read

Engineering advanced cancer therapies with synthetic biology.

Nat Rev Cancer 2019 Mar 5. Epub 2019 Mar 5.

Synthetic Biology Group, Research Laboratory of Electronics, Massachusetts Institute of Technology, Cambridge, MA, USA.

Engineered immune-cell-based cancer therapies have demonstrated robust efficacy in B cell malignancies, but challenges such as the lack of ideal targetable tumour antigens, tumour-mediated immunosuppression and severe toxicity still hinder their therapeutic efficacy and broad applicability. Synthetic biology can be used to overcome these challenges and create more robust, effective adaptive therapies that enable the specific targeting of cancer cells while sparing healthy cells. In this Progress article, we review recently developed gene circuit therapies for cancer using immune cells, nucleic acids and bacteria as chassis. Read More

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http://dx.doi.org/10.1038/s41568-019-0121-0DOI Listing
March 2019
5 Reads

Embedding a positive research culture that fosters innovation.

Nat Rev Cancer 2019 Feb 28. Epub 2019 Feb 28.

Cancer Research UK, Angel Building, London, UK.

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http://www.nature.com/articles/s41568-019-0127-7
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February 2019
1 Read

The mechanics of tumour formation.

Nat Rev Cancer 2019 Feb 26. Epub 2019 Feb 26.

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-019-0124-xDOI Listing
February 2019

Adapting to change.

Authors:
Ulrike Harjes

Nat Rev Cancer 2019 Feb 25. Epub 2019 Feb 25.

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-019-0126-8DOI Listing
February 2019
2 Reads

Microbiota and immune cell interplay.

Authors:
Anna Dart

Nat Rev Cancer 2019 Feb 19. Epub 2019 Feb 19.

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-019-0122-zDOI Listing
February 2019
1 Read

The evolving landscape of biomarkers for checkpoint inhibitor immunotherapy.

Nat Rev Cancer 2019 Mar;19(3):133-150

Human Oncology and Pathogenesis Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.

Checkpoint inhibitor-based immunotherapies that target cytotoxic T lymphocyte antigen 4 (CTLA4) or the programmed cell death 1 (PD1) pathway have achieved impressive success in the treatment of different cancer types. Yet, only a subset of patients derive clinical benefit. It is thus critical to understand the determinants driving response, resistance and adverse effects. Read More

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http://dx.doi.org/10.1038/s41568-019-0116-xDOI Listing
March 2019
2 Reads

Shaping a Nature Reviews Cancer article.

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Nat Rev Cancer 2019 Mar;19(3):121

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http://www.nature.com/articles/s41568-019-0120-1
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March 2019
3 Reads

Targeting endovascular progenitors controls cancer.

Authors:
Jordan Hindson

Nat Rev Cancer 2019 Mar;19(3):128-129

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-019-0119-7DOI Listing
March 2019
1 Read

Epigenetic therapy in immune-oncology.

Nat Rev Cancer 2019 Mar;19(3):151-161

Princess Margaret Cancer Centre, University Health Network (UHN), Toronto, Ontario, Canada.

DNA methylation inhibitors have become the mainstay for treatment of certain haematological malignancies. In addition to their abilities to reactivate genes, including tumour suppressors, that have acquired DNA methylation during carcinogenesis, they induce the expression of thousands of transposable elements including endogenous retroviruses and latent cancer testis antigens normally silenced by DNA methylation in most somatic cells. This results in a state of viral mimicry in which treated cells mount an innate immune response by turning on viral defence genes and potentially expressing neoantigens. Read More

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http://dx.doi.org/10.1038/s41568-019-0109-9DOI Listing
March 2019
1 Read

Senolytic helpers.

Authors:
Ulrike Harjes

Nat Rev Cancer 2019 Mar;19(3):128-129

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-019-0115-yDOI Listing
March 2019
2 Reads

Methylated clusters.

Authors:
Anna Dart

Nat Rev Cancer 2019 Mar;19(3):125

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-019-0114-zDOI Listing
March 2019
3 Reads

Glioblastoma is 'hot' for personalized vaccines.

Nat Rev Cancer 2019 Mar;19(3):129

Senior Editor, Nature Communications, .

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http://dx.doi.org/10.1038/s41568-019-0118-8DOI Listing
March 2019
6 Reads

Unmasking cancer cell character.

Nat Rev Cancer 2019 Mar;19(3):130

Senior Editor, Nature Reviews Drug Discovery, .

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http://www.nature.com/articles/s41568-019-0117-9
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March 2019
5 Reads

Author Correction: Every step of the way: integrins in cancer progression and metastasis.

