Featured
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Letter |
The evolutionary history of lethal metastatic prostate cancer
The subclonal composition of human prostate tumours and their metastases has been mapped by whole-genome sequencing, thus establishing the evolutionary trees behind the development and spread of these cancers; an important observation was that metastases could be re-seeded multiple times, and spread from one tumour to another was frequently seen.
- Gunes Gundem
- , Peter Van Loo
- & G. Steven Bova
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Letter |
IL-17-producing γδ T cells and neutrophils conspire to promote breast cancer metastasis
Tumours maximize their chance of metastasizing by evoking a systemic inflammatory cascade in mouse models of spontaneous breast cancer metastasis.
- Seth B. Coffelt
- , Kelly Kersten
- & Karin E. de Visser
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Letter |
Therapy-induced tumour secretomes promote resistance and tumour progression
Tumour cells respond to an effective, targeted drug treatment with BRAF, ALK or EGFR kinase inhibitors by inducing a complex network of secreted signals that promote tumour growth, dissemination and metastasis of drug-resistant cancer cell clones, and increase the survival of drug-sensitive tumour cells, potentially contributing to incomplete tumour regression.
- Anna C. Obenauf
- , Yilong Zou
- & Joan Massagué
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Letter |
Metastasis-suppressor transcript destabilization through TARBP2 binding of mRNA hairpins
Linear sequence elements within messenger RNAs are known to be targeted by regulatory factors such as microRNAs for degradation, a process that has been implicated in disease; now, non-linear regulatory structural elements within mRNAs are shown also to be targeted, with the resulting mRNA destabilization mediating breast cancer metastasis.
- Hani Goodarzi
- , Steven Zhang
- & Sohail F. Tavazoie
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Outlook |
Biology: Three known unknowns
Even as cancer therapies improve, basic questions about drug resistance, tumour spread and the role of normal tissue remain unanswered.
- Katherine Bourzac
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Outlook |
Mechanics: The forces of cancer
The way cells physically interact with each other and their environment could help researchers understand the invasion and metastasis of solid tumours.
- Erika Jonietz
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Research Highlights |
Pathway from breast to bone
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Letter |
SHARP1 suppresses breast cancer metastasis by promoting degradation of hypoxia-inducible factors
SHARP1, which is itself regulated by the p63 metastasis suppressor, regulates the invasive and metastatic phenotype in triple-negative breast cancer (TNBC) through inhibition of hypoxia-inducible factors, and this process operates independently from oxygen levels.
- Marco Montagner
- , Elena Enzo
- & Stefano Piccolo
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Letter |
RNA sequencing of pancreatic circulating tumour cells implicates WNT signalling in metastasis
A new method allows the collection of circulating tumour cells (CTCs) despite their rarity; transcriptome sequencing of CTCs could allow identification of pathways involved in metastasis.
- Min Yu
- , David T. Ting
- & Daniel A. Haber
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Outlook |
Perspective: The right trials
The system for clinical trials must be redesigned if there is to be a decline in breast cancer metastasis, argues Patricia S. Steeg.
- Patricia S. Steeg
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Outlook |
Metastasis: The rude awakening
If detected early, most cases of breast cancer seem to be curable. But the tumour's deadly offspring could be sleeping in the body.
- Jocelyn Rice
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Letter |
Deleted in colorectal carcinoma suppresses metastasis in p53-deficient mammary tumours
In a mouse model of mammary carcinoma, loss of deleted in colorectal cancer (DCC) promotes metastasis formation, and in cell cultures derived from p53-deficient mouse mammary tumours DCC expression controls netrin-1-dependent cell survival, supporting the function of DCC as a context-dependent tumour suppressor that limits survival of disseminated tumour cells.
- Paul Krimpenfort
- , Ji-Ying Song
- & Anton Berns
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News & Views |
Evolution after tumour spread
A genetic study of brain cancers in mice and humans reveals distinct mutations in primary tumours and their metastases, suggesting that the two disease 'compartments' may require different treatments.
- Steven C. Clifford
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Research Highlights |
Tumour cells lend a hand
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Letter |
A microRNA regulon that mediates endothelial recruitment and metastasis by cancer cells
The microRNA miR-126 suppresses the formation of breast cancer metastases via the suppression of several novel pro-angiogenic genes that cooperate in the recruitment of endothelial cells, leading to the formation of metastatic colonies.
- Kim J. Png
- , Nils Halberg
- & Sohail F. Tavazoie
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Letter |
Interactions between cancer stem cells and their niche govern metastatic colonization
For the initiation of metastasis, there must be a small population of cancer stem cells at the secondary site and, to maintain this population and allow proliferation, infiltrating cancer cells must induce the expression of stromal periostin.
