Matrix metalloproteases and epithelial-to-mesenchymal transition: Implications for carcinoma metastasis

The epithelial to mesenchymal transition (EMT) is characterized by the loss of epithelial characteristics and the gain of mesenchymal attributes in epithelial cells. It has been associated with physiological and pathological processes requiring epithelial cell migration and invasion. Initially, EMT was observed in embryological and adult development with many well characterized examples including the conversions of epiblast to primary mesenchyme (gastrulation), somite to sderotome, somite to dermis, myotome to migratory myoblast, dorsal neural tube to neural crest, placodal ectoderm to cranial ganglion precursor, intermediate mesoderm to nephric mesenchyme, lateral mesoderm to connective/muscular tissue, endocardium to cardiac cushion mesenchyme and trophectoderm invasion.[1],[2] In addition, evidence is mounting to support an important role of EMT pathways in the progression of carcinoma to metastasis providing epithelial tumour cells with the ability to migrate, invade the surrounding stroma and disseminate in secondary organs.[3]–[5

Matrix Metalloproteases and Epithelia-to-mesenchymal transition: implications for carcinoma metastasis.

The epithelial to mesenchymal transition (EMT) is characterized by the loss of epithelial characteristics and the gain of mesenchymal attributes in epithelial cells. It has been associated with physiological and pathological processes requiring epithelial cell migration and invasion. Initially, EMT was observed in embryological and adult development with many well characterized examples including the conversions of epiblast to primary mesenchyme (gastrulation), somite to sderotome, somite to dermis, myotome to migratory myoblast, dorsal neural tube to neural crest, placodal ectoderm to cranial ganglion precursor, intermediate mesoderm to nephric mesenchyme, lateral mesoderm to connective/muscular tissue, endocardium to cardiac cushion mesenchyme and trophectoderm invasion.[1],[2] In addition, evidence is mounting to support an important role of EMT pathways in the progression of carcinoma to metastasis providing epithelial tumour cells with the ability to migrate, invade the surrounding stroma and disseminate in secondary organs.[3]–[5

Report from Working Group 2: Higgs Physics at the HL-LHC and HE-LHC

The discovery of the Higgs boson in 2012, by the ATLAS and CMS experiments, was a success achieved with only a percent of the entire dataset foreseen for the LHC. It opened a landscape of possibilities in the study of Higgs boson properties, Electroweak Symmetry breaking and the Standard Model in general, as well as new avenues in probing new physics beyond the Standard Model. Six years after the discovery, with a conspicuously larger dataset collected during LHC Run 2 at a 13 TeV centre-of-mass energy, the theory and experimental particle physics communities have started a meticulous exploration of the potential for precision measurements of its properties. This includes studies of Higgs boson production and decays processes, the search for rare decays and production modes, high energy observables, and searches for an extended electroweak symmetry breaking sector. This report summarises the potential reach and opportunities in Higgs physics during the High Luminosity phase of the LHC, with an expected dataset of pp collisions at 14 TeV, corresponding to an integrated luminosity of 3~ab$^{-1}$. These studies are performed in light of the most recent analyses from LHC collaborations and the latest theoretical developments. The potential of an LHC upgrade, colliding protons at a centre-of-mass energy of 27 TeV and producing a dataset corresponding to an integrated luminosity of 15~ab$^{-1}$, is also discussed