Nat Rev Cancer 2019 Mar;19(3):179

Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.

In the originally published article, pertuzumab was incorrectly described as an anti-PI3K therapy in the section 'Integrins in anticancer therapy'. The sentence should read 'In mouse mammary tumour models, increased collagen levels and increased β1 integrin and SRC activity have been demonstrated to accompany, and promote, combined resistance to anti-human epidermal growth factor receptor 2 (HER2; also known as ERBB2) (trastuzumab and pertuzumab) and anti-PI3K (buparlisib) therapies164.' This has now been corrected in all versions of the original article. Read More

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http://www.nature.com/articles/s41568-019-0112-1
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March 2019
6 Reads

Author Correction: Cancer in wildlife: patterns of emergence.

Nat Rev Cancer 2019 Jan 31. Epub 2019 Jan 31.

Department of Pathology, Microbiology, and Immunology, School of Veterinary Medicine, University of California, Davis, CA, USA.

In the originally published article, the aetiology of the single case of B cell lymphoma found in the Mountain gorilla was incorrectly referred to as Gibbon lymphocryptovirus 1 in Table 1. The correct aetiology is Gbb lymphocryptovirus 1. This has now been corrected in both the html and PDF versions of the article. Read More

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http://www.nature.com/articles/s41568-019-0113-0
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January 2019
5 Reads

Immune control by amino acid catabolism during tumorigenesis and therapy.

Nat Rev Cancer 2019 Mar;19(3):162-175

Institute of Cellular Medicine, Faculty of Medical Sciences, Framlington Place, Newcastle University, Newcastle-upon-Tyne, UK.

Immune checkpoints arise from physiological changes during tumorigenesis that reprogramme inflammatory, immunological and metabolic processes in malignant lesions and local lymphoid tissues, which constitute the immunological tumour microenvironment (TME). Improving clinical responses to immune checkpoint blockade will require deeper understanding of factors that impact local immune balance in the TME. Elevated catabolism of the amino acids tryptophan (Trp) and arginine (Arg) is a common TME hallmark at clinical presentation of cancer. Read More

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http://www.nature.com/articles/s41568-019-0106-z
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March 2019
13 Reads

Trafficking signals for metastasis.

Nat Rev Cancer 2019 Mar;19(3):127

Nature Reviews Cancer, .

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http://www.nature.com/articles/s41568-019-0111-2
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March 2019
9 Reads

The global cancer burden: necessity is the mother of prevention.

Nat Rev Cancer 2019 Mar;19(3):123-124

International Agency for Research on Cancer, Lyon, France.

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http://www.nature.com/articles/s41568-019-0110-3
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March 2019
9 Reads

Organoid 2.0.

Authors:
Anna Dart

Nat Rev Cancer 2019 Mar;19(3):126-127

Nature Reviews Cancer, .

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http://www.nature.com/articles/s41568-019-0108-x
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March 2019
6 Reads

Rare ribosomopathies: insights into mechanisms of cancer.

Nat Rev Cancer 2019 Jan 22. Epub 2019 Jan 22.

Department of Biochemistry and Molecular Genetics, University of Louisville, Louisville, KY, USA.

Long thought to be too big and too ubiquitous to fail, we now know that human cells can fail to make sufficient amounts of ribosomes, causing a number of diseases collectively known as ribosomopathies. The best characterized ribosomopathies, with the exception of Treacher Collins syndrome, are inherited bone marrow failure syndromes, each of which has a marked increase in cancer predisposition relative to the general population. Although rare, emerging data reveal that the inherited bone marrow failure syndromes may be underdiagnosed on the basis of classical symptomology, leaving undiagnosed patients with these syndromes at an elevated risk of cancer without adequate counselling and surveillance. Read More

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http://dx.doi.org/10.1038/s41568-019-0105-0DOI Listing
January 2019
6 Reads

Publisher Correction: Expanding the search.

Authors:
Anna Dart

Nat Rev Cancer 2019 Feb;19(2):119

Nature Reviews Cancer, .

The originally published Research Highlight incorrectly credited the image. The correct credit line should read Dennis Hallinan/Alamy Stock Photo. This has now been corrected in all versions of the original article. Read More

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http://www.nature.com/articles/s41568-019-0107-y
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February 2019
5 Reads

Fasting in oncology: a word of caution.

Nat Rev Cancer 2019 Mar;19(3):177

Medical Oncology Unit, Fondazione IRCCS Policlinico San Matteo and Department of Internal Medicine, University of Pavia, Pavia, Italy.

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http://dx.doi.org/10.1038/s41568-018-0098-0DOI Listing
March 2019
4 Reads

Reply to 'Fasting in oncology: a word of caution'.

