Publications by authors named "Anna Perdrix-Rosell"
Article Synopsis
- Cancer cells depend on their specific tumor microenvironment (TME) for growth, and the relationship between them has been a topic of inquiry, though it's unclear if this connection is established from the beginning or if cancer cells naturally dominate their environment over time.
- In a study, researchers altered the secretions of aggressive breast cancer cells to create a non-traditional TME, and although tumors initially formed, this atypical environment eventually hindered long-term cancer growth.
- The study revealed that this atypical TME led to the infiltration of macrophages with anti-tumor properties, which are linked to better outcomes in less aggressive breast cancers, indicating promising prognostic potential based on these genetic signatures.
Melanoma is a highly aggressive tumour that can metastasize very early in disease progression. Notably, melanoma can disseminate using amoeboid invasive strategies. We show here that high Myosin II activity, high levels of ki-67 and high tumour-initiating abilities are characteristic of invasive amoeboid melanoma cells.
View Article and Find Full Text PDFDespite substantial clinical benefit of targeted and immune checkpoint blockade-based therapies in melanoma, resistance inevitably develops. We show cytoskeletal remodeling and changes in expression and activity of ROCK-myosin II pathway during acquisition of resistance to MAPK inhibitors. MAPK regulates myosin II activity, but after initial therapy response, drug-resistant clones restore myosin II activity to increase survival.
View Article and Find Full Text PDFTriple-negative breast cancers (TNBCs) have poor prognosis and lack targeted therapies. Here we identified increased copy number and expression of the PIM1 proto-oncogene in genomic data sets of patients with TNBC. TNBC cells, but not nonmalignant mammary epithelial cells, were dependent on PIM1 for proliferation and protection from apoptosis.
View Article and Find Full Text PDFIn addition to its role in membrane abscission during cytokinesis, viral budding, endosomal sorting, and plasma membrane repair [1], the endosomal sorting complex required for transport-III (ESCRT-III) machinery has recently been shown to seal holes in the reforming nuclear envelope (NE) during mitotic exit [2, 3]. ESCRT-III also acts during interphase to repair the NE upon migration-induced rupture [4, 5], highlighting its key role as an orchestrator of membrane integrity at this organelle. While NE localization of ESCRT-III is dependent upon the ESCRT-III component CHMP7 [3], it is unclear how this complex is able to engage nuclear membranes.
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