Featured
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Article |
The genomic and transcriptomic architecture of 2,000 breast tumours reveals novel subgroups
Integrative analysis of copy number and gene expression in 2,000 primary breast tumours with long-term clinical follow-up revealed putative cis-acting driver genes, novel subgroups and trans-acting aberration hotspots that modulate subgroup-specific gene networks.
- Christina Curtis
- , Sohrab P. Shah
- & Samuel Aparicio
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Letter |
The clonal and mutational evolution spectrum of primary triple-negative breast cancers
Primary triple-negative breast cancers are shown to vary widely and continuously in the degree of clonal evolution and mutational content at the time of diagnosis, with implications for future studies of the disease.
- Sohrab P. Shah
- , Andrew Roth
- & Samuel Aparicio
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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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Research Highlights |
Drug drives cancer stem cells
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News & Views |
Reprogramming clinical outcome
On binding to its target hormone, the oestrogen-receptor protein modulates the expression of many genes. Changes in the receptor's interaction with DNA have now been linked to clinical outcome in patients with breast cancer. See Letter p.389
- Geneviève Deblois
- & Vincent Giguère
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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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Research Highlights |
Spoilers of chemotherapy
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Research Highlights |
Lifting the brakes on cancer
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News |
The computer will see you now
‘Computational pathologist’ diagnoses different grades of breast cancer.
- Heidi Ledford
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Research Highlights |
Gene signature links to drug target
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News |
Breast-cancer gene keeps DNA under wraps
BRCA1 mechanism may explain how other tumour suppressors work.
- Alla Katsnelson
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Letter |
Functional genomics reveal that the serine synthesis pathway is essential in breast cancer
- Richard Possemato
- , Kevin M. Marks
- & David M. Sabatini
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Research Highlights |
Breast-cancer weaknesses found
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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 & Views |
Macrophages limit chemotherapy
A major hurdle to successful cancer treatment is tumour resistance to chemotherapy. White blood cells called macrophages often infiltrate tumours in large numbers, and now appear to promote tumour chemoresistance.
- Michele De Palma
- & Claire E. Lewis
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News |
Fifty genome sequences reveal breast cancer's complexity
Decoding of ten trillion bases yields no simple patterns or silver bullets.
- Meredith Wadman
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Letter |
Tumour evolution inferred by single-cell sequencing
Although it is known that tumours are genetically heterogeneous it has so far been difficult to dissect this heterogeneity at a single cell level. This paper combines whole-genome amplification and next-generation sequencing of flow-sorted nuclei from breast tumours to investigate their population structure and evolution. In contrast to gradual models of tumour progression, the results indicate that tumours grow by punctuated clonal expansions with few persistent intermediates.
- Nicholas Navin
- , Jude Kendall
- & Michael Wigler
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Research Highlights |
Cyclin through drug resistance
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Article |
TRIM24 links a non-canonical histone signature to breast cancer
A crystal structure of the tandem PHD and bromodomain regions of the transcription and chromatin regulator TRIM24 reveals combinatorial recognition of dual marks on the histone H3 tail. TRIM24 is involved in activation of oestrogen-dependent genes and is aberrantly expressed in breast cancer.
- Wen-Wei Tsai
- , Zhanxin Wang
- & Michelle Craig Barton
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Technology Feature |
Interactome under construction
Developing techniques are helping researchers to build the protein interaction networks that underlie all cell functions.
- Laura Bonetta
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Research Highlights |
Cancer: Metabolic link to breast cancer
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Research Highlights |
Cancer biology: Tumours pave their own path
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News |
Bone-disease drug could treat breast cancer
Hormone therapy causes cancer through a molecule already implicated in osteoporosis.
- Ewen Callaway
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Letter |
RANK ligand mediates progestin-induced mammary epithelial proliferation and carcinogenesis
Progestins, used in hormone replacement therapy and contraceptives, have been suggested to promote the development of breast cancer. These authors show that the ability of progestins to induce mammary tumours in mouse models is mediated by RANKL (receptor activator of NF-KB ligand). Inhibition of RANKL could reduce tumorigenesis in hormone-induced and other mouse mammary gland tumour models, suggesting a new therapeutic approach.
- Eva Gonzalez-Suarez
- , Allison P. Jacob
- & William C. Dougall
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Letter |
Osteoclast differentiation factor RANKL controls development of progestin-driven mammary cancer
Progestins, used in contraceptives and hormone replacement therapy, have been linked to breast cancer. These authors provide a mechanistic basis for this association. They show in a mouse model that synthetic progestins can promote mammary tumour formation by inducing RANKL (receptor activator of NF-KB ligand), which acts on mammary epithelial cells through the RANKL receptor RANK.
- Daniel Schramek
- , Andreas Leibbrandt
- & Josef M. Penninger
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News |
Breast cancer protein is finally purified
Isolation of BRCA2 could help understanding of cancer risk and aid drug screening.
- Alla Katsnelson
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Research Highlights |
Cancer therapeutics: Nano tumour killer
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Letter |
Progesterone induces adult mammary stem cell expansion
Reproductive history influences breast cancer risk but the cellular mechanisms are unclear. Here it is shown that ovarian hormones regulate the size of the mammary stem cell pool in mice. The size of this pool increases when progesterone levels increase during the reproductive cycle. Progesterone probably regulates stem cell numbers through a paracrine mechanism involving induction of RANKL and Wnt in luminal cells.
- Purna A. Joshi
- , Hartland W. Jackson
- & Rama Khokha
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News & Views |
Cues from steroid hormones
The steroid hormones oestrogen and progesterone have a role in sickness and in health. In breast tissue, both roles probably work through a single mechanism: controlling the number and activity of mammary stem cells.
- John P. Lydon
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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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Letter |
Control of mammary stem cell function by steroid hormone signalling
The ovarian hormones oestrogen and progesterone increase breast cancer risk but the cellular mechanisms are unclear. Here it is shown that the size of the mammary stem cell pool in mice is regulated by steroid hormone signalling, although these cells lack the receptors for oestrogen and progesterone. The augmented pool could lead to clonal expansion of a mutated cell, possibly accounting for the increased incidence of breast cancer associated with pregnancy.
- Marie-Liesse Asselin-Labat
- , François Vaillant
- & Jane E. Visvader
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News |
Breast cancer gene patents judged invalid
Court ruling may spell bad news for biotech industry.
- Meredith Wadman
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News |
Lawsuit rekindles gene-patent debate
Criticism of exclusive licences puts university policies in the spotlight.
- Brendan Borrell