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Stem, immune and nervous cells all forces for tumor progression

One of the difficulties for preventing the evolution of a tumor is that cancer progression can be promoted by undifferentiated or migrating cells whose states could follow different directions. At the 40th edition of Barcelona Biomed conferences at the Institute for Research in Biomedicine (IRB Barcelona), which took place from Nov. 27 to 29, 2023, and is entitled “Cancer in Context: Cellular, Tissue, and Organismal Determinants of Malignant Fates,” Angela Nieto presented her latest data on epithelial-to-mesenchymal transition (EMT).

Barcelona
Comunidad-autonoma-de-cataluna
Spain
Angela-nieto
Institute-for-research
Barcelona-biomed
Organismal-determinants
Malignant-fates
Epithelial-mesenchymal-transition
Emt
Colorectal-cancer
Brain-cancer

Cancer drug prevents EMT, metastasis and more

Blocking epithelial–mesenchymal transition (EMT) in tumours reduces their ability to give rise to metastases and sensitises the tumour cells to chemotherapy.

Bruxelles
Bruxelles-capitale
Belgium
France
Justine-lengrand
Cancer
Netris-pharma
Niversité-libre-de-bruxelles
Mt
Epithelial-mesenchymal-transition
Etrin-1

New insights into how aggressive cancer cells proliferate and propagate the disease

Not all cancer metastases have the same destructive effect. Researchers demonstrate different mechanisms in experiments.

Zurich
Züsz
Switzerland
Germany
Heidelberg
Baden-wüberg
Munich
Bayern
Danielle-ellis
Christina-scheel
Skin-cancer-center
Skin-cancer-center-at-ruhr-university-bochum

"A tEMTing target? Clinical and experimental evidence for epithelial-me" by Benjamin Genenger, Jay R. Perry et al.

Cutaneous squamous cell carcinoma (cSCC) is a disease with globally rising incidence and poor prognosis for patients with advanced or metastatic disease. Epithelial-mesenchymal transition (EMT) is a driver of metastasis in many carcinomas, and cSCC is no exception. We aimed to provide a systematic overview of the clinical and experimental evidence for EMT in cSCC, with critical appraisal of type and quality of the methodology used. We then used this information as rationale for potential drug targets against advanced and metastatic cSCC. All primary literature encompassing clinical and cell-based or xenograft experimental studies reporting on the role of EMT markers or related signalling pathways in the progression of cSCC were considered. A screen of 3443 search results yielded 86 eligible studies comprising 44 experimental studies, 22 clinical studies, and 20 studies integrating both. From the clinical studies a timeline illustrating the alteration of EMT markers and related signalli

Cutaneous-squamous-cell-carcinoma
Epithelial-mesenchymal-transition
Metastasis
Systematic-review
Targeted-therapy
Rokinase-plasminogen-activator-system
V-induced

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