Please use this identifier to cite or link to this item: http://hdl.handle.net/10889/11463
Title: Mutant KRAS promotes malignant pleural effusion formation
Other Titles: -
Authors: Agalioti, Theodora
Giannou, Anastasios
Krontira, Anthi
Kanellakis, Nikolaos
Kati, Danai
Vreka, Malamati
Pepe, Mario
Spella, Magda
Lilis, Ioannis
Zazara, Dimitra
Nikolouli, Eirini
Spiropoulou, Nikolitsa
Papadakis, Andreas
Papadia, Konstantina
Voulgaridis, Apostolos
Stamou, Panagiota
Meiners, Silke
Eickelberg, Oliver
Snyder, Linda
Antimisiaris, Sophia
Kardamakis, Dimitrios
Psallidas, Ioannis
Marazioti, Antonia
Stathopoulos, Georgios
Keywords: Malignant pleural effusion
Mutant KRAS
CCL2
Keywords (translated): Κακοήθης υπεζωκοτική συλλογή
Source: Nature communications
Abstract: Malignant pleural effusion (MPE) is the lethal consequence of various human cancers metastatic to the pleural cavity. However, the mechanisms responsible for the development of MPE are still obscure. Here we show that mutant KRAS is important for MPE induction in mice. Pleural disseminated, mutant KRAS bearing tumour cells upregulate and systemically release chemokine ligand 2 (CCL2) into the bloodstream to mobilize myeloid cells from the host bone marrow to the pleural space via the spleen. These cells promote MPE formation, as indicated by splenectomy and splenocyte restoration experiments. In addition, KRAS mutations are frequently detected in human MPE and cell lines isolated thereof, but are often lost during automated analyses, as indicated by manual versus automated examination of Sanger sequencing traces. Finally, the novel KRAS inhibitor deltarasin and a monoclonal antibody directed against CCL2 are equally effective against an experimental mouse model of MPE, a result that holds promise for future efficient therapies against the human condition.
Abstract (translated): --
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