Nat Rev Cancer 2019 Mar;19(3):178

IFOM, FIRC Institute of Molecular Oncology, Milano, Italy.

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http://dx.doi.org/10.1038/s41568-018-0100-xDOI Listing
March 2019
14 Reads

Modelling cancer in microfluidic human organs-on-chips.

Nat Rev Cancer 2019 Feb;19(2):65-81

Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA, USA.

One of the problems that has slowed the development and approval of new anticancer therapies is the lack of preclinical models that can be used to identify key molecular, cellular and biophysical features of human cancer progression. This is because most in vitro cancer models fail to faithfully recapitulate the local tissue and organ microenvironment in which tumours form, which substantially contributes to the complex pathophysiology of the disease. More complex in vitro cancer models have been developed, including transwell cell cultures, spheroids and organoids grown within flexible extracellular matrix gels, which better mimic normal and cancerous tissue development than cells maintained on conventional 2D substrates. Read More

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http://dx.doi.org/10.1038/s41568-018-0104-6DOI Listing
February 2019
6 Reads

Get to know your epigenetic target.

Nat Rev Cancer 2019 Feb;19(2):62-63

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0103-7DOI Listing
February 2019
3 Reads

Expanding the search.

Authors:
Anna Dart

Nat Rev Cancer 2019 Mar;19(3):126-127

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0101-9DOI Listing
March 2019
2 Reads

Maintaining the tumour's diet.

Authors:
Ulrike Harjes

Nat Rev Cancer 2019 Feb;19(2):62-63

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0097-1DOI Listing
February 2019
7 Reads

Therapeutically exploiting STAT3 activity in cancer - using tissue repair as a road map.

Nat Rev Cancer 2019 Feb;19(2):82-96

Olivia Newton-John Cancer Research Institute and La Trobe University School of Cancer Medicine, Heidelberg, Victoria, Australia.

The tightly orchestrated temporal and spatial control of signal transducer and activator of transcription 3 (STAT3) activity in epithelial, immune and stromal cells is critical for wound healing and tissue repair. Excessive STAT3 activation within cancer cells and cells of the tumour microenvironment can be viewed as a neoplastic mimic of an inflammation-driven repair response that collectively promotes tumour progression. In addition to the canonical transcriptional pathways by which STAT3 promotes stem cell-like characteristics, survival, proliferation, metastatic potential and immune evasion, cytoplasmic STAT3 activity fuels tumour growth by metabolic and other non-transcriptional mechanisms. Read More

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http://dx.doi.org/10.1038/s41568-018-0090-8DOI Listing
February 2019
2 Reads

Genomic evolution of cancer models: perils and opportunities.

Nat Rev Cancer 2019 Feb;19(2):97-109

Broad Institute of Harvard and MIT, Cambridge, MA, USA.

Cancer research relies on model systems, which reflect the biology of actual human tumours to only a certain extent. One important feature of human cancer is its intra-tumour genomic heterogeneity and instability. However, the extent of such genomic instability in cancer models has received limited attention in research. Read More

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http://www.nature.com/articles/s41568-018-0095-3
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February 2019
25 Reads

Your genomic inheritance matters.

Nat Rev Cancer 2019 Feb;19(2):63

Senior Editor, Nature Communications, .

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http://dx.doi.org/10.1038/s41568-018-0099-zDOI Listing
February 2019
6 Reads

Checkpoint ahead - be prepared to stop!

Authors:
Anna Dart

Nat Rev Cancer 2019 Feb;19(2):61

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0096-2DOI Listing
February 2019
2 Reads

Radiation promotes systemic responses.

Authors:
Jordan Hindson

Nat Rev Cancer 2019 Jan;19(1):4-5

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0094-4DOI Listing
January 2019
2 Reads

Regulatory networks in AML.

Nat Rev Cancer 2019 Jan;19(1):6-7

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0092-6DOI Listing
January 2019
2 Reads

Immunosuppressive lymphatics.

Authors:
Anna Dart

Nat Rev Cancer 2019 Jan;19(1):6-7

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0091-7DOI Listing
January 2019
2 Reads

Post-GWAS in prostate cancer: from genetic association to biological contribution.

Nat Rev Cancer 2019 Jan;19(1):46-59

Cancer Program, School of Biomedical Sciences, Institute of Health and Biomedical Innovation, Queensland University of Technology, Brisbane, Queensland, Australia.

