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Approaching real-time terahertz imaging with photo-induced coded apertures and compressed sensing
Photo-induced coded-aperture imaging (PI-CAI) based on compressed sensing (CS) at 590 GHz using a WR-1.5 (500–750 GHz) vector network analyser is demonstrated. For a 256-pixel (16 × 16) frame, the acquisition time can be reduced by 40%, as compared with PI-CAI without CS, while maintaining high imaging quality. On the basis of this approach, it is envisioned that real-time (26 fps) THz imaging with 1000 pixels (32 × 32) can be realised using high-speed digital micromirror device chipsets and optimised data-acquisition software.
Journal Article
Matrix viscoelasticity controls spatiotemporal tissue organization
Biomolecular and physical cues of the extracellular matrix environment regulate collective cell dynamics and tissue patterning. Nonetheless, how the viscoelastic properties of the matrix regulate collective cell spatial and temporal organization is not fully understood. Here we show that the passive viscoelastic properties of the matrix encapsulating a spheroidal tissue of breast epithelial cells guide tissue proliferation in space and in time. Matrix viscoelasticity prompts symmetry breaking of the spheroid, leading to the formation of invading finger-like protrusions, YAP nuclear translocation and epithelial-to-mesenchymal transition both in vitro and in vivo in a Arp2/3-complex-dependent manner. Computational modelling of these observations allows us to establish a phase diagram relating morphological stability with matrix viscoelasticity, tissue viscosity, cell motility and cell division rate, which is experimentally validated by biochemical assays and in vitro experiments with an intestinal organoid. Altogether, this work highlights the role of stress relaxation mechanisms in tissue growth dynamics, a fundamental process in morphogenesis and oncogenesis.Viscoelasticity is a universal mechanical feature of the extracellular matrix. Here the authors show that the extracellular matrix viscoelasticity guides tissue growth and symmetry breaking, a fundamental process in morphogenesis and oncogenesis.
Journal Article
Epigenetic analysis leads to identification of HNF1B as a subtype-specific susceptibility gene for ovarian cancer
HNF1B is overexpressed in clear cell epithelial ovarian cancer, and we observed epigenetic silencing in serous epithelial ovarian cancer, leading us to hypothesize that variation in this gene differentially associates with epithelial ovarian cancer risk according to histological subtype. Here we comprehensively map variation in
HNF1B
with respect to epithelial ovarian cancer risk and analyse DNA methylation and expression profiles across histological subtypes. Different single-nucleotide polymorphisms associate with invasive serous (rs7405776 odds ratio (OR)=1.13,
P
=3.1 × 10
−10
) and clear cell (rs11651755 OR=0.77,
P
=1.6 × 10
−8
) epithelial ovarian cancer. Risk alleles for the serous subtype associate with higher
HNF1B
-promoter methylation in these tumours. Unmethylated, expressed
HNF1B
, primarily present in clear cell tumours, coincides with a CpG island methylator phenotype affecting numerous other promoters throughout the genome. Different variants in
HNF1B
associate with risk of serous and clear cell epithelial ovarian cancer; DNA methylation and expression patterns are also notably distinct between these subtypes. These findings underscore distinct mechanisms driving different epithelial ovarian cancer histological subtypes.
HNF1B is overexpressed in the clear cell subtype and epigenetically silenced in the serous subtype of ovarian cancer. Pearce and colleagues now show that genetic variants in HNF1B are differentially associated with risks of developing these two cancer subtypes, possibly through an epigenetic mechanism.
Journal Article
TIMPs: versatile extracellular regulators in cancer
Key Points
Tissue inhibitors of metalloproteinases (TIMPs) control diverse metalloproteinases and their wide range of substrates, regulating tissue homeostasis.
TIMPs are tightly involved in the development of most cancer hallmarks.
TIMP-regulated proteolytic processing affects major signalling pathways.
TIMP genetic models suggest TIMPs have a role in adult stem cell niches.
TIMP1 and TIMP3 have contrasting correlations with prognosis in human cancers: TIMP1 increase and TIMP3 reduction indicate poor prognosis.
TIMPs have the potential to function as biomarkers in patient body fluids.
The four tissue inhibitors of metalloproteinases (TIMPs) regulate proteolysis of a vast range of matrix and cell surface proteins, affecting tumour architecture and cell signalling. This Review article analyses the role of TIMPs in cancer and their potential as targets and biomarkers.
A compelling long-term goal of cancer biology is to understand the crucial players during tumorigenesis in order to develop new interventions. Here, we review how the four non-redundant tissue inhibitors of metalloproteinases (TIMPs) regulate the pericellular proteolysis of a vast range of matrix and cell surface proteins, generating simultaneous effects on tumour architecture and cell signalling. Experimental studies demonstrate the contribution of TIMPs to the majority of cancer hallmarks, and human cancers invariably show TIMP deregulation in the tumour or stroma. Of the four TIMPs, TIMP1 overexpression or TIMP3 silencing is consistently associated with cancer progression or poor patient prognosis. Future efforts will align mouse model systems with changes in TIMPs in patients, will delineate protease-independent TIMP function, will pinpoint therapeutic targets within the TIMP–metalloproteinase–substrate network and will use TIMPs in liquid biopsy samples as biomarkers for cancer prognosis.
Journal Article
Identification and molecular characterization of a new ovarian cancer susceptibility locus at 17q21.31
Epithelial ovarian cancer (EOC) has a heritable component that remains to be fully characterized. Most identified common susceptibility variants lie in non-protein-coding sequences. We hypothesized that variants in the 3′ untranslated region at putative microRNA (miRNA)-binding sites represent functional targets that influence EOC susceptibility. Here, we evaluate the association between 767 miRNA-related single-nucleotide polymorphisms (miRSNPs) and EOC risk in 18,174 EOC cases and 26,134 controls from 43 studies genotyped through the Collaborative Oncological Gene–environment Study. We identify several miRSNPs associated with invasive serous EOC risk (odds ratio=1.12,
P
=10
−8
) mapping to an inversion polymorphism at 17q21.31. Additional genotyping of non-miRSNPs at 17q21.31 reveals stronger signals outside the inversion (
P
=10
−10
). Variation at 17q21.31 is associated with neurological diseases, and our collaboration is the first to report an association with EOC susceptibility. An integrated molecular analysis in this region provides evidence for
ARHGAP27
and
PLEKHM1
as candidate EOC susceptibility genes.
Most confirmed susceptibility variants for epithelial ovarian cancer lie in non-protein-coding sequences. Here Permuth-Wey and colleagues investigate variants in 3′ untranslated regions (UTRs) and uncover a new susceptibility locus.
Journal Article