- Ilaria Malanchi
- , Albert Santamaria-Martínez
- & Joerg Huelsken
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Research Highlights |
Tissues stretch to let tumours move
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Research Highlights |
When push comes to shove in cancer
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Letter |
CCL2 recruits inflammatory monocytes to facilitate breast-tumour metastasis
- Bin-Zhi Qian
- , Jiufeng Li
- & Jeffrey W. Pollard
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Research Highlights |
Immune cells promote metastasis
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News |
Cancer theory faces doubts
A leading explanation for how disease migrates falls short on clinical evidence.
- Heidi Ledford
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Letter |
The patterns and dynamics of genomic instability in metastatic pancreatic cancer
Pancreatic cancer is highly aggressive, usually because of widespread metastasis. Here, next-generation DNA sequencing has been used to detect genomic rearrangements in 13 patients with pancreatic cancer and to explore clonal relationships among metastases. The results reveal not only considerable inter-patient heterogeneity, but also ongoing genomic instability and evolution during the development of metastases.
- Peter J. Campbell
- , Shinichi Yachida
- & P. Andrew Futreal
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Letter |
Distant metastasis occurs late during the genetic evolution of pancreatic cancer
Here, whole-genome sequencing has been used to analyse primary pancreatic tumours and one or more metastases from the same patients. The findings show that tumours are composed of several geographically distinct subclones, and allow maps to be produced showing how metastatic cancer clones evolve within the primary tumour. Moreover, a quantitative analysis of the timing of the genetic evolution of pancreatic cancer has been performed.
- Shinichi Yachida
- , Siân Jones
- & Christine A. Iacobuzio-Donahue
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Letter |
TAp63 suppresses metastasis through coordinate regulation of Dicer and miRNAs
The aberrant expression of microRNAs and of the enzymes that control their processing has been reported in tumours, but the mechanisms involved are not clear. It is now shown that TAp63, a member of the p53 family of tumour suppressors, suppresses tumorigeneis and metastasis by directly controlling the expression of Dicer (a microRNA-processing enzyme) and Dicer-regulated microRNAs.
- Xiaohua Su
- , Deepavali Chakravarti
- & Elsa R. Flores
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Letter |
Human melanoma-initiating cells express neural crest nerve growth factor receptor CD271
In this work, the neural crest stem cell marker CD271 is implicated as a cancer stem cell marker, allowing identification and prospective isolation of melanoma cancer stem cells.
- Alexander D. Boiko
- , Olga V. Razorenova
- & Irving L. Weissman
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Letter |
Migrastatin analogues target fascin to block tumour metastasis
Analogues of migrastatin — a natural product secreted by Streptomyces — are potent inhibitors of tumour cell migration and metastasis. Here, the underlying mechanism is elucidated: these migrastatin analogues target and inhibit the activity of the actin-bundling protein fascin. Hence proteins such as fascin might present new molecular targets for cancer treatments.
- Lin Chen
- , Shengyu Yang
- & Xin-Yun Huang
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Letter |
Long non-coding RNA HOTAIR reprograms chromatin state to promote cancer metastasis
Large intervening non-coding RNAs (lincRNAs) are pervasively transcribed in the genome. Here it is shown that lincRNAs in the HOX genetic loci are dysregulated during breast cancer progression in human cells, and that expression levels of the lincRNA called HOTAIR can predict whether a tumour will metastasize. Moreover, enforced expression of HOTAIR can lead to altered patterns of binding of the PRC2 protein to the genome.
- Rajnish A. Gupta
- , Nilay Shah
- & Howard Y. Chang
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Article |
Genome remodelling in a basal-like breast cancer metastasis and xenograft
Massively parallel DNA sequencing allows entire genomes to be screened for genetic changes associated with tumour progression. Here, the genomes of four DNA samples from a 44-year-old African-American patient with basal-like breast cancer were analysed. The samples came from peripheral blood, the primary tumour, a brain metastasis and a xenograft derived from the primary tumour. The findings indicate that cells with a distinct subset of the primary tumour mutation might be selected during metastasis and xenografting.
- Li Ding
- , Matthew J. Ellis
- & Elaine R. Mardis
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News & Views |
Genomics of metastasis
Cancer cells that invade other parts of the body do so by accumulating genomic aberrations. Analysis of the genomic differences between primary and metastatic tumours should aid the understanding of this process.
- Joe Gray
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Research Highlights |
Cancer biology: Cellular battering ram