Genome-wide association studies (GWAS) have been successful in deciphering the genetic component of predisposition to many human complex diseases including prostate cancer. Germline variants identified by GWAS progressively unravelled the substantial knowledge gap concerning prostate cancer heritability. With the beginning of the post-GWAS era, more and more studies reveal that, in addition to their value as risk markers, germline variants can exert active roles in prostate oncogenesis. Read More

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http://dx.doi.org/10.1038/s41568-018-0087-3DOI Listing
January 2019
2 Reads
37.400 Impact Factor

The lung microenvironment: an important regulator of tumour growth and metastasis.

Nat Rev Cancer 2019 Jan;19(1):9-31

Department of Cardiothoracic Surgery, Weill Cornell Medicine, New York, NY, USA.

Lung cancer is a major global health problem, as it is the leading cause of cancer-related deaths worldwide. Major advances in the identification of key mutational alterations have led to the development of molecularly targeted therapies, whose efficacy has been limited by emergence of resistance mechanisms. US Food and Drug Administration (FDA)-approved therapies targeting angiogenesis and more recently immune checkpoints have reinvigorated enthusiasm in elucidating the prognostic and pathophysiological roles of the tumour microenvironment in lung cancer. Read More

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http://dx.doi.org/10.1038/s41568-018-0081-9DOI Listing
January 2019
5 Reads

A year of ups and downs.

Authors:

Nat Rev Cancer 2019 Jan;19(1)

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http://dx.doi.org/10.1038/s41568-018-0093-5DOI Listing
January 2019
2 Reads

Cytokinesis defects and cancer.

Nat Rev Cancer 2019 Jan;19(1):32-45

Oncode Institute, Utrecht, Netherlands.

Whole-genome and centrosome duplication as a consequence of cytokinesis failure can drive tumorigenesis in experimental model systems. However, whether cytokinesis failure is in fact an important cause of human cancers has remained unclear. In this Review, we summarize evidence that whole-genome-doubling events are frequently observed in human cancers and discuss the contribution that cytokinesis defects can make to tumorigenesis. Read More

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http://dx.doi.org/10.1038/s41568-018-0084-6DOI Listing
January 2019
2 Reads

A source of calcium.

Authors:
Ulrike Harjes

Nat Rev Cancer 2019 Jan;19(1)

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0089-1DOI Listing
January 2019
2 Reads

Cancer chromatin accessed.

Nat Rev Cancer 2019 Jan;19(1)

Nature Communications, .

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http://dx.doi.org/10.1038/s41568-018-0088-2DOI Listing
January 2019
1 Read

Cooperation among cancer cells: applying game theory to cancer.

Nat Rev Cancer 2019 Feb;19(2):110-117

Brady Urological Institute, Johns Hopkins School of Medicine, Baltimore, MD, USA.

Cell cooperation promotes many of the hallmarks of cancer via the secretion of diffusible factors that can affect cancer cells or stromal cells in the tumour microenvironment. This cooperation cannot be explained simply as the collective action of cells for the benefit of the tumour because non-cooperative subclones can constantly invade and free-ride on the diffusible factors produced by the cooperative cells. A full understanding of cooperation among the cells of a tumour requires methods and concepts from evolutionary game theory, which has been used successfully in other areas of biology to understand similar problems but has been underutilized in cancer research. Read More

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http://dx.doi.org/10.1038/s41568-018-0083-7DOI Listing
February 2019
2 Reads

Dividing paths in fatty liver disease.

Authors:
Ulrike Harjes

Nat Rev Cancer 2019 Jan;19(1)

Nature Reviews Cancer, .

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http://www.nature.com/articles/s41568-018-0086-4
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January 2019
12 Reads

N-mA marks the spot.

Authors:
Anna Dart

Nat Rev Cancer 2019 Jan;19(1):4-5

Nature Reviews Cancer, .

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http://www.nature.com/articles/s41568-018-0085-5
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January 2019
9 Reads

Stress management in T cells.

Authors:
Ulrike Harjes

Nat Rev Cancer 2018 Dec;18(12):724-725

Nature Reviews Cancer, .

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http://dx.doi.org/10.1038/s41568-018-0082-8DOI Listing
December 2018
2 Reads

mTOR signalling and cellular metabolism are mutual determinants in cancer.

Nat Rev Cancer 2018 Dec;18(12):744-757

Biozentrum, University of Basel, Basel, Switzerland.

Oncogenic signalling and metabolic alterations are interrelated in cancer cells. mTOR, which is frequently activated in cancer, controls cell growth and metabolism. mTOR signalling regulates amino acid, glucose, nucleotide, fatty acid and lipid metabolism. Read More

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http://www.nature.com/articles/s41568-018-0074-8
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http://dx.doi.org/10.1038/s41568-018-0074-8DOI Listing
December 2018
32